Mean arterial pressure effects

In a third study the time course of the effects of intravenous and intracoronary injections of cysteinyl leukotrienes on metabolic parameters and systemic and coronary hemodynamics was examined in patients with normal coronary arteries [32]. LTD4 (3 nmol, injected into the left coronary artery) induced an early (20 s), transient fall in mean arterial pressure paralleled by rises in heart rate and plasma levels of epinephrine and norepinephrine, all of which had returned to baseline by 10 min. CVR rose at 10 and 15 min and myocardial oxygen extraction at 15 min. Thus, small doses of cysteinyl leukotrienes may induce both an early, transient fall in mean arterial pressure, with secondary sympathoadrenergic activation, and a later increase in small coronary arteriolar resistance. 

Aim for a 10-15% reduction in mean arterial pressure (MAP) ° Nitroprusside—0.25-0.5 mcg/kg/min continuous IV infusion increase in increments of 0.25-0.5 mcg/kg/min until desired hemodynamic effect. Usual doses up to 2-3 mcg/kg/min. High-alert medication—read package insert before use... 

Aldosterone acts on the distal tubule of the nephron to increase sodium reabsorption. The mechanism of action involves an increase in the number of sodium-permeable channels on the luminal surface of the distal tubule and an increase in the activity of the Na+-K+ ATPase pump on the basilar surface of the tubule. Sodium diffuses down its concentration gradient out of the lumen and into the tubular cells. The pump then actively removes the sodium from cells of the distal tubule and into the extracellular fluid so that it may diffuse into the surrounding capillaries and return to the circulation. Due to its osmotic effects, the retention of sodium is accompanied by the retention of water. In other words, wherever sodium goes, water follows. As a result, aldosterone is very important in regulation of blood volume and blood pressure. The retention of sodium and water expands the blood volume and, consequently, increases mean arterial pressure. 

Figure 15.4 Effects of the autonomic nervous system on mean arterial pressure. The baroreceptors, chemoreceptors, and low-pressure receptors provide neural input to the vasomotor center in the brainstem. The vasomotor center integrates this input and determines the degree of discharge by the sympathetic and parasympathetic nervous systems to the cardiovascular system. Cardiac output and total peripheral resistance are adjusted so as to maintain mean arterial pressure within the normal range.

Figure 15.5 Effects of sympathetic and parasympathetic nervous activity on mean arterial pressure. The parasympathetic nervous system innervates the heart and therefore influences heart rate and cardiac output. The sympathetic nervous system innervates the heart and veins and thus influences cardiac output. This system also innervates the arterioles and therefore influences total peripheral resistance. The resulting changes in cardiac output and total peripheral resistance regulate mean arterial pressure.

Renal blood flow has a direct effect on GFR, which in turn has a direct effect on urine output. As RBF increases, GFR and urine output increase. Conversely, as RBF decreases, GFR and urine output decrease. Furthermore, any change in urine output affects plasma volume and blood pressure. Therefore, the regulation of RBF and GFR are important considerations. According to Ohm s law (Q = AP/R), RBF is determined by mean arterial pressure (MAP) and the resistance of the afferent arteriole (Raffart) ... 

T Renin — T angiotensin II —> T aldosterone -4 T Na+ reabsorption Net effects 4 urine output T blood volume T mean arterial pressure... 

Net effects 4 urine output 4 blood volume 4 mean arterial pressure... 

Fig. 6.1 (a) in vitro GTN tolerance and CHF 2363 CHF 2363 on mean arterial pressure peak cross-tolerance concentration-response curves effect induced on mean arterial pressure (MAP) for relaxation of noradrenaline-contracted rat by intravenous infusion of CHF 2363 (open aortic strips by GTN (O) and CHF 2363 (A) columns) and IS-5-MN (cross-hatched before (open symbols) and after (solid symbols) columns) in the anaesthetised rat. Adapted 90min exposure to 550pM GTN. (b) Effect of from Ref. [37] with permission. 

Iron(III)-TMPyP rapidly catalyzes the isomerization of ONO2 to NO3 (447) and the reaction also involves formation of an oxoFe(IV) intermediate. Iron(III)-TMPyP has been shown to have significant cytoprotective effects on cells both in vitro and in vivo and does not elevate mean arterial pressure suggesting a lack of interaction with NO (448). 

