We are searching data for your request:
Upon completion, a link will appear to access the found materials.
From what I have read regarding blood pressure and blood flow, I've come to the conclusion that, apart from the osmolarity of blood, the only determinant of how much oxygen/nutrients the tissues get per unit time, is blood flow.
Does blood pressure (not systemic, but within a theoretical capillary) have absolutely no effect on this, and if so, why? Intuitively, it seems to me that if the force by blood on the walls of a capillary increases, that would imply a higher number of molecules touching endothelial cells, and thus a higher likelihood of molecule transport per unit time.
Or is it perhaps that they both have positive effects on oxygenation/nutrient transport; but blood flow's effect greatly excels that of blood pressure?
Does capillary blood pressure have any effect on how much oxygen or nutrient gets distributed to tissues? - Biology
The kidneys regulate the body’s osmotic pressure in mammals.
Explain how the kidneys serve as the main osmoregulatory organs in mammalian systems, using the functional properties of nephrons
- Kidneys regulate the osmotic pressure of a mammal’s blood through extensive filtration and purification, in a process known as osmoregulation.
- Kidneys filter the blood urine is the filtrate that eliminates waste from the body via the ureter into the bladder.
- The kidneys are surrounded by three layers: renal fascia, perirenal fat capsule, and the renal capsule.
Kidneys: The Main Osmoregulatory Organ
The kidneys are a pair of bean-shaped structures that are located just below and posterior to the liver in the peritoneal cavity. Adrenal glands, also called suprarenal glands, sit on top of each kidney. Kidneys regulate the osmotic pressure of a mammal’s blood through extensive filtration and purification in a process known as osmoregulation. All the blood in the human body is filtered many times a day by the kidneys. These organs use almost 25 percent of the oxygen absorbed through the lungs to perform this function. Oxygen allows the kidney cells to efficiently manufacture chemical energy in the form of ATP through aerobic respiration. Kidneys eliminate wastes from the body urine is the filtrate that exits the kidneys.
Kidneys’ location and function: Kidneys filter the blood, producing urine that is stored in the bladder prior to elimination through the urethra. They are located in the peritoneal cavity.
Externally, the kidneys are surrounded by three layers. The outermost layer, the renal fascia, is a tough connective tissue layer. The second layer, the perirenal fat capsule, helps anchor the kidneys in place. The third and innermost layer is the renal capsule. Internally, the kidney has three regions: an outer cortex, a medulla in the middle, and the renal pelvis in the region called the hilum of the kidney. The hilum is the concave part of the bean-shape where blood vessels and nerves enter and exit the kidney it is also the point of exit for the ureters.
Structure of the kidney: Externally, the kidney is surrounded by the renal fascia, the perirenal fat capsule, and the renal capsule. Internally, the kidney is most importantly filled with nephrons that filter blood and generate urine.
Because the kidney filters blood, its network of blood vessels is an important component of its structure and function. The arteries, veins, and nerves that supply the kidney enter and exit at the renal hilum. Renal blood supply starts with the branching of the aorta into the renal arteries (which are each named based on the region of the kidney they pass through) and ends with the exiting of the renal veins to join the inferior vena cava. The renal arteries split into several segmental arteries upon entering the kidneys. Each segmental artery splits further into several interlobar arteries that enter the renal columns, which supply the renal lobes. The interlobar arteries split at the junction of the renal cortex and medulla to form the arcuate arteries. The arcuate, “bow shaped” arteries form arcs along the base of the medullary pyramids. Cortical radiate arteries, as the name suggests, radiate out from the arcuate arteries, branch into numerous afferent arterioles, and then enter the capillaries supplying the nephrons.
31.4 Blood Flow and Blood Pressure Regulation
In this section, you will explore the following questions:
Connection for AP ® Courses
The information in this section is not within the scope for AP ® . However, the exchange of oxygen and carbon dioxide at capillary beds is an application of diffusion, a phenomenon we explored in detail in an earlier chapter. In addition, because many persons suffer from high blood pressure, often called the “silent killer,” you might find it informative to know how blood pressure is regulated and why lack of appropriate regulation is detrimental.
Blood pressure (BP) is the pressure exerted by blood on the walls of a blood vessel that helps to push blood through the body. Systolic blood pressure measures the amount of pressure that blood exerts on vessels while the heart is beating. The optimal systolic blood pressure is 120 mmHg. Diastolic blood pressure measures the pressure in the vessels between heartbeats. The optimal diastolic blood pressure is 80 mmHg. Many factors can affect blood pressure, such as hormones, stress, exercise, eating, sitting, and standing. Blood flow through the body is regulated by the size of blood vessels, by the action of smooth muscle, by one-way valves, and by the fluid pressure of the blood itself.
