Vascular capacitance

RV function. Another technique to assess RV function is the measurements of isovolumic relaxation time (IVRT). Prolonged right ventricular IVRT in IPAH patients was found to be the strongest predictor of clinical status and survival (35). Another novel method of predicting outcomes in patients with IPAH is Doppler measurement of pulmonary vascular capacitance, which is calculated by utilization of the relationship between stroke volume and pulmonary pulse pressure. In multivariate analysis, echo-calculated pulmonary vascular capacitance correlated more strongly with outcomes than invasively measured mPAP, RA pressure, and pulmonary vascular resistance (PVR) (36). 

Mahapatra S, Nishimura RA, Oh JK, et al. The prognostic value of pulmonary vascular capacitance determined by Doppler echocardiography in patients with pulmonary arterial hypertension. J Am Soc Echocardiogr 2006 19 1045-50. 

Rothe, C. F. and Gaddis, M. L. 1990. Autoregulation of cardiac output by passive elastic characteristics of the vascular capacitance system. Circulation 81 360. 

The arteries are composed of elastin and collagen fibers and smooth muscles in a complex circumferential organization with a variable helix. Accordingly, the arteries are compliant vessels, and their wall stiffness increases with deformation, as in all other connective tissues. Because of their ability to expand as transmural pressure increases, blood vessels may function to store blood volume under pressure. In this sense, Aey fimction as capacitance elements, similar to storage tanks. The linear relationship between the volume V and the pressure defines the capacitance of the storage element, or the vascular capacitance ... 

Hydralazine. Hydrala2iae causes vasodilation ia all primary vascular beds and has more pronounced effects on capacitance than on resistance blood vessels. Despite the hypotension it produces, hydrala2iae iacreases renal blood flow and cardiac output. PRA iacreases with its use. Tachycardia, headache, di22iaess, and water and sodium retention are principal side effects of hydrala2iae therapy. 

Nasal vasculature may offer some insight into this question, though research to date has been equivocal. Nasal turbinate vessels can be classified as either capacitance vessels or resistive vessels. Capacitance vessels appear to vasodilate in response to infection while resistance vessels appear to respond to cold stimuli by vasoconstriction. Buccal vascular structures also respond to thermal stimuli but appear to respond principally to cutaneous stimuli. How pharyngeal and tracheobronchial submucosal vessels react to thermal stimuli is not known, though cold-induced asthma is believed to result from broncho-spasms caused by susceptible bronchial smooth muscle responding to exposure to cold dry air.- This asthmatic response suggests an inadequate vascular response to surface cooling. 

The relative contributions of Ca2+ entry via CCE and second messenger-operated pathways to the Ca2+ signals evoked by physiological stimuli in the A7r5 vascular smooth muscle cell line. For simplicity, I refer to the second of these pathways as a non-capacitative Ca2+ entry (NCCE) pathway. 

The inhibition of sympathetic tone to the venous system (capacitance vessels) results in increased pooling of blood in the venous vascular bed with consequent decreased venous return to the heart and decreased cardiac output. This phenomenon is more pronounced in upright positions because of the effect of gravity. The hemodynamic effects of ganglionic blockers include decreases in cardiac output, renal blood flow, cerebral blood flow and orthostatic hypotension(20,21). 

O -Adrenoceptor antagonists (o -blockers) are competitive inhibitors at the level of Q -adrenoceptors. These receptors are found in many organs and tissues, but their predominant functional importance is to mediate the vasoconstrictor effects of endogenous catecholamines (noradrenaline, adrenaline) released from the sympathetic nerve endings. Conversely, Q -adrenoceptor antagonism by means of an a-blocker will inhibit this constrictor activity and hence cause vasodilatation. This vasodilator effect occurs in both resistance vessels (arterioles) and capacitance vessels (veins), since a-adrenoceptors are present in both types of vascular structures. Accordingly, both cardiac afterload and preload will be lowered, in particular when elevated. 

