Veins and arteries meet at roam

Circulatory system and the heart (video) | Khan Academy

veins and arteries meet at roam

Arteries carry blood [ away from / toward ] the heart. Veins carry Veins and arteries meet at ___capillaries__, where nutrients are exchanged with body tissues. meet specific demands in physiological and pathological situations throughout Markers preferentially expressed by EC from arteries and veins. recruitment, and roaming of putative endothelial progenitor cells (EPC). Taking Shape by GONSOFUS, released 26 April 1. Too Good 2. Like It Hot 3. Love In My Soul 4. Veter (Wind) 5. Music Takes You Higher 6. No Se Vaya 7.

In this sense, some organs present their primary vascularisation focused exclusively on vasculogenesis such as the lung, while other organs such as the kidneys are vascularised by both vasculogenesis and angiogenesis.

Indeed, it is proposed that embryonic leaflets are associated with distinct neovascularisation processes, where organs from endodermal origin are vascularised by vasculogenesis and ectodermal organs by angiogenesis [ 81 ]. In a pathological context, vasculogenesis is important during tumoural development, especially when angiogenesis is inhibited by antitumoural therapies. An increase in circulating EPC populations has been shown in patients with cancer, suggesting a possible role of vasculogenesis during tumoural neovascularisation [ 82 ].

Furthermore, several studies have been showing a correlation between the reduction of EPC and worsening of reendothelialisation in injured vessels, metabolic diseases, diabetes, atherosclerosis, and endothelial dysfunction [ 83 ]. Angiogenesis Angiogenesis, differently from vasculogenesis, is the process by which new blood vessels are formed from preexisting vessels.

It is relevant in both physiological and pathological conditions, occurring by two different mechanisms: Sprouting angiogenesis is the formation of new blood vessels in response to proangiogenic factors and involves retraction of pericytes, migration, and proliferation of EC that give origin to branches with a lumen, which are stabilised by pericyte recruitment and deposition of a new basement membrane [ 84 ].

This process is initiated by tissue hypoxia and it is seen occurring in physiological processes such as embryonic development, particularly important for the vascular network expansion initially formed by the vasculogenesis, in the wound healing process, during ischaemic tissue vascularisation, and in pathological conditions, such as solid tumours formation, eye diseases, and inflammatory disorders as rheumatoid arthritis and psoriasis [ 85 — 88 ].

In turn, intussusception angiogenesis consists in the repeated insertion of new, slender, transcapillary tissue pillars, which increase in size and allow capillary network growth [ 89 ]. This angiogenesis type is more efficient compared to sprouting since it only requires a reorganisation of EC without initial cell migration and proliferation, being, therefore, an economic process of neovascularisation regarding metabolic and energetic demands. Intussusception occurs throughout life but is more significant during vascular development in embryos; however it also may occur from preexistent capillaries and the current methods for their evaluation remain failed and expensive, which limits the advances and knowledge about this type of angiogenesis [ 9091 ].

The existence of these two types of angiogenesis suggests a form of heterogeneity regarding the cells, factors, and stimulus among them. In addition, the preference for one or another process indicates the importance of each type of angiogenesis in a particular condition or stage of embryonic development. Despite this hypothesis, more studies are necessary to address the factors and conditions determining the heterogeneity during sprouting and intussusceptive angiogenesis in different blood-organ barriers and tissues.

Angiogenesis process is controlled by a range of angiogenic stimulators and inhibitors, on a way that the balance of these factors maintains the turnover of endothelial cells. However, under conditions such as reduced pO2, low pH, hypoglycaemia, mechanic stress, inflammatory stimuli, and tumoural development, there is an increase of proangiogenic factors, inducing endothelial proliferation, and migration, triggering a so-called angiogenic switch [ 7492 ].

Pathological conditions induce the activation of different molecular pathways during angiogenesis when compared to physiological states. Mutations in oncogenes and tumour suppressor genes, and growth factor misbalanced activities are crucial to trigger pathological angiogenesis.

In sprouting angiogenesis, EC present three distinct phenotypes which play different roles in the sprouting vessel, named angiogenic tip, stalk, and phalanx cells. In relation to their morphology, tip cells show organised stress fibres with numerous probing filopodia that permit migrating toward angiogenic factors, but they do not form lumen and are minimally proliferative []. Stalk cells are seen behind tip cells and are highly proliferative, form lumens, and lay down extracellular matrix, but do not extend filopodia.