How Blood Flows Through the Body
Blood is pushed through the body by the action of the pumping heart. With each rhythmic pump, blood is pushed under high pressure and velocity away from the heart, initially along the main artery, the aorta. In the aorta, the blood travels at 30 cm/sec. As blood moves into the arteries, arterioles, and ultimately to the capillary beds, the rate of movement slows dramatically to about 0.026 cm/sec, one-thousand times slower than the rate of movement in the aorta. While the diameter of each individual arteriole and capillary is far narrower than the diameter of the aorta, and according to the law of continuity, fluid should travel faster through a narrower diameter tube, the rate is actually slower due to the overall diameter of all the combined capillaries being far greater than the diameter of the individual aorta.
The slow rate of travel through the capillary beds, which reach almost every cell in the body, assists with gas and nutrient exchange and also promotes the diffusion of fluid into the interstitial space. After the blood has passed through the capillary beds to the venules, veins, and finally to the main venae cavae, the rate of flow increases again but is still much slower than the initial rate in the aorta. Blood primarily moves in the veins by the rhythmic movement of smooth muscle in the vessel wall and by the action of the skeletal muscle as the body moves. Because most veins must move blood against the pull of gravity, blood is prevented from flowing backward in the veins by one-way valves. Because skeletal muscle contraction aids in venous blood flow, it is important to get up and move frequently after long periods of sitting so that blood will not pool in the extremities.
Blood flow through the capillary beds is regulated depending on the body’s needs and is directed by nerve and hormone signals. For example, after a large meal, most of the blood is diverted to the stomach by vasodilation of vessels of the digestive system and vasoconstriction of other vessels. During exercise, blood is diverted to the skeletal muscles through vasodilation while blood to the digestive system would be lessened through vasoconstriction. The blood entering some capillary beds is controlled by small muscles, called precapillary sphincters, illustrated in Figure 31.18. If the sphincters are open, the blood will flow into the associated branches of the capillary blood. If all of the sphincters are closed, then the blood will flow directly from the arteriole to the venule through the thoroughfare channel (see Figure 31.18). These muscles allow the body to precisely control when capillary beds receive blood flow. At any given moment only about 5-10% of our capillary beds actually have blood flowing through them.
Clinical Relevance – Carbon Monoxide Poisoning
Carbon Monoxide (CO) is a colourless, odourless gas that can be released from faulty boilers or combustion engines. Carbon Monoxide poisoning occurs when CO reacts with haemoglobin at the site of oxygen binding. Haemoglobin has an affinity for CO that is 210x greater than its affinity for oxygen. This means that once carbon monoxide binds to haemoglobin, it is irreversible.
Symptoms of CO poisoning are headache, nausea and tiredness, but interestingly, respiration rate is usually spared as the partial pressure of oxygen dissolved in the blood is maintained at normal levels. Haemoglobin bound to CO has a cherry-red colour and this may be visible in nails beds and mucous membranes of patients with CO poisoning. Treatment is with 100% oxygen and referral for hyperbaric oxygen treatment. CO poisoning is fatal when 70-80% of haemoglobin is bound with carbon monoxide.
Carbon Dioxide Expulsion
Your muscles produce more energy as skeletal movements and contractions increase during exercise. Carbon dioxide is a toxic byproduct of energy production in your muscles. Your circulation system has chemoreceptors that detect changes in oxygen and carbon dioxide concentrations in your blood. Chemoreceptors send signals to your brain that increase your respiration rate when they detect rising carbon dioxide levels. Your circulatory system's veins work harder circulating waste-rich blood back to your heart during exercise your heart contracts and pushes the blood into the pulmonary artery and your lungs absorb carbon dioxide from the pulmonary artery and expel the toxic gas from your body each time you exhale.
What Are the Coronary Arteries?
Like all organs, your heart is made of tissue that requires a supply of oxygen and nutrients. Although its chambers are full of blood, the heart receives no nourishment from this blood. The heart receives its own supply of blood from a network of arteries, called the coronary arteries.
Two major coronary arteries branch off from the aorta near the point where the aorta and the left ventricle meet:
- Right coronary artery supplies the right atrium and right ventricle with blood. It branches into the posterior descending artery, which supplies the bottom portion of the left ventricle and back of the septum with blood.
- Left main coronary artery branches into the circumflex artery and the left anterior descending artery. The circumflex artery supplies blood to the left atrium, as well as the side and back of the left ventricle. The left anterior descending artery supplies the front and bottom of the left ventricle and the front of the septum with blood.
These arteries and their branches supply all parts of the heart muscle with blood.
When the coronary arteries narrow to the point that blood flow to the heart muscle is limited (coronary artery disease), a network of tiny blood vessels in the heart that aren't usually open (called collateral vessels) may enlarge and become active. This allows blood to flow around the blocked artery to the heart muscle, protecting the heart tissue from injury.
