Browsing by Subject "blood flow"
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Item Coronary Perfusion Pressure-Induced Changes in Coronary Vascular Volume in the Canine Right Ventricle(1997-12-01) Yu, Ying; H. Fred Downey; Robert T. Mallet; Michael L. SmithYu, Ying, Coronary Perfusion Pressure-induced Changes in Coronary Vascular Volume in the Canine Right Ventricle. Master of Science (Biomedical Sciences), December 1997; 33 pp; 4 tables; 5 figures; bibliography, 24 titles. Changes in coronary perfusion pressure cause changes in myocardial contractile function and oxygen consumption (MVO2), particularly in the right ventricle (RV). This study determined the effects of right coronary (RC) perfusion pressure (RCP) on RC vascular volume (RCB) and its relationship to MVO2 of in situ, working canine hearts, and also investigated whether changes in MVO2 are due primarily to altered RCP or RC blood flow (RCF). In 15 open chest, anesthetized dogs, the RC artery was cannulated and perfused with arterial blood diverted from a femoral artery. To blunt RCP-induced changes in RCF, vasopressin was infused into the RC perfusion line in seven dogs. RCV was measured by an indicator dilution method as RCP was varied without vasopressin (RCP=60, 100, 140, and 180 mmHg) and with vasopressin (RCP=60 and 100 mmHg). Without vasopressin, changes in RCP induced changes in MVO2 which were associated with changes in RCV and RCF. With vasopressin, increasing RCP from 60 mmHg to 100 mmHg produced no changes in RCF, RCV, or MVO2. These results indicate that RCP-induced changes in RV MVO2 are mediated by RCV and/or RCF, but not by RCP per se.Item Deltoid Opioid Receptor Phenotype Modulation of Hindlimb Vascular Conduction(2008-10-06) Barlow, Matthew A.; Raven, Peter B.; Gwirtz, Patricia A.; Dillon, Glenn H.Barlow, Matthew A. Deltoid Opioid Receptor Phenotype Modulation of Hindlimb Vascular Conduction. Doctor of Philosophy (Integrative Physiology), Oct 6th, 2008, 136 pp, 1 table 26 figures. Hypertension, diabetes mellitus and their presumed precursor the metabolic syndrome are part of a complex disease process associated with insulin resistance. Neurovascular complications in diabetics commonly involve the lower limbs resulting in a vicious cycle of autonomic neuropathy, painful occlusive claudication and resulting immobility that precipitates inactivity and progressive disability. The fixed neural and vascular diseases evolve slowly and the early events in this progressive decline in function are poorly understood. Sympathetic vasoconstriction is a major component of blood flow regulation in muscle. Active vasoconstriction in the lower limbs depends on continued transmission of efferent vasomotor signals through the lumbar sympathetic chain ganglia. Opioid receptors actively reduce normal ganglionic transmission presumably by lowering acetylcholine release. In the heart, the subtypes of delta-opioid receptors (DORs) facilitate (DOR-1, vagotonic) and inhibit (DOR-2, vagolytic) cholinergic transmission in the heart. The DOR-2 mediated inhibitory effects in heart are alterable and can change rapidly. Diabetes impairs vascular control. Ganglionic transmission is metabolically vulnerable during high fat feeding and insulin resistance. We hypothesized that the DOR-2 stimulation significantly facilitates vasodilation by reducing cholinergic transmission within the sympathetic chain ganglion. The ability to activate DOR-1 stimulation facilitates to cause further vasoconstriction in the anesthetized and surgically instrumented state of the dog did not show dose dependent activation. The DOR-1 activity in the insulin resistant dogs appears to be decreased as the DOR-1 blockade had no effect on the dose responses in the heart or the hindlimb. Enhanced sympathetic tone through BCO by increasing and reducing cholinergic transmission in the lumbar sympathetic ganglion shows an enhanced pro-constrictor phenotype under stresses of severe hypotension possibly through a DOR-1 mediated activation.Item Interaction of Neural and Local Mechanisms in the Control of Skeletal Muscle Blood Flow(2003-12-01) Wray, David Walter; Michael L. SmithWray, David Walter, Interaction of Neural and Local Mechanisms in the Control of Skeletal Muscle Blood Flow. Doctor of Philosophy (Biomedical Science), December, 2003, 181 pp., 1 table, 19 illustrations, references, 139 titles. The current project sought to characterize the interaction of neural and local mechanisms of skeletal muscle blood flow control through exogenous and endogenous α-andrenoreceptor activation. We hypothesized that α1- and α2-adrenoreceptors in the human leg would exhibit differential distribution and responsiveness, and that unilateral knee-extensor exercise would attenuate α-adrenoreceptor-mediated vasoconstriction in an intensity-dependent manner. We also hypothesized that carotid baroreflex (CBR)-mediated sympathoexcitation would provoke less vasoconstriction during exercise than at rest. Intra-arterial infusion of phenylephrine (PE, α1-agonist) or BHT-933 (α2-agonist) reduced femoral blood flow (FBF) by approximately 60% at rest, but during exercise (27W) the degree of vasoconstriction evoked by PE and BHT was significantly reduced. During ramped (7W-37W) exercise, BHT did not reduce FBF at any intensity, while some degree of PE-induced vasoconstriction was evident at all but the highest exercise intensity. Using sinusoidal neck pressure, CBR-mediated changes in heart rate (HR), arterial blood pressure (ABP) muscle sympathetic nerve activity (MSNA), FBF, and tissue oxygenation (TOm) were seen at rest. During 7w exercise, CBR-mediated control of ABP, FBF, and Tom was attenuated. We conclude that exercise attenuates α-adrenergic responsiveness to exogenous and endogenous activation to ensure sufficient muscle blood flow while maintaining systemic ABP homeostasis.