Blood flow through a vessel

The flow of blood through a vessel is determined by two factors  

The relationship among blood flow (Q, ml/min), the pressure gradient (AP, mmHg), and vascular resistance (R, mmHg/ml/min) is described by Ohm s law  

The second factor that determines the flow of blood through a vessel is resistance. In contrast to the pressure gradient, blood flow through a vessel 

Friction also develops as blood contacts the vessel wall while flowing through it. Therefore, the greater the vessel surface area in contact with the blood, the greater the amount of friction developed and the greater is the resistance to blood flow. Two factors determine the vessel surface area length of the vessel and vessel radius. 

The longer the vessel, the more the blood comes into contact with the vessel wall and the greater the resistance is. However, vessel length in the body remains constant. Therefore, as with blood viscosity, it is not a variable factor causing changes in resistance. 

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Ohm s law, which correlates the effects of blood pressure and vascular resistance on blood flow through a vessel (Q = AP/R), may also be applied to blood flow through the entire systemic circulation, or cardiac output ... 

These reports suggested a novel mechanism for the control of vascular caliber (Figure 29.1). In this construct, as the RBC is increasingly deformed by increments in the velocity of blood flow through a vessel and/or by reductions in vascular diameter, it releases ATP that stimulates endothelial synthesis of NO resulting in relaxation of vascular smooth muscle and, thereby, an increase in vascular caliber. This vasodilation results in a decrease in vascular resistance as well as a decrease in the stimulus for RBC deformation and ATP release. Indeed, it has been proposed that RBC-derived ATP contributes to vascular resistance in both the pulmonary and systemic circulation. 

The nitrates, such as isosorbide (Isordil) and nitroglycerin, have a direct relaxing effect on die smooth muscle layer of blood vessels. The result of diis effect is an increase in the lumen of die artery or arteriole and an increase in the amount of blood flowing through diese vessels. An increased blood flow results in an increase in die oxygen supply to surrounding tissues. 

It is assumed that there is perfect heat transfer between tissue and blood in the capillaries and the temperature of blood leaving the capillaries is equal to the local tissue temperature. This is not strictly correct, but it seems to be a reasonable approximation. Recently Keller (30) has pointed out that blood flowing through small vessels may serve as an effective heat transfer medium which, in effect, increases the apparent thermal conductivity of tissue. 

A patient had a sudden heart attack caused by inadequate blood flow through the vessels of the heart. As a consequence, there was an inadequate supply of oxygen to generate ATP in his cardiomyocytes. 

The device functions as a physical barrier to prevent blood flow through the vessel, but due to the gelatinous and bioabsorbable nature of the foam on saturation, it does not provide a scaffold for clot formation and connective tissue ingrowth (Speakman, 1964). Gelfoam treatments can lead to downstream embolization due to the nature of the particles and may have a connection with infections, potentially caused by air bubbles trapped in the materials during the mixing process used to prepare the foam. 

Capillaries 1/R results in increased filtration of fluid across capillaries as well as a decrease in the number of perfused capillaries. The mechanisms underlying these responses are still not clearly defined but may be related to decreased NO levels in capillary endothelial cells as a result of oxidant stress, as described above. Lower NO levels may increase capillary permeability, and increase the rate of filtration of fluid into the tissue. The resulting edema was proposed to compress the capillaries sufficiently to impede blood flow through these vessels. 

Coronary vasodilator. A drug that enhances blood flow through the blood vessels of the heart. 

Acute coronary syndromes most often result from a physical disruption of the fibrous cap, either frank cap fracture or superficial endothelial erosion, allowing the blood to make contact with the thrombogenic material in the lipid core or the subendothelial region of the intima. This contact initiates the formation of a thrombus, which can lead to a sudden and dramatic blockade of blood flow through the affected artery. If the thrombus is nonocclusive or transient, it may either be clinically silent or manifest as symptoms characteristic of unstable angina. Importantly, if collateral vessels have previously formed, for example, due to chronic ischemia produced by multi vessel disease, even total occlusion of one coronary artery may not lead to an acute myocardial infarction. 

The main function of vascular smooth muscle is to distribute blood flow through selective vasoconstriction and vasomotion. The latter is clearly associated with oscillations in [Ca2+]j, but it was long thought that tonic contraction was initiated by SR Ca2+ release and maintained by a steady state elevation of [Ca2+] dependent on influx. However, confocal microscopy of intact blood vessels has... 

The blood vessels in skeletal muscle contain both a-and Pz-adrenoceptors. Norepinephrine constricts these blood vessels and reduces blood flow through an interaction with a-adrenoceptors. Isoproterenol dilates the vessels in skeletal muscle and consequently increases blood flow through the tissue by interaction with the Pz-adrenoceptors. Epinephrine has a more complex ac-... 

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