The American journal of physiology
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Hypothermia is known to protect myocardium during ischemia, but its role in induction of a protective stress response before ischemia has not been evaluated. As cold incites stress responses in other tissues, including heat shock protein induction and signaling mitochondrial biogenesis, we postulated that hypothermia in perfused hearts would produce similar phenomena while reducing injury during subsequent ischemia. Studies were performed in isolated perfused rabbit hearts (n = 77): a control group (C) and a hypothermic group (H) subjected to decreasing infusate temperature from 37 to 31 degrees C over 20 min. ⋯ Inducible heat shock protein (HSP70-1) mRNA was elevated nearly 4-fold after ischemia in C hearts and 12-fold in H hearts. These data indicate that hypothermia preserves myocardial function and ATP stores during subsequent ischemia and reperfusion. Signaling for mitochondrial biogenesis indexed by ANT1 and beta-F1-ATPase mRNA levels is also preserved during a marked increase in HSP70-1 mRNA.
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On the basis of the windkessel model, the stroke volume-to-aortic pulse pressure ratio (SV/PP) has been proposed as an estimate of total arterial compliance, but recent studies have questioned this approximation. Aortic pressure was obtained at rest in 31 adults undergoing cardiac catheterization (47 +/- 14 yr): controls (n = 7), patients with dilated cardiomyopathy (n = 10), and patients with other cardiac diseases (n = 14). We calculated PP, mean aortic pressure (MAoP), heart period (T), SV (thermodilution cardiac output/heart rate), total peripheral resistance (R), total arterial compliance estimated by area method (Carea), and the time constant of aortic pressure decay in diastole (RCarea). ⋯ These results implied that PP/MAoP and T/RCarea were proportionally related (T/RCarea = 1.18PP/MAoP - 0.07; r = 0.96; P < 0.001). We conclude that for humans at rest 1) SV/PP gave a reliable estimate of Carea, and 2) T normalized by the time constant of aortic pressure decay in diastole was proportionally related to PP/MAoP. This last relationship could be considered an aspect of the coupling between the left ventricle and its load.
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In earlier work, mathematical models of the urine concentration mechanism were developed incorporating the features of renal anatomy. However, several anatomic observations showed inconsistencies in the modeling representation of the outer stripe (OS) anatomy. In this study, based on observations from comparative anatomy and morphometric studies, we propose a new structural model of outer medullary anatomy, different from that previously presented [A. ⋯ J. Clin. Invest. 93: 212-222, 1994).
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This study investigated the effects of bilateral injections of a serotonin (5-HT) receptor agonist into the lateral parabrachial nucleus (LPBN) on the intake of NaCl and water induced by 24-h water deprivation or by sodium depletion followed by 24 h of sodium deprivation (injection of the diuretic furosemide plus 24 h of sodium-deficient diet). Rats had stainless steel cannulas implanted bilaterally into the LPBN. Bilateral LPBN injections of the serotonergic 5-HT1/2 receptor antagonist methysergide (4 micrograms/200 nl at each site) increased hypertonic NaCl intake when tested 24 h after sodium depletion and after 24 h of water deprivation. ⋯ In contrast, the intake of a palatable solution (0.06 M sucrose) under body fluid-replete conditions was not changed after bilateral LPBN methysergide injections. The results show that serotonergic mechanisms in the LPBN modulate water and sodium intake induced by volume depletion and sodium loss. The finding that sucrose intake was not affected by LPBN serotonergic blockade suggests that the effects of the methysergide treatment on the intakes of water and NaCl are not due to a mechanism producing a nonspecific enhancement of all ingestive behaviors.
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The effects of lung injury, positive end-expiratory pressure (PEEP), and norepinephrine on heterogeneity of regional pulmonary blood flow (rPBF, radioactive microspheres) were investigated. We hypothesized that lung injury increases heterogeneity of rPBF and that PEEP ventilation reduces these effects. Heterogeneity of rPBF is scale dependent and was therefore assessed in detail. ⋯ Norepinephrine, in part, further reduced gradients (right, 50 +/- 58%; P < or = 0.05; left, 102 +/- 94%; P = NS). We conclude that oleic acid- and glass bead-induced lung injury produces abnormal distribution of rPBF. Of these changes, application of PEEP only reverses perfusion gradients.