In addition, stalk cells show attenuated DLL-4 expression due to an inhibition promoted by NOTCH signalling from adjacent tip cells, while they present Ang-2 receptor and Tie-2, two components not present in tip cells [, ]. Phalanx cells are morphologically cobblestone-shaped and have lower migratory and proliferative capacities, but present high expression of VEGFR-1, which is responsible for interposing the proangiogenic effects of VEGF and keeping phalanx cells in a quiescent state, together with a high expression of VE-cadherin.

Thus, phalanx cells seem to respond to VEGF in a different way than tip cells []. Under physiological conditions, EC in the blood form a monolayer of phalanx cells interconnected by junctional molecules ensheathed by pericytes, which suppress EC proliferation. In sprouting angiogenesis, when proangiogenic signals such as VEGF, FGF, or chemokines are released by any of the aforementioned stimuli, pericytes detach and liberate themselves from the basement membrane by proteolytic degradation, mainly by MMP [ ].

At the same time, VEGF increases the permeability of the vessel and plasma proteins extravasate, forming a provisional extracellular matrix ECM on which EC migrate and initiate branch formation.

veins and arteries meet at roam

They are able to integrate attractive and repulsive directional cues presented by the microenvironment and define the route in which the new sprouts grow []. The proliferation of stalk cells is responsible by branch elongation, while tip cells direct the growth of the branch vessel by filopodia and lamellipodia []. Tip cell fusion and branch anastomosis are facilitated by macrophages that express angiopoietin receptor TIE-2, NRP1 receptor a specific receptor for semaphorinsand VEGF, acting to modulate intercellular adhesion [ ].

In addition, to support this idea, Fantin and colleagues [ ] demonstrated that macrophages expressing TIE-2 and NRP1 comprised the major population of tissue macrophages acting on brain vascularisation and they were able to interact with tip cells, promoting vascular anastomosis and indicating a new target to antiangiogenic therapies.

Finally, a lumen is formed by one of three processes: Mural cells such as pericytes and smooth muscle cells are recruited and promote stabilisation of the new vessel while parallel matrix deposition and specific vascular bed adaptations occur [, ]. In an intussusceptive angiogenesis process, the new blood vessel is formed from a preexisting vessel following an intraluminal pillar formation and interendothelial reorganisation.

Then, a central perforation is formed and pericytes and myofibroblasts stabilise the new vessel, a step followed by the joining and fusion with adjacent pillars and final division, giving rise to two vessels []. This process shows three main patterns of vascularisation: The intussusceptive angiogenesis mechanism is important to growth and vascular remodelling, besides being present in pathological contexts such as tumour development.

Few experimental models are available to study mechanisms, factors, and in which conditions intussusceptive angiogenesis occurs, since it is occurring in an intravascular compartment.

Meet the heart! - Circulatory system physiology - NCLEX-RN - Khan Academy

Therefore, the discovery of new experimental approaches is required to elucidate this neovascularisation process. De Paepe and colleagues [ ] described an aberrant nonsprouting angiogenesis in human fetal lung xenografts that was associated with bronchopulmonary dysplasia of preterm newborn BPD -associated dysangiogenesis.

In this situation, lungs are able to change vascular pattern formation from a sprouting phenotype to an intussusceptive phenotype, showing a linear and nonsprouting vasculature probably due a mechanism that includes IGF signalling dysregulation and hypoxia, not yet clarified. In addition, a proper formation of the pulmonary microvasculature seems to be necessary to the normal alveolar and lung development [ — ].

In addition to the heterogeneity of EC and angiogenic processes, in many conditions such as tumourigenesis, the formed vascular bed varies considerably depending on the type and site of the tumour. This heterogeneity could explain, at least in part, the resistance of some tumour types to antiangiogenic therapies [ ].

In general, the tumour vasculature is characterized by exacerbated angiogenesis and abnormal tortuous blood vessels, discontinuous EC, and scarce pericyte coverage, which favour the extravasation of tumour cells [ 73]. EC from tumours differ from healthy EC for a range of reasons, but mainly due to their expression of a subset of genes that could vary depending on tumour type, exhibition of a proangiogenic and stem-like phenotype, and chromosomal abnormalities [].