Increased blood pressure reasonable?
My Kepler Bb humanoids have their arteries and veins doubled up(quadrupled if you are looking at the coronary arteries and veins). This makes sense because they have 2 hearts and both of those are 4 chambered hearts just like ours. If the arteries and veins weren't doubled up that would basically mean 1 8 chambered heart instead of 2 4 chambered hearts.
So since the 2 hearts are in sync with each other from embryonic development until a health problem affects 1 heart and the other heart compensates in response to it, it makes sense, to me at least that blood pressure would be increased even if left ventricular pressure stayed the same.
Assuming that the pressure-volume loop of the left ventricle and in fact all 4 chambers of the heart stayed as is, for the first few inches of aorta and the last few inches of venae cavae, the blood pressure would be the same. But most arteries and veins would not have the heart and their own muscular walls as the only sources of blood pressure.
You also have the fact that the arteries and veins are spaced so closely that they would push against each other as the hearts pump in or out of sync.
So the blood pressure in 1 artery would affect the blood pressure in the other artery. But lowering the blood pressure is just not feasible because the closer arterial pressure is to venous pressure, the less blood that flows and since less blood flow = less oxygen transport which is the exact opposite of why I doubled up most of the blood vessels in the first place(and quadrupled in the case of coronary arteries and veins), hypotension is just a no, regardless of how much it would lower pressure from arteries being next to each other.
So this leaves me with only 1 option I know of if I want to keep this double circulatory system. That is to raise the blood pressure in the arteries(so maybe what would be stage 1 hypertension for us would be normal blood pressure for my humanoids). This will increase blood flow because now there is more of a gradient between the arteries and veins. Bigger pressure gradient = more blood flow = more oxygen transport.
Since my humanoids naturally have a slower heart rate due to 2 hearts being in sync, this works well(at least I think it does). What is bradycardia for us is normal for them.
But would raising arterial blood pressure to increase blood flow despite the fact that now there is more force from each artery pushing on the artery next to it work to significantly increase oxygen transport(which is why I doubled things up(quadrupled for coronary))?
According to the Texas Heart Institute, the heart is a continuously pumping muscle&mdashmade of four chambers&mdashthat beats throughout a person&rsquos lifespan. The heart is essentially a pump that pushes oxygen-rich blood through arteries to tissues, organs and cells, according to the institute. Blood returns to the heart through venules, which are small blood vessels, and veins. Four valves regulate blood flow in the heart from both veins and arteries. The heart, therefore, is the main component of the cardiovascular system that ensures that all veins, capillaries and arteries receive the blood necessary to nourish cells.
The pressure of the blood flow in the body is produced by the hydrostatic pressure of the fluid (blood) against the walls of the blood vessels. Fluid will move from areas of high to low hydrostatic pressures. In the arteries, the hydrostatic pressure near the heart is very high and blood flows to the arterioles where the rate of flow is slowed by the narrow openings of the arterioles. During systole, when new blood is entering the arteries, the artery walls stretch to accommodate the increase of pressure of the extra blood during diastole, the walls return to normal because of their elastic properties. The blood pressure of the systole phase and the diastole phase, graphed in [link], gives the two pressure readings for blood pressure. For example, 120/80 indicates a reading of 120 mm Hg during the systole and 80 mm Hg during diastole. Throughout the cardiac cycle, the blood continues to empty into the arterioles at a relatively even rate. This resistance to blood flow is called peripheral resistance .