Fig. 3. Haemodynamic effects of different types of calcium antagonists. Drawn lines nifedipine and other rapidly an short-acting dihydropyridines. Dotted lines verapamil and diltiazem. MAP = mean arterial pressure HR = heart rate CO = cardiac output TPR = total peripheral resistance UE = urinary excretion of Na and H2O. Note the reflex tachycardia, provoked by nifedipine.

Isoproterenol (isoprenaline) is a very potent 3-receptor agonist and has little effect on receptors. The drug has positive chronotropic and inotropic actions because isoproterenol activates 3 receptors almost exclusively, it is a potent vasodilator. These actions lead to a marked increase in cardiac output associated with a fall in diastolic and mean arterial pressure and a lesser decrease or a slight increase in systolic pressure (Table 9-4 Figure 9-6). 

NO has a significant effect on vascular smooth muscle tone and blood pressure. Numerous endothelium-dependent vasodilators, such as acetylcholine and bradykinin, act by increasing intracellular calcium levels, which induces NO synthesis (Figure 19-2). Mice with a knockout mutation in the eNOS gene display increased vascular tone and elevated mean arterial pressure, indicating that eNOS is a fundamental regulator of blood pressure. The effects of vasopressor drugs are increased by inhibition of NOS. 

Flalothane, desflurane, enflurane, sevoflurane, and isoflurane all decrease mean arterial pressure in direct proportion to their alveolar concentration. With halothane and enflurane, the reduced arterial pressure appears to be caused by a reduction in cardiac output because there is little change in systemic vascular resistance despite marked changes in individual vascular beds (eg, an increase in cerebral blood flow). In contrast, isoflurane, desflurane, and sevoflurane have a depressant effect on arterial pressure as a result of a decrease in systemic vascular resistance with minimal effect on cardiac output. 

Both somatostatin and octreotide cause transient increases in mean arterial pressure and mean pulmonary pressure when given intravenously to patients with cirrhosis, more marked with bolus administration than with continuous infusion (5). This may be either direct or mediated by inhibition of gut vasodilatory peptides (SEDA-24, 505 6) and is not usually associated with significant clinical effects. 

Terlipressin has similar, but less pronounced, systemic hemodynamic effects to vasopressin, including increases in mean arterial pressure and reduced heart rate (9). Of 105 patients who had continuous terlipressin infusions for... 

Nasta et al. also tried to investigate the relationship between cholesterol and mood states in the initial puerperal period. Their results showed that reduced plasma cholesterol concentration was associated with major feelings of fatigue and depressed mood [79]. In addition, West et al. compared the effects of transdermal versus oral estrogens on the vascular resistance index, mean arterial pressure, serum lipid concentrations, norepinephrine, and left ventricular structure in 10 postmenopausal women. The results showed that oral and transdermal estrogen significantly decreased the vascular resistance index, mean arterial pressure, norepinephrine, and total and low-density lipoprotein cholesterol to a similar extent [80],... 

SK F 38393 is about ten times less potent than dopamine as a renal vasodilator in anesthetized dogs, and shows only about half the maximal renal vasodilator effect. However, while at high doses dopamine increased mean arterial pressure and heart rate, high doses of SK F 38393 increased only blood pressure. 

Seymour AA, Swerdel JN, Delaney NG, Rom M and Cushman DW (1987) Effects of ring opened antrial natriuretic peptide (ANP) on mean arterial pressure MAP and renal excretion in SHR. Fed Proc 46 1296... 

Because the monkey is the most sensitive species for the effects on complement, we have opted to perform cardiovascular safety studies as part of subchronic study protocols using implanted telemetry units in selected monkeys (two/sex in at least two different treatment groups, including the high dose) to measure ECG, mean arterial pressure, heart rate, and body temperature. These parameters are then recorded at frequent intervals for a 24-hour period prior to treatment to establish circadian fluctuations and normal response to various stimuli encountered during the day. This technique enables us to assess both acute alterations related to complement activation after single doses and chronic safety after repeated administration. 

After adequate fluid resuscitation has been established, inotropic support is usually required. Noradrenaline is the inotrope of choice for septic shock its potent a-adrenergic effect increases the mean arterial pressure and its modest Pj effect may raise cardiac output, or at least maintain it as the peripheral vascular resistance increases. Dobutamine may be added further to augment cardiac output. 

Gulati, A. Singh, G. Rebello, S. Sharma, A.C. Effect of diaspirin cross-linked and stroma-reduced hemoglobin on mean arterial pressure and endothelin-1 concentration in rats. Life Sci. 1995, 56, 1433-1442. 

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