All these peculiarities contribute to the transformation of tumour angiogenesis in a complex process and, consequently, foment discussions about angiogenic modulation in relation to tissue heterogeneity, especially with respect to therapies and the advent of new imaging tools for diagnostic purposes.

It has already been observed that the density of the initial microvasculature in the primary tumour site is determinant to tumoural progression and further neovascularisation. In conclusion, angiogenesis is characterized by a heterogeneous and complex process which includes a range of factors worthy of being subject of studies for future applications. Furthermore, these complexities, especially regarding cellular and functional heterogeneity, allow greater understanding and provide subsidies for appropriate experimental design choices to test scientific hypotheses.

Arteriogenesis Arteriogenesis refers to the formation of collateral arterioles, allowing increased blood flow to tissues and being a crucial compensation mechanism to restore tissue perfusion where the main vascular pathway has been obstructed [ ].

In adults, arteriogenesis can occur in response to various stimuli, including changes in haemodynamic forces, such as shear stress, and in the metabolic demands of tissues, as in hypoxic conditions [ ].

For this reason, postnatal arteriogenesis plays an essential role in restoring blood supply in several pathological situations, in which the metabolic demand is greater than the amount of blood perfusing the tissue [].

The arteriogenic process may occur by two distinct mechanisms, de novo formation, or remodelling of preexisting collateral arterioles.

The first one involves the formation and expansion of new vessels from a preexisting arteriolar network, localised near to an occluded artery, reconnecting the distal arterial segment [ 26 ]. The second one involves the remodelling of preexisting vessels, promoting gradual enlargement of arterioles until they are able to increase blood flow and restore local perfusion [ ].

During embryonic development, de novo arteriogenesis consists in the differentiation and maturation of the primary vascular plexus, induced by the increase in blood pressure. The consequent increase in shear stress in the new capillary network stimulates local recruitment of smooth muscle cells and proliferation of endothelial cells, leading to the formation of mature arteries [ — ]. There is evidence that arteriogenesis by de novo formation can also happen in the adult; however, this issue remains controversial.

Some authors believe that the newly detected collaterals could be native collaterals not detected before remodelling or even preexistent capillaries that undergo arterialisation [ — ]. Nevertheless, the presence of new collateral arterioles was detected after acute arterial occlusion in murine brain [ ] and heart [ 26 ], as well as after apical resection in neonatal murine heart [ ]. Of note, these new collateral formations occurred in areas with apparent absence of preexisting connections.

In addition, one cannot rule out the possibility of remodelling occurrence not only in preexisting collaterals, but also in the presumed de novo formed arteriole to increase their calibre, making this discussion even more complex and difficult to address in vivo. Considering the difficulty to distinguish new arteriole formation from remodelling of preexistent ones, the mechanisms involved in de novo arteriogenesis remain poorly understood.

The augment of shear stress in the arterial tree along with tissue hypoxia generated by a major artery occlusion is believed to be the main trigger for the beginning of the de novo process [ 26]. While evidence about de novo arteriogenesis in adults is scarce, the dominant form of postnatal arteriogenesis appears to be largely dependent on the remodelling of preexistent collateral vessels [ ].

The postnatal collateral remodelling may be divided into three phases: When a major vessel occlusion promotes the drop-in of perfusion pressure at a distal point, this reduction leads to an increased flow through preexisting collateral arteries.

The resultant increased wall shear stress is the main trigger for the initiation phase of arteriogenesis [ ]. Shear stress activates the endothelium of collateral vessels. Activated endothelial cells, by their turn, stimulate the recruitment of local and bone marrow inflammatory cells, through the expression of chemokines as tumour necrosis factor TNFVEGF, and CCL-2 and adhesion molecules such as selectins, intercellular adhesion molecule 1 iCAM1and vascular adhesion molecule 1 vCAM1 [].

The early recruited inflammatory cells are neutrophils, which help to degrade extracellular matrix, enabling vessels to expand [ ]. The released CCL-2 chemokine, in turn, promotes the recruitment of circulating monocytes expressing the receptor CCR2 to the affected region [].