In therapeutic doses, hydralazine produces little effect on nonvascular smooth muscle or on the heart. Its pharmacological actions are largely confined to vascular smooth muscle and occur predominantly on the arterial side of the circulation venous capacitance is much less affected. Because cardiovascular reflexes and venous capacitance are not affected by hydralazine, postural hypotension is not a clinical concern. Hydralazine treatment does, however, result in an increase in cardiac output. This action is brought about by the combined effects of a reflex increase in sympathetic stimulation of the heart, an increase in plasma renin, and salt and water retention. These effects limit the hypotensive usefulness of hydralazine to such an extent that it is rarely used alone. 

Alpha receptors are widely expressed in vascular beds, and their activation leads to arterial and venoconstriction. Their direct effect on cardiac function is of relatively less importance. A relatively pure agonist such as phenylephrine increases peripheral arterial resistance and decreases venous capacitance. The enhanced arterial resistance usually leads to a dose-dependent rise in blood pressure (Figure 9-... 

Physiologically, in both normal and hypertensive individuals, blood pressure is maintained by moment-to-moment regulation of cardiac output and peripheral vascular resistance, exerted at three anatomic sites (Figure 11-1) arterioles, postcapillary venules (capacitance vessels), and heart. A fourth anatomic control site, the kidney, contributes to maintenance of blood pressure by regulating the volume of intravascular fluid. Baroreflexes, mediated by autonomic nerves, act in combination with humoral mechanisms, including the renin-angiotensin-aldosterone system, to coordinate function at these four control sites and to maintain normal blood pressure. Finally, local release of vasoactive substances from vascular endothelium may also be involved in the regulation of vascular resistance. For example, endothelin-1 (see Chapter 17) constricts and nitric oxide (see Chapter 19) dilates blood vessels. 

Direct vasodilators, which reduce pressure by relaxing vascular smooth muscle, thus dilating resistance vessels and—to varying degrees—increasing capacitance as well. 

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. 

The primary direct result of an effective dose of nitroglycerin is marked relaxation of veins with increased venous capacitance and decreased ventricular preload. Pulmonary vascular pressures and heart size are significantly reduced. In the absence of heart failure,... 

Vascular smooth muscle tone is regulated by adrenoceptors consequently, catecholamines are important in controlling peripheral vascular resistance and venous capacitance. Alpha receptors increase arterial resistance, whereas 2 receptors promote smooth muscle relaxation. There are major differences in receptor types in the various vascular beds (Table 9-4). The skin vessels have predominantly receptors and constrict in the presence of epinephrine and norepinephrine, as do the splanchnic vessels. Vessels in skeletal muscle may constrict or dilate depending on whether ffor 13 receptors are activated. Consequently, the overall effects of a sympathomimetic drug on blood vessels depend on the relative activities of that drug at and 8receptors and the anatomic sites of the vessels affected. In addition, Di receptors promote vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels. Activation of the Di receptors in the renal vasculature may play a major role in the natriuresis induced by pharmacologic administration of dopamine. 

The hypotensive action of guanethidine early in the course of therapy is associated with reduced cardiac output, due to bradycardia and relaxation of capacitance vessels. With long-term therapy, peripheral vascular resistance decreases. Compensatory sodium and water retention may be marked... 

Hypertension is defined as a sustained diastolic blood pressure greater than 90 mm Hg accompanied by an elevated systolic blood pressure (>140 mm Hg). Hypertension results from increased peripheral vascular smooth muscle tone, which leads to increased arteriolar resistance and reduced capacitance of the venous system. Elevated blood pressure is an extremely common disorder, affecting approximately 15% of the population of the United States (60 million people). Although many of these individuals have no symptoms, chronic hypertension—either systolic or diastolic—can lead to congestive heart failure, myocardial infarction, renal damage, and cerebrovascular accidents. The incidence of morbidity and mortality significantly decreases when hypertension is diagnosed early and is properly treated. 

Midodrine is a prodrug, whose active metabolite is relatively selective for vascular postjunctional alphai-adrenoceptors and therefore increases peripheral resistance by arteriolar constriction, with some veno-constriction in capacitance vessels (1). It has minimal activity in the central nervous system, since it does not cross the blood-brain barrier. It can be given orally and has a systemic availabihty of over 90% by this route. The half-life of the active deglycinated metabolite is relatively short (2-3 hours). The dosage range is 2.5-10 mg tds, and is usually toward the upper end of this range. 

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