American journal of physiology. Heart and circulatory physiology
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Am. J. Physiol. Heart Circ. Physiol. · Oct 2009
Autonomic effects on the spectral analysis of heart rate variability after exercise.
Although frequency-domain analysis of heart rate variability (HRV) has been performed in the setting of exercise and recovery from exercise, the relationship of specific frequency components to sympathetic and parasympathetic inputs has not been validated in this setting. The aim of this study is to evaluate the relationship of frequency components of HRV to sympathetic and parasympathetic modulation in the setting of recovery after exercise using selective autonomic blockade. Normal subjects (n = 27, 17 men, 53 +/- 7 yr old) underwent bicycle stress testing on four separate days. ⋯ Root mean square (detrended SD) and rMSSD were highly correlated with the square root of the total power (r = 0.96) and high-frequency power (r = 0.95), respectively. Although there are marked reductions in the frequency-domain measures in recovery versus rest, the fluctuations in the low- and high-frequency bands respond to autonomic blockade in the expected fashion. Time-domain measures of HRV were highly correlated with frequency-domain measures and therefore provide a computationally more efficient assessment of autonomic influences during recovery from exercise that is less susceptible to anomalies of frequency-domain analysis.
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Am. J. Physiol. Heart Circ. Physiol. · Oct 2009
Transfer of nitric oxide by blood from upstream to downstream resistance vessels causes microvascular dilation.
The discovery that hemoglobin, albumin, and glutathione carry and release nitric oxide (NO) may have consequences for movement of NO by blood within microvessels. We hypothesize that NO in plasma or bound to proteins likely survives to downstream locations. To confirm this hypothesis, there must be a finite NO concentration ([NO]) in arteriolar blood, and upstream resistance vessels must be able to increase the vessel wall [NO] of downstream arterioles. ⋯ When isoproterenol was applied to the upstream vessels, they dilated, but neither the [NO] or diameter downstream arterioles increased. These observations indicate that NO can move in blood from upstream to downstream resistance vessels. This mechanism allows larger vessels that generate large [NO] to influence vascular tone in downstream vessels in response to both flow and receptor stimuli.
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Am. J. Physiol. Heart Circ. Physiol. · Oct 2009
Melatonin protects against heart ischemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening.
Melatonin, a well-known antioxidant, has been shown to protect against ischemia-reperfusion myocardial damage. Mitochondrial permeability transition pore (MPTP) opening is an important event in cardiomyocyte cell death occurring during ischemia-reperfusion and therefore a possible target for cardioprotection. In the present study, we tested the hypothesis that melatonin could protect heart against ischemia-reperfusion injury by inhibiting MPTP opening. ⋯ Similar results were obtained following treatment of ischemic-reperfused rat heart with cyclosporine A, a known inhibitor of MPTP opening. In addition, melatonin prevents mitochondrial NAD(+) release and mitochondrial cytochrome c release and, as previously shown, cardiolipin oxidation associated with ischemia-reperfusion. Together, these results demonstrate that melatonin protects heart from reperfusion injury by inhibiting MPTP opening, probably via prevention of cardiolipin peroxidation.