During the growth phase, the macrophages play an essential paracrine role, recruiting other bone marrow cells as well as modulating smooth muscle and endothelial cell proliferation.

In addition, macrophages modulate matrix remodelling by aiding on basement membrane degradation, through MMP-2 and MMP-9 secretion []. The inflammatory signalling cascades induce the differentiation of smooth muscle cells from a contractile phenotype to a synthetic phenotype. This differentiation is characterized by the downregulation of actin, myosin, desmin and calponin expression, and upregulation of fibronectin [ ].

The replacement of contractile material for endoplasmic reticulum and free ribosomes is also observed in smooth muscle cells []. SMC with this phenotype are directed to migration, proliferation, and production of a fibronectin-based transitional matrix [ ], essential for the remodelling process. The proliferation of smooth muscle and endothelial cells leads to collateral vessel luminal expansion and tortuous elongation.

As luminal diameter increases, distal perfusion is restored and blood flow resistance decreases, as well as shear stress. Finally, the collateral vessel passes through the maturation phase.

With the decline on shear stress, the endothelium function of collateral vessel normalises and the inflammatory response decreases, initiating inflammation resolution and reduction of cell proliferation, as well as the return of SMC to a contractile phenotype [ ]. At this point, the arterioles with lower resistance provide most of the blood flow and continue to remodel outward, stabilising and maturing into dominant collateral. At the same time, small collateral vessels that may not maintain sufficient hemodynamic stimulation undergo neointimal hyperplasia and eventual regression [].

Important signalling pathways associated with neovascularisation processes will be better discussed later in this manuscript. However, it is interesting to point out how some of these pathways can mediate distinct actions during arteriogenesis in different organs and tissues. The resultant NO production and release by EC exert an important vasodilatation effect, increasing the flow through collateral vessels and, thereby, possibly augmenting flow-induced remodelling [ ]. In addition, this axis activation is essential for sustained interactions of the endothelium with pericytes and vascular SMC, as well as maintenance of vascular stability [].

The pathway activation after ligation to delta-like ligand Dll from arterioles EC leads to perivascular macrophage maturation and antiinflammatory polarisation, improving collateral remodelling [ ]. On arterial occlusive diseases, such as peripheral artery disease, myocardial infarction, and ischaemic stroke, the restoration of blood flow to the affected tissue must be quick so its viability and function can be preserved. Collateral vessels can effectively bypass arterial obstructions and are more likely to induce effective reperfusion of tissues than proliferation of capillary network [ ].

However, the number of arteriolar collaterals was shown to vary widely among organs as heart, brain, and lower extremities, and even among individuals.

In fact, clinical outcome in patients with arterial occlusive diseases appears to be directly correlated to the number of preexistent collaterals in the affected area and their capacity of remodelling [].

It was shown that the arteriole network remodelling process also can negatively affect tissues extensively damaged by hypoxia. In ischaemic hindlimbs, the formation of new arterioles with an aberrantly smooth muscle cells cover was observed, presenting increased interprocess spacing and haphazard actin microfilament bundles [ ], which affected the restoration of blood perfusion effectiveness.

Interestingly, animal model studies have shown that even the speed of the arteriogenesis process may vary among different organs and tissues. For example, it was observed that the maximum remodelling of collaterals in murine ischaemic brain occurs up to 3 days after arterial occlusion [ ], significantly faster than in the ischaemic heart 3 to 7 days [ 26 ] and skeletal muscle 3 to 4 weeks [].

The reason for this difference still needs to be elucidated, but one hypothesis suggested is that specific tissue characteristics in the location adjacent to the collateral vessels can affect the time required for reorganisation of the surrounding matrix and cells before outward remodelling can proceed [ ].

In conclusion, arteriogenesis is a complex multifactorial process, stimulated by changes in the haemodynamic forces and in the metabolic demands, and is essential to restore the adequate blood supply to organs and tissues after acute or chronic major artery occlusion.

Understanding and clarifying the heterogeneity of mechanisms involved in this neovascularisation process are crucial to develop effective clinical approaches for many arterial obstructive diseases.

veins and arteries meet at roam

Lymphangiogenesis The lymphatic system is known for its primary function of draining fluids in the interstitial space, redirecting them to blood vessels. It is a drainage system, from and to which immune cells responsible for the defence of the organism may emerge and go [ ]. In addition to this function, it is active in other contexts, namely, in the regulation of blood pressure, in the differentiation and modulation of immune and inflammatory cells, in lipid metabolism, and in atherosclerosis and metastasis.

