American journal of physiology. Heart and circulatory physiology
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Am. J. Physiol. Heart Circ. Physiol. · Jul 2002
Increasing P(50) does not improve DO(2CRIT) or systemic VO(2) in severe anemia.
Reducing the hemolobin (Hb)-O(2) binding affinity facilitates O(2) unloading from Hb, potentially increasing tissue mitochondrial O(2) availability. We hypothesized that a reduction of Hb-O(2) affinity would increase O(2) extraction when tissues are O(2) supply dependent, reducing the threshold of critical O(2) delivery (DO(2 CRIT)). We investigated the effects of increased O(2) tension at which Hb is 50% saturated (P(50)) on systemic O(2) uptake (VO(2) (SYS)), DO(2 CRIT), lactate production, and acid-base balance during isovolemic hemodilution in conscious rats. ⋯ Arterial lactate was lower in RSR13-treated than in control animals when animals were O(2) supply dependent. The decrease in base excess, arterial pH, and bicarbonate during O(2) supply dependence was significantly less after RSR13 than after saline. These findings demonstrate that during O(2) supply dependence caused by severe anemia, reducing Hb-O(2) binding affinity does not affect VO(2) (SYS) or DO(2 CRIT) but appears to have beneficial effects on oxidative metabolism and acid base balance.
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Am. J. Physiol. Heart Circ. Physiol. · May 2002
Effect of endovascular cooling on myocardial temperature, infarct size, and cardiac output in human-sized pigs.
Mild hypothermia reduces myocardial infarct size in small animals; however, the extent of myocardial protection in large animals with greater thermal mass remains unknown. We evaluated the effects of mild endovascular cooling on myocardial temperature, infarct size, and cardiac output in 60- to 80-kg isoflurane-anesthetized pigs. We occluded the left anterior descending coronary artery for 60 min, followed by reperfusion for 3 h. ⋯ Salvaged myocardium showed normal sestamibi uptake, confirming intact microvascular flow and myocyte viability. Cardiac output was maintained in hypothermic hearts because of an increase in stroke volume, despite a decrease in heart rate. Mild endovascular cooling to 34 degrees C lowers myocardial temperature sufficiently in human-sized hearts to cause a substantial cardioprotective effect, preserve microvascular flow, and maintain cardiac output.
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Am. J. Physiol. Heart Circ. Physiol. · Feb 2002
Clinical Trial Controlled Clinical TrialHypovolemia and neurovascular control during orthostatic stress.
Humans exposed to real or simulated microgravity experience decrements in blood pressure regulation during orthostatic stress that may be related to autonomic dysregulation and/or hypovolemia. We examined the hypothesis that hypovolemia, without the deconditioning effects of bed rest or spaceflight, would augment the sympathoneural and vasomotor response to graded orthostatic stress. Radial artery blood pressure (tonometry), stroke volume (SV), brachial blood flow (Doppler ultrasound), heart rate (electrocardiogram), peroneal muscle sympathetic nerve activity (MSNA; microneurography), and estimated central venous pressure (CVP) were recorded during five levels (-5, -10, -15, -20 and -40 mmHg) of randomly assigned lower body negative pressure (LBNP) (n = 8). ⋯ During hypovolemia, there was an upward shift in the %DeltaMSNA/DeltaCVP, DeltaFVR/DeltaCVP, and DeltaTPR/DeltaCVP relationships during 0 to -20 mmHg LBNP. In contrast to normovolemia, blood pressure increased at -40 mmHg LBNP during hypovolemia due to larger gains in the %DeltaMSNA/DeltaCVP and DeltaTPR/DeltaCVP relationships. It was concluded that acute hypovolemia augmented the neurovascular component of blood pressure control during moderate orthostasis, effectively compensating for decrements in SV and cardiac output.
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Am. J. Physiol. Heart Circ. Physiol. · Jan 2002
Comparative StudyEffect of a maldistribution of microvascular blood flow on capillary O(2) extraction in sepsis.
Inherent in the remote organ injury caused by sepsis is a profound maldistribution of microvascular blood flow. Using a 24-h rat cecal ligation and perforation model of sepsis, we studied O(2) transport in individual capillaries of the extensor digitorum longus (EDL) skeletal muscle. ⋯ Capillary O(2) extraction increased threefold (P < 0.05) and was directly related to the degree of stopped flow in the EDL. Thus impaired O(2) transport in early stage sepsis is likely the result of a microcirculatory dysfunction.
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Am. J. Physiol. Heart Circ. Physiol. · Jan 2002
Comparative StudyBeneficial effects of the Ca(2+) sensitizer levosimendan in human myocardium.
Levosimendan has been reported to increase cardiac Ca(2+) sensitivity, thereby not enhancing intracellular Ca(2+) or diastolic tension. This may be advantageous for the treatment of heart failure patients. Therefore, the present study investigates the mode of action of levosimendan in both failing and nonfailing (NF) human myocardium. ⋯ After application of isoprenaline, levosimendan shortened relaxation and contraction kinetics. Levosimendan did not change the systolic Ca(2+) transient but it improved the force-frequency relationship in DCM. In conclusion, levosimendan improves contraction in failing human myocardium under conditions with already increased intracellular Ca(2+).