American journal of physiology. Heart and circulatory physiology
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Am. J. Physiol. Heart Circ. Physiol. · Jan 2005
Right atrial dimension-pressure relation during volume expansion is unaltered by pregnancy in the rat.
Blood volume expands significantly during pregnancy, but afferent signals from cardiac receptors are reduced. In addition, during exogenous volume expansion, right atrial pressure (RAP) increases more for equivalent volumes in pregnant animals, implying reduced atrial compliance. To examine possible gestational alterations in atrial dimension during volume expansion, we compared the effects of volume expansion on RAP and right atrial dimension (RAD) in pregnant vs. virgin rats. ⋯ Despite increased basal RAD in pregnant rats, the slope of the RAD-RAP relation during volume expansion was similar in the two groups. Results indicate that resting RAD is increased in pregnant rats and that the change in dimension during volume loads is similar to that in virgin rats. Thus, during pregnancy, the right atrium appears to accommodate the increased blood volume, and reduced afferent signaling most likely is due to mechanisms other than mechanical alterations of the atrium by expanded volume.
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Am. J. Physiol. Heart Circ. Physiol. · Dec 2004
Effect of sepsis on skeletal muscle oxygen consumption and tissue oxygenation: interpreting capillary oxygen transport data using a mathematical model.
Inherent in the inflammatory response to sepsis is abnormal microvascular perfusion. Maldistribution of capillary red blood cell (RBC) flow in rat skeletal muscle has been characterized by increased 1) stopped-flow capillaries, 2) capillary oxygen extraction, and 3) ratio of fast-flow to normal-flow capillaries. On the basis of experimental data for functional capillary density (FCD), RBC velocity, and hemoglobin O2 saturation during sepsis, a mathematical model was used to calculate tissue O2 consumption (Vo2), tissue Po2 (Pt) profiles, and O2 delivery by fast-flow capillaries, which could not be measured experimentally. ⋯ Average (minimum) Pt decreased from 43 (40) mmHg in control to 34 (27) and 26 (15) mmHg in AS and ES, respectively, and clustering fast-flow capillaries (increased flow heterogeneity) reduced minimum Pt to 14.5 mmHg. Thus, although fast capillaries prevented tissue dysoxia, they did not prevent increased hypoxia as the degree of microvascular injury increased. The model predicts that decreased FCD, increased fast flow, and increased Vo2 in sepsis expose skeletal muscle to significant regions of hypoxia, which could affect local cellular and organ function.
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Am. J. Physiol. Heart Circ. Physiol. · Dec 2004
Comparative StudyDiffering effects of epinephrine, norepinephrine, and vasopressin on survival in a canine model of septic shock.
During sepsis, limited data on the survival effects of vasopressors are available to guide therapy. Therefore, we compared the effects of three vasopressors on survival in a canine septic shock model. Seventy-eight awake dogs infected with differing doses of intraperitoneal Escherichia coli to produce increasing mortality were randomized to receive epinephrine (0.2, 0.8, or 2.0 microg.kg(-1).min(-1)), norepinephrine (0.2, 1.0, or 2.0 microg.kg(-1).min(-1)), vasopressin (0.01 or 0.04 U/min), or placebo in addition to antibiotics and fluids. ⋯ In this study, the effects of vasopressors were independent of severity of infection but dependent on the type and dose of vasopressor used. Epinephrine adversely affected organ function, systemic perfusion, and survival compared with norepinephrine and vasopressin. In the ranges studied, norepinephrine and vasopressin have more favorable risk-benefit profiles than epinephrine during sepsis.
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Am. J. Physiol. Heart Circ. Physiol. · Nov 2004
Theoretical considerations in the dynamic closed-loop baroreflex and autoregulatory control of total peripheral resistance.
The most important goal of this study is to enhance our understanding of the crucial functional relationships that determine the behavior of the systemic circulation and its underlying physiological regulatory mechanisms with minimal modeling. To the present day, much has been said about the indirect hydraulic effects of right atrial pressure (PRA) via cardiac output (CO) on arterial pressure (Pa) through the heart and pulmonary circulation or the direct regulatory effects of PRA on Pa through the cardiopulmonary baroreflex; however, very little attention has been given to the hydraulic influence that PRA exerts directly through the systemic circulation. ⋯ With this in mind, we emphasize the analytic algebraic analysis of the systemic circulation composed of arteries, veins, and its underlying physiological regulatory mechanisms of baroreflex and autoregulatory modulation of total peripheral resistance (TPR), where the behavior of the system can be analytically synthesized from an understanding of its minimal elements. As a result of this analysis, we present a novel mathematical method to determine short-term TPR fluctuations, which accounts for the entirety of observed Pa fluctuations, and propose a new cardiovascular system identification method to delineate the actual actions of the physiological mechanisms responsible for the dynamic couplings between CO, Pa, PRA, and TPR in an individual subject.
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Am. J. Physiol. Heart Circ. Physiol. · Nov 2004
Selective decontamination of the digestive tract attenuated the myocardial inflammation and dysfunction that occur with burn injury.
This study examined the effects of oral antibiotics to selectively decontaminate the digestive tract (SDD) on postburn myocardial signaling, inflammation, and function. We hypothesized that antibiotic therapy to eliminate pathogens from the gastrointestinal (GI) tract would reduce myocardial inflammatory responses and improve postburn myocardial performance. Sprague-Dawley rats received polymyxin E (15 mg), tobramycin (6 mg), and 5-flucytosin (100 mg) by oral gavage twice daily for 3 days preburn and 24 h postburn. ⋯ Vehicle-treated burn injury increased myocardial PKCepsilon/p38 MAPK expression, promoted NF-kappaB nuclear translocation, promoted TNF-alpha, IL-1beta, IL-6, and IL-10 secretion, and impaired myocardial function. SDD attenuated burn-related proinflammatory myocardial signaling, cytokine secretion, and myocardial contractile defects. Our data suggest that burn-related loss of GI barrier function and translocation of microbial products serve as upstream mediators of postburn myocardial inflammatory signaling and dysfunction.