In turn, the physiological role of lymphatic vasculature is conditioned by other pathological events, such as obesity, chronic inflammation, and autoimmune diseases [ ]. Lymphatic vessels present a morphological heterogeneity, being, therefore, subdivided into capillaries and collectors. The capillaries are responsible for the absorption of the extravasated fluid, whereas the collectors are transporters.

With regard to the cellular morphology, capillaries are formed by button-type joints and collectors are made of the zipper types. In addition, lymphatic endothelial cells from capillaries are surrounded by dendritic cells, recruited by chemokines such as CCL, and expressing high levels of the lymphatic vessel endothelial receptor 1 LYVE-1in opposition to lymphatic EC from collectors [ ]. Lymphatic capillaries are formed after the establishment of blood vasculature in a process in which venous endothelial cells undergo lymphatic speciation by presenting markers of the lymphatic vasculature such as LYVE-1, prospero homeobox protein 1 PROX-1and VEGFR-3 [ ].

The mechanism by which new lymphatic vessels are formed is called lymphangiogenesis and, in the embryonic period, some veins present a lymphatic capacity when they present endothelial cells that express PROX-1, SOX, and LYVE At a later stage, they begin to express VEGFR-3 and, following a gradient concentration of VEGF-C, they migrate, proliferate, and form a primitive lymphatic sac, expressing new lymph markers and originating a lymphatic plexus where maturation and remodelling occur.

Cellular and Molecular Heterogeneity Associated with Vessel Formation Processes

Smooth muscle cells are recruited and form leaflets that allow the lymphatic vessel to become functional. The expansion of this vascular network occurs mainly by lymphangiogenesis, although in recent years the process of lymphovasculogenesis has been referred to as a possible process that occurs after the embryonic phase. In lymphovasculogenesis, the haemogenic endothelium produces haematopoietic stem cells HSC that will serve the new lymphatic vascular formation, similar to what occurs in the process of vasculogenesis [ ].

The main difference between lymphovasculogenesis and lymphangiogenesis is the origin of the cells that give rise to the vasculature. In the first context, the cells come from preexisting vessels, and in the second they are derived from the haemogenic endothelium or, as more recently discussed, from circulating progenitor cells that were transdifferentiated into lymphangioblasts, revealing heterogeneity in the cells that originated from lymphatic vessels [].

Although studies from already addressed the existence of circulating lymphatic progenitor cells, only more recently these reports become more usual. Lee and colleagues [ ] have demonstrated that bone marrow-derived cells expressing the protein podoplanin, characteristic of lymphatic vasculature, contributed to postnatal neovascularisation, indicating which progenitor cells could participate in lymphatic neoformation.

These authors characterized these cells immunophenotypically and demonstrated that they express lymphatic cell markers such as LYVE-1 and VEGFR-3, besides podoplanin when cultured in vitro. Likewise, when these cells were tested in vivo in cell therapy models, they incorporated the neoformed lymphatic vasculature in corneal, ear, skin, and tumour models, and continued to express the markers of lymphatic cells.

These findings open a promising field of study and provide new perspectives to the treatment of diseases that affect the lymphatic system. New approaches have been focused on determining markers, the origin, and niches for isolation of lymphatic precursor cells [ 21], on generating pure lymphatic endothelial cells from pluripotent stem cells and studying their effects on wound repair [ ], and on clarifying the mechanisms by which lymphatic endothelial precursor cells are mobilised in pathological and physiological contexts [ ].

Lymphangiogenesis occurs physiologically in restricted situations, such as during the embryonic period for expansion of the lymphatic network of the embryo, during female reproductive cycle, and in mammary gland genesis [ ].

In fact, lymphangiogenesis is more seen occurring in pathological conditions. Lymphatic vascular dysfunction can cause oedema formation, due to failed draining of the interstitial contents, or may contribute to the formation of new lymphatics that are associated with metastatic dissemination to distant lymph nodes and organs, and rejection of grafts. Lymphangiogenesis is also seen during obesity, since excess lymph in the interstitium leads to the production of proinflammatory cytokines and hypertrophy of adipocytes.

