Understanding the role and control of vascular capacitance (the venous system) in the maintenance of cardiovascular homeostasis is the long-range goal of this project. Vascular capacitance is important in people following hemorrhage or fluid loss (shock), during exercise in a hot environment, as we change our orientation from lying to standing (orthostatic hypotension), or in cardiovascular deconditioning in a zero-gravity environment. Vascular capacitance may be important in the etiology of hypertension or in compensation during congestive heart failure. I plan to quantify the magnitude of overall vascular passive elastic recoil following changes in blood flow (cardiac output) that leads to redistribution of blood volume between the peripheral tissue and the heart. This is a crucial determinant of cardiac output. All of the venous return blood will be collected into a reservoir at a set pressure and pumped back to the body at various rates. The importance of reflexes will be assessed by using various sympathetic blocking agents. Using an ultrasonic distance meter, I expect to show that venous collapse is a physiologically insignificant factor in the distribution of blood between the peripheral tissues and the thorax. Changes in unstressed volume of isolated veins will be studied under various degrees of sympathetic stimulation to further explore this important concept and characteristic of vascular capacitance. The role of beta-adrenergic receptors in the reflex control of vascular capacitance will be evaluated by measuring changes in hepatic outflow resistance and the cardiovascular response to hemorrhage, bilateral carotid occlusion and beta-adrenergic agonists before and after receptor blockade. I expect to show that both alpha- and beta-adrenergic receptors, in physiologic concentrations, cause general body venoconstriction. Computer simulations will be tested with the data obtained and will be used to consolidate the mass of information currently available. Indicator dilution techniques for estimating organ blood volume, methods for measuring the mean vascular filling pressure of organs, and the method for estimating mean circulatory filling pressure technique will be critically evaluated. The constant cardiac output reservoir and the mean circulatory filling pressure techniques will be critically compared to test whether these two methods for measuring changes in general venomotor tone are complementary, consistent and accurate.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Method to Extend Research in Time (MERIT) Award (R37)
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Experimental Cardiovascular Sciences Study Section (ECS)
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Indiana University-Purdue University at Indianapolis
Schools of Medicine
United States
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Rothe, C F; Maass-Moreno, R (2000) Active and passive liver microvascular responses from angiotensin, endothelin, norepinephrine, and vasopressin. Am J Physiol Heart Circ Physiol 279:H1147-56
Rothe, C F; Maass-Moreno, R (1998) Hepatic venular resistance responses to norepinephrine, isoproterenol, adenosine, histamine, and ACh in rabbits. Am J Physiol 274:H777-85
Maass-Moreno, R; Rothe, C F (1997) Distribution of pressure gradients along hepatic vasculature. Am J Physiol 272:H2826-32