Hemodynamics, normalization

In normal human subjects, ANP infusion for one hour causes increased absolute and fractional sodium excretion, urine flow, GFR, and water clearance (53—55). As shown in many in vitro and in vivo animal studies, ANP achieves this by direct effect on the sodium reabsorption in the inner medullary collecting duct, ie, by reducing vasopressin-dependent free-water and sodium reabsorption leading to diuresis and by indirect effect through increased hemodynamic force upon the kidney. ANP inhibits the release of renin and aldosterone resulting in the decreased plasma renin activity and aldosterone concentration (56,57). 

We examined the effects of selective activation of histamine Hj receptors on coronary hemodynamics in two groups patients with atypical chest pain and normal coronary arteries, and patients with vasospastic angina [48]. Selective Hj receptor stimulation was achieved by infusing histamine intravenously (0.5 pg/kg/min) for 5 min after pretreatment with cimetidine to antagonize the H2 receptors. Heart rate was kept constant (100 beats/min) by coronary sinus pacing. 

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. 

Maintain fluid and hemodynamic support Expect normal mentation after recovery... 

With advancing age, the patient with essential hypertension progressively changes his hemodynamic pattern into one of normal cardiac output with increased peripheral arteriolar constriction and, finally, later in the natural course of the disease into one of lower cardiac output and further increase in peripheral vascular resistance ). 

Niarchos AP, Pickering TG Wallace JM, Case DB, Laragh JH. (1980) Hemodynamic effects of the converting enzyme inhibitor teprotide in normal- and high-renin hypertension. Clin Pharmacol Ther 28 592-601. 

The hemodynamic effects of sotalol are related to its 3-adrenoceptor antagonist activity. Accordingly, decreases in resting heart rate and in exercise-induced tachycardia are seen in patients receiving sotalol. A modest reduction in systolic pressure and in cardiac output may occur. The reduction in cardiac output is a consequence of lowering the heart rate, since stroke volume is unaffected by sotalol treatment. In patients with normal ventricular function, cardiac output is maintained despite the decrease in heart rate because of the simultaneous increase in the stroke volume. 

The net cardiovascular effects of atropine in patients with normal hemodynamics are not dramatic tachycardia may occur, but there is... 

In vitro, U-II is a potent constrictor of vascular smooth muscle its activity depends on the type of blood vessel and the species from which it was obtained. Vasoconstriction occurs primarily in arterial vessels, where U-II can be more potent than endothelin 1, making it the most potent known vasoconstrictor. However, under some conditions, U-II may cause vasodilation. In vivo, U-II has complex hemodynamic effects, the most prominent being regional vasoconstriction and cardiac depression. In some ways, these effects resemble those produced by ET-1. Nevertheless, the role of the peptide in the normal regulation of vascular tone and blood pressure in humans appears to be minor. 

Hemodynamic studies indicate that blood pressure lowering by clonidine results from reduction of cardiac output due to decreased heart rate and relaxation of capacitance vessels, with a reduction in peripheral vascular resistance, particularly when patients are upright (when sympathetic tone is normally increased). 

The mechanisms by which tolerance develops are not completely understood. As noted above, diminished release of nitric oxide may be partly responsible for tolerance to nitroglycerin. Systemic compensation also plays a role in tolerance in the intact human. Initially, significant sympathetic discharge occurs and after one or more days of therapy with long-acting nitrates, retention of salt and water may reverse the favorable hemodynamic changes normally caused by nitroglycerin. 

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