Lymphoedema is classically observed in the infectious disease filariasis, but also in some cardiovascular and genetic conditions [ ]. Similar to angiogenesis, this process involves three general steps, among which are the activation and migration of lymphatic endothelial cells, their proliferation, and lumen formation. In this case, the profile selection into either tip or stalk cells also occurs, although the factors and pathways coordinating it are not well defined as for angiogenesis.

Tip cells begin to migrate and emit filopodia, while stalk cells continue proliferating and allowing vessel elongation. Lumen formation occurs by intracellular vacuolisation and, finally, there is remodelling and maturation of the vessel [].

VEGF is also the main factor to stimulate lymphatic sprouting. Differently from sprouting angiogenesis, the NOTCH pathway is not active in lymphangiogenesis [ ].

Blood Vessels: Arteries, Capillaries & More

Lymphangiogenesis during inflammatory conditions is also mediated by VEGF. Inflammatory macrophages secrete large amounts of VEGF and stimulate local lymphatic sprouting, which aids in the supply of inflammatory cells and drainage of exudate.

It has also been argued that inflammatory macrophages could become incorporated into lymphatic vessels and transdifferentiate into lymphatic endothelial cells, but this hypothesis is not fully accepted by the scientific community [ ].

veins and arteries meet at roam

Some studies, however, have demonstrated the important role of macrophages in the formation of lymphatic vessels. They are named lymphangiogenic macrophages and, during inflammatory processes, they show direct and indirect effects on lymphangiogenesis. Direct effects were related to the production of prolymphangiogenic factors, and the indirect ones were attributed to their contribution to the mobilising of more macrophages from bone marrow and the amplifying of the immune response, further stimulating lymphangiogenesis.

In addition, the activation of Toll-like receptors TLR during inflammatory contexts leads to increased production of VEGF-C and -D by macrophages, inducing the proliferation of lymphatic endothelial cells [].

In a tumoural context, lymphangiogenesis is associated with tumour malignancy. Tumour lymphatic vessels as well as blood vessels are compromised. Tumour cells and tumour stroma release lymphangiogenic factors that increase the sprouting of lymphatic vessels, which are also essential for tumour progression. Tumour-associated macrophages can secrete lymphangiogenic factors as well as incorporation into the new lymphatic vasculature, contributing to lymphangiogenesis and dissemination of micrometastases and metastases to distant lymph nodes and organs [].

The interaction of tumour cells with lymphatic cells can be promoted by interstitial fluid resulting from lymphatic drainage via autologous chemotaxis involving the chemokine CCL and its receptor, CCR-7, expressed by tumour cells. The production of lymphangiogenic factors such as VEGF-C and -D stimulates the formation and enlargement of lymphatics in the vicinity of the tumour, increasing the surface area for interaction between the cells. VEGF-C also promotes the invasiveness of tumour cells in an autocrine manner and upregulates the production of CCL by lymphatic vessels [ ].

In view of this knowledge, as well as in angiogenesis, some therapeutic strategies involving the use of antilymphangiogenic agents and blocking of VEGF signalling have been proposed and studied to successfully inhibit tumour growth. Anti-VEGF and anti-VEGF-C monoclonal antibodies, as well as antibodies against specific parts of the VEGFR-2 receptor, were produced, yet there are no approved drugs able to only block lymphangiogenesis, which could benefit some pathologies that do not necessarily require the blocking of angiogenic processes [].

Cellular Heterogeneity and Blood-Organ Barriers Different processes of neovascularisation occur in response to a range of stimuli, factors, and mediators. Then as we go towards the heart from the lungs, we have a vein, but it's oxygenated. So that's this little loop here that we start and I'm going to keep going over the circulation pattern because the heart can get a little confusing, especially because of its three-dimensional nature.

But what we have is, the heart pumps de-oxygenated blood from the right ventricle. You're saying, hey, why is it the right ventricle? That looks like the left side of the drawing, but it's this dude's right-hand side, right? This is this guy's right hand. And this is this dude's left hand. He's looking at us, right? We don't care about our right or left. We care about this guy's right and left. And he's looking at us. He's got some eyeballs and he's looking at us. So this is his right ventricle.

