American journal of physiology. Heart and circulatory physiology
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Am. J. Physiol. Heart Circ. Physiol. · Sep 2003
Pathophysiology of orthostatic hypotension after bed rest: paradoxical sympathetic withdrawal.
Although orthostatic hypotension is a common clinical syndrome after spaceflight and its ground-based simulation model, 6 degrees head-down bed rest (HDBR), the pathophysiology remains unclear. The authors' hypothesis that a decrease in sympathetic nerve activity is the major pathophysiology underlying orthostatic hypotension after HDBR was tested in a study involving 14-day HDBR in 22 healthy subjects who showed no orthostatic hypotension during 15-min 60 degrees head-up tilt test (HUT) at baseline. After HDBR, 10 of 22 subjects demonstrated orthostatic hypotension during 60 degrees HUT. ⋯ In contrast, orthostatic activation of total MSNA was preserved throughout 60 degrees HUT in subjects who did not develop orthostatic hypotension. These data support the hypothesis that a decrease in sympathetic nerve activity is the major pathophysiological factor underlying orthostatic hypotension after HDBR. It appears that the diminished sympathetic activity, in combination with other factors associated with HDBR (e.g., hypovolemia), may predispose some individuals to postural hypotension.
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Am. J. Physiol. Heart Circ. Physiol. · Sep 2003
An integrative model of coupled water and solute exchange in the heart.
Physiologists have devised many models for interpreting water and solute exchange data in whole organs, but the models have typically neglected key aspects of the underlying physiology to present the simplest possible model for a given experimental situation. We have developed a physiologically realistic model of microcirculatory water and solute exchange and applied it to diverse observations of water and solute exchange in the heart. Model simulations are consistent with the results of osmotic weight transient, tracer indicator dilution, and steady-state lymph sampling experiments. The key model features that permit this unification are the use of an axially distributed blood-tissue exchange region, inclusion of a lymphatic drain in the interstitium, and the independent computation of transcapillary solute and solvent fluxes through three different pathways.
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Am. J. Physiol. Heart Circ. Physiol. · Sep 2003
Ketamine blocks Ca2+-activated K+ channels in rabbit cerebral arterial smooth muscle cells.
Although ketamine and Ca2+-activated K+ (KCa) channels have been implicated in the contractile activity regulation of cerebral arteries, no studies have addressed the specific interactions between ketamine and the KCa channels in cerebral arteries. The purpose of this study was to examine the direct effects of ketamine on KCa channel activities using the patch-clamp technique in single-cell preparations of rabbit middle cerebral arterial smooth muscle. We tested the hypothesis that ketamine modulates the KCa channel activity of the cerebral arterial smooth muscle cells of the rabbit. ⋯ Ketamine had little effect on either the voltage-dependency or open- and closed-time histograms of KCa channel. The present study clearly demonstrates that ketamine inhibits KCa channel activities in rabbit middle cerebral arterial smooth muscle cells. This inhibition of KCa channels may represent a mechanism for ketamine-induced cerebral vasoconstriction.
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Am. J. Physiol. Heart Circ. Physiol. · Aug 2003
Contribution of systemic vascular resistance and total arterial compliance to effective arterial elastance in humans.
The respective contribution of systemic vascular resistance (R) and total arterial compliance (C) to the arterial load remains to be established in humans. Effective arterial elastance (Ea), i.e., the left ventricular end-systolic pressure (LVESP)-over-stroke volume ratio, is a reliable estimate of arterial load. It is widely accepted that Ea mainly relates to mean aortic pressure (MAP) and thus to the R-to-T ratio (R/T ratio), where T is cycle length. ⋯ The sensitivity of Ea to a change in R/T was 2.5 times higher than to a similar change in 1/C in both normotensive and hypertensive adults. The LVESP was more strongly related to systolic aortic pressure (SAP; r2 = 0.94) than to MAP (r2 = 0.83), and LVESP matched 90% SAP (bias = 0 +/- 5mmHg). An alternative model of Ea is proposed, in which Ea is proportional to the heart rate x SAP product-over-cardiac index ratio whatever the MAP.
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Am. J. Physiol. Heart Circ. Physiol. · Aug 2003
Effects of hyperoxia on local and remote microcirculatory inflammatory response after splanchnic ischemia and reperfusion.
Splanchnic ischemia-reperfusion (I/R) causes tissue hypoxia that triggers local and systemic microcirculatory inflammatory responses. We evaluated the effects of hyperoxia in I/R induced by 40-min superior mesenteric artery (SMA) occlusion and 120-min reperfusion in four groups of rats: 1) control (anesthesia only), 2) sham operated (all surgical procedures without vascular occlusion; air ventilation), 3) SMA I/R and air, 4) SMA I/R and 100% oxygen ventilation started 10 min before reperfusion. Leukocyte rolling and adhesion in mesenteric microvessels, pulmonary microvascular blood flow velocity (BFV), and macromolecular (FITC-albumin) flux into lungs were monitored by intravital videomicroscopy. ⋯ Oxygen therapy attenuated the increase in mesenteric leukocyte rolling and adherence (P < 0.0001) and maintained microvascular patency at values not significantly different from sham-operated animals. Hyperoxia also attenuated the decrease in pulmonary capillary BFV and shear rates, reduced leukocyte infiltration in the lungs (P < 0.001), and prevented the increase in pulmonary macromolecular leak (P < 0.001), maintaining it at values not different from sham-operated animals. The data suggest that beneficial effects of normobaric hyperoxia in splanchnic I/R are mediated by attenuation of both local and remote inflammatory microvascular responses.