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Nature of Flow of a Liquid
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Total peripheral resistance of the systemic circulation. If the cardiac output (CO) is 6.6 L/min (110 cm3/s), the MAP 95 mmHg and the mean velocity of flow 16 cm/s, then or A useful conversion to remember is If mean blood flow velocity is used to calculate resistance, we have
The Systemic Circulation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
As explained earlier, total peripheral resistance is one of the main factors affecting mean arterial blood pressure. As arterioles are the main component of peripheral resistance, alterations in their radius affect mean arterial blood pressure. Generalized arteriolar constriction, as by an increase in sympathetic nervous system outflow, increases total peripheral resistance, and mean arterial blood pressure rises as a consequence.
Diabetes Mellitus and Ischemic Heart Disease
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
In DM patients of type II (Table 38), a hyperkinetic syndrome is noted. The high level of the cardiac index — 3.46 l/m2 (against 2.78 in healthy persons) is mainly ensured by a growth in the stroke index. In type II DM patients, the total peripheral resistance is lowered to 1217.0 dyn·s·cm−5 (in healthy persons it is 1508.4). It is quite logical to assume that a growth in the ventricular ejection and drop in the peripheral resistance are aimed at increasing the supply of oxygen under conditions of lowering its partial stress in the tissues. The growth in the ventricular ejection in type II DM patients is doubtlessly due to the increase in the mass of the myocardium of the left ventricle. Hypertrophy of the myocardium in DM is explained by disturbance of metabolism and dystrophic changes, especially by diabetic microangiopathies. When comparing other parameters of echocardiography (the ejection fraction, extent of shortening of the front-rear dimension of the left ventricle during systole), we failed to note considerable distinctions. Most likely, the growth in the mess of the myocardium of the left ventricle in type II DM compensates the drop in the contractility of the cardiac myocytes.
Drug repurposing strategies and key challenges for COVID-19 management
Published in Journal of Drug Targeting, 2022
Shubham Mule, Ajit Singh, Khaled Greish, Amirhossein Sahebkar, Prashant Kesharwani, Rahul Shukla
In the worst of cases, this infection may become so severe that it starts spreading systemically through blood circulation and produce systemic inflammatory response syndrome. Permeability of systemic blood vessels is increased which ultimately causes leakage of blood fluids in interstitial spaces, because of which reduction in blood volume is seen. On top of that, systemic vasodilation produced by inflammatory mediators causes a reduction in total peripheral resistance. A decrease in both, blood volume and total peripheral resistance is collectively responsible for the drastic decrease in blood pressure. The patient becomes hypotensive, and the possibility of potential septic shock cannot be denied. As the blood pressure is reduced, blood perfusion to multiple organs is obstructed. If such conditions persist then it may lead to multi-system organ failure. Decreased blood perfusion to the kidney can ultimately lead to renal failure hence kidney’s ability to excrete of bilirubin, creatinine, urea, etc. will be disturbed and these substances may start building up in blood and tissues. Similarly, damage to the liver will cause the release of intracellular enzymes like alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in addition to fibrinogen, and IL-6.
The emerging significance of circadian rhythmicity in microvascular resistance
Published in Chronobiology International, 2022
Jeffrey T. Kroetsch, Darcy Lidington, Steffen-Sebastian Bolz
On a simplistic level, the vascular system is separated into a macro- and a microvascular component, each with distinct functional characteristics: macrovessels conduct blood over long distances with minimal resistance (conduit vessels), while microvessels are specialized to control blood flow resistance and interface with highly specialized microenvironments within various tissues. Since the tissue microenvironments are unique, it is not surprising that the microvascular elements within each tissue are also highly specialized. For example, the renal microcirculation permits the passage of molecules and fluids, while the cerebral microcirculation is largely impermeable (i.e., blood–brain barrier). Thus, it is important to recognize that molecular control mechanisms identified in one particular microvascular bed cannot be assumed to operate in another microvascular bed. Collectively, the microvascular resistance generated by the resistance arteries and pre-capillary arterioles locally controls capillary blood flow and hence, tissue/organ perfusion. The sum of the resistances generated by each microvascular bed constitutes the variable component of total peripheral resistance (TPR).
Effects of acute moderate-intensity exercise at different duration on blood pressure and endothelial function in young male patients with stage 1 hypertension
Published in Clinical and Experimental Hypertension, 2021
Yan Yan, Zhengzhen Wang, Yan Wang, Xuemei Li
Our study indicated that both 20 and 40 min of bicycle ergometry at 40%~50% HRR elicited an increase in plasma NO concentration, and the increasing magnitude of 40 min exercise was greater than that of 20 min (Figure 3). The increase in blood flow during exercise leads to an increase in vascular shear force, which is one of the main reasons for the body to regulate the release of NO (40). The shear force, which is generated due to exercise, has positive effects rather than the negative effects caused by the shear force in certain pathological conditions (41). A previous study has documented that a bout of acute exercise of moderate intensity increases the release of NO, causes vasodilation, and decreases the total peripheral resistance (42). The study by Rao et al. (43) suggested that blood vessels were insensitive to α-adrenergic stimulation following acute exercise. It is this insensitive response that promotes vasodilation and decreases total peripheral resistance. The decrease in α-adrenergic sensitive may be related to NO increase. In other words, increased levels of NO not only improve vasodilation but also reduce the sensitivity of blood vessels to the sympathetic nervous system. The increase in shear force following exercise stimulates the production of NO, and NO may reduce the production of endothelin-1 by inhibiting superoxide (44), but further research is needed to explore this pathway.