Actually, let me just start off with the whole cycle. So we have de-oxygenated blood coming from the rest of the body, right? The name for this big pipe is called the inferior vena cava-- inferior because it's coming up below. Actually, you have blood coming up from the arms and the head up here. They're both meeting right here, in the right atrium. Let me label that. I'm going to do a big diagram of the heart in a second. And why are they de-oxygenated? Because this is blood returning from our legs if we're running, or returning from our brain, that had to use respiration-- or maybe we're working out and it's returning from our biceps, but it's de-oxygenated blood.

It shows up right here in the right atrium. It's on our left, but this guy's right-hand side. From the right atrium, it gets pumped into the right ventricle. It actually passively flows into the right ventricle. The ventricles do all the pumping, then the ventricle contracts and pumps this blood right here-- and you don't see it, but it's going behind this part right here.

It goes from here through this pipe. So you don't see it. I'm going to do a detailed diagram in a second-- into the pulmonary artery. We're going away from the heart. This was a vein, right? This is a vein going to the heart. This is a vein, inferior vena cava vein.

This is superior vena cava. Then I'm pumping this de-oxygenated blood away from the heart to the lungs. Now this de-oxygenated blood, this is in an artery, right? This is in the pulmonary artery. It gets oxygenated and now it's a pulmonary vein. And once it's oxygenated, it shows up here in the left-- let me do a better color than that-- it shows up right here in the left atrium. Atrium, you can imagine-- it's kind of a room with a skylight or that's open to the outside and in both of these cases, things are entering from above-- not sunlight, but blood is entering from above.

On the right atrium, the blood is entering from above. And in the left atrium, the blood is entering-- and remember, the left atrium is on the right-hand side from our point of view-- on the left atrium, the blood is entering from above from the lungs, from the pulmonary veins.

Veins go to the heart. Then it goes into-- and I'll go into more detail-- into the left ventricle and then the left ventricle pumps that oxygenated blood to the rest of the body via the non-pulmonary arteries. So everything pumps out. Let me make it a nice dark, non-blue color. So it pumps it out through there.

You don't see it right here, the way it's drawn. It's a little bit of a strange drawing. It's hard to visualize, but I'll show it in more detail and then it goes to the rest of the body. Let me show you that detail right now. So we said, we have de-oxygenated blood. Let's label it right here. This is the superior vena cava. This is a vein from the upper part of our body from our arms and heads.

This is the inferior vena vaca. This is veins from our abdomen and from our legs and the rest of our body. So it it first enters the right atrium. Remember, we call the right atrium because this is someone's heart facing us, even though this is on the left-hand side. It enters through here. It's coming from veins. Then it shows up in the right ventricle, right? These are valves in our heart. And it passively, once the right ventricle pumps and then releases, it has a vacuum and it pulls more blood from the right atrium.

It pumps again and then it pushes it through here. Now this blood right here-- remember, this one still is de-oxygenated blood. De-oxygenated blood goes to the lungs to become oxygenated. So this right here is the pulmonary-- I'm using the word pulmonary because it's going to or from the lungs. It's dealing with the lungs. And it's going away from the heart. It's the pulmonary artery and it is de-oxygenated.

Circulatory system and the heart

Then it goes to the heart, rubs up against some alveoli and then gets oxygenated and then it comes right back. Now this right here, we're going to the heart. So that's a vein. It's in the loop with the lungs so it's a pulmonary vein and it rubbed up against the alveoli and got the oxygen diffused into it so it is oxygenated. And then it flows into your left atrium.

Now, the left atrium, once again, from our point of view, is on the right-hand side, but from the dude looking at it, it's his left-hand side. So it goes into the left atrium. Now in the left ventricle, after it's done pumping, it expands and that oxygenated blood flows into the left ventricle. Then the left ventricle-- the ventricles are what do all the pumping-- it squeezes and then it pumps the blood into the aorta.

This is an artery. Why is it an artery? Because we're going away from the heart. Is it a pulmonary artery? No, we're not dealing with the lungs anymore. We dealt with the lungs when we went from the right ventricle, went to the lungs in a loop, back to the left atrium. Now we're in the left ventricle.