Glycans and Glycosaminoglycans as Clinical Biomarkers and Therapeutics - Part A
Alpha-fetoprotein (AFP) was identified as a new fraction of alpha globulins in human fetal serum by Bergstrand and Czar in 1956. 1 Abelev discovered that serum AFP was mainly produced by yolk sac endoderm and fetal liver in the embryo. The synthesis of AFP was also observed after partial hepatectomy in adult mice, in hepatoma-bearing mice, and in tissue culture of hepatoma. 2,3 In 1964, Tatarinov was the first one to report that serum AFP levels are elevated in the sera of liver cancer patients. 4
AFP and serum albumin belong to a large family of albumins. Moreover, the AFP and albumin genes are present in tandem in the same transcriptional orientation on chromosome 4. 5,6 The molecular biology studies showed that AFP consists of 591 amino acids and is modified with one N-glycan chain at the 232nd Asn residue. 7–10 AFP is an analog of serum albumin. 5 The role of the AFP primarily is to transport heavy metal ions and various insoluble molecules in fetus blood circulation, such as copper and nickel, fatty acids, bilirubin, and medications. 11
During fetal development, the embryonic hepatocytes are the main site for the synthesis of AFP followed by the yolk sac. The gastrointestinal mucosa from the endoderm can also produce AFP in small amount. From 6 weeks of gestation, AFP begins to be produced. The AFP content in the blood and urine of pregnant women continues to increase, which reaches a peak at 12–15 weeks. The AFP level in fetal plasma can be up to 3 mg/mL and then gradually decreases. The AFP level in umbilical cord blood at birth can reach to 10–100 mg/L. After birth, AFP synthesis is quickly inhibited and its content decreased to 50 μg/L. AFP level in the blood of infants is close to that of the adult by the age of 8–12 months. 12,13 Generally, the plasma AFP concentration in the male is slightly higher than that in the female. 14
Increased serum AFP levels have been approved and used as a clinical biomarker for liver cancer detection since 1980s. 11 When liver cancer occurs, the liver cells restore the function of producing AFP. As the disease progresses, serum AFP levels will increase sharply. 15,16 Before the onset of symptoms, AFP has gradually increased for many months in liver cancer patients. At that time, most of liver cancer patients have no obvious symptoms and the tumor sizes are relatively small. In general, increased serum AFP concentrations are considered to be reliable for the diagnosis of liver cancer. 17–19 Different cohort studies showed that increased serum AFP levels for detecting early liver cancer have the sensitivity ranging from 39% to 65% and the specificity ranging from 76% to 97%. 20,21
Early detection of liver cancer leads to improved survival however, the high false-negative rate makes the serum AFP level-based early detection strategies for liver cancer ineffective. To enhance the sensitivity and specificity of AFP as a biomarker, attention was turned to the different glycoforms of AFP as biomarkers since different cells make different N-glycan structures. The ground-breaking work was published by two independent research groups in 1981. 22,23 There are three major families of AFP glycoforms (AFP-L1, AFP-L2, and AFP-L3), which differ in their affinity for the Lens culinaris agglutinin (LCA), which recognizes fucosylated core region of bi- and triantennary complex-type N-Glycan structures. Using the LCA, AFP can be fractionated into three glycoforms: AFP-L1, AFP-L2, and AFP-L3. 22,23 AFP-L1 does not contain the LCA-binding sites, which is the main component of AFP. AFP-L1 isoform is typically associated with inflammatory liver diseases, such as chronic hepatitis and cirrhosis. AFP-L2 is most abundant in pregnant women. Serum AFP-L3 levels are highest in liver cancer patients and can be used in the absence of elevated AFP levels to detect liver cancer at early stage. 24
While traditional AFP assay requires a serum AFP level above 20 ng/mL, AFP-L3 assay requires an AFP level above 10 ng/mL and the highly sensitive assay for AFP-L3 requires AFP levels as low as 2 ng/mL. 25 AFP-L3 has a better specificity for early liver cancer detection than AFP, but its sensitivity is low (37%–60%). 26,27 The high-sensitive AFP-L3 assay improves the sensitivity from 37% to approximately 50%, 26,28 which means that false-negative rate is still at 50%.
In pregnant women, fetal AFP levels can be detected in serum and urine. Since AFP could be quickly cleared from the mother's serum via her kidneys, maternal urine AFP levels correlate with fetal serum AFP levels. Maternal serum AFP levels peak near the end of the first trimester and decrease rapidly after birth. 17 Infants’ AFP levels are usually achieved to a normal adult range over the first year of life. 29 AFP in maternal amniotic fluid or maternal plasma can be used for prenatal surveillance of the fetus. Elevated AFP levels in serum and amniotic fluid in pregnant women may indicate fetal spina bifida, anencephaly, congenital esophageal atresia, or multiple fetuses. 30–33 However, the function of AFP in adult humans is largely unknown. 34
It is reported that when the serum AFP concentration is higher than 30 ng/mL, the body's immune function will be inhibited. 35 In adults, serum AFP levels are elevated in most of patients with primary liver cancer. 36 Extremely high serum levels of AFP are mainly seen in patients with primary liver cancer, whereas the serum AFP levels in patients with metastatic liver cancer are generally lower than 424 ng/mL. Alcoholic cirrhosis, acute viral hepatitis, and HBsAg carriers show a slight increase in AFP levels during compensatory liver regeneration. 37 In addition, the AFP positive rate is 50% in germ cell tumors and the AFP levels are significantly elevated in patients with advanced nonspermatogenic embryonic cell tumors. 38,39 Patients with other gastrointestinal tumors, such as pancreatic cancer or lung cancer, may also be elevated to varying degrees. 40–43 There is no literature reported that AFP levels are related to tumor size, malignancy, and stage.
Since the serum AFP levels in patients suffering from different cancer or noncancer diseases have not been systematically studied and compared, such information would be needed to understand the molecular nature and the meaning of elevated serum AFP levels. Thus, in current study a total of 66,682 clinical lab test results of serum AFP levels from healthy individuals and patients with 47 different types of diseases during the past 5 years were retrieved and analyzed.