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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of temperature on naloxone treatment in canine hemorrhagic shock were examined in 24 dogs hemorrhaged to a mean arterial blood pressure of 35 mm Hg (ambient temperature, 21 degrees C). After two hours of hypotension, the blood reservoir was clamped with no return of shed blood. Dogs were divided into three groups: Control (n = 8) received normal saline (0.5 cc/kg/hr); naloxone-cold (n = 8) and -warm (n = 8) received naloxone (2 mg/kg bolus and 2 mg/kg/hr constant infusion). Body temperature was maintained in four dogs with a warming blanket, and four dogs received no external warming. Rectal temperature fell to 34.2 +/- 0.9 degrees C in naloxone-cold animals; naloxone-warm animals were maintained at 38.6 +/- 0.1 degrees C by external warming. Control dogs rapidly deteriorated after reservoir clamping (survival, 18.6 +/- 5 min). Naloxone infusion significantly increased survival regardless of body temperature (cold, 125 +/- 21 min; warm, 199 +/- 13 min). Naloxone transiently increased mean arterial pressure and dP/dt in the colder dogs, while coronary perfusion, myocardial oxygen metabolism, and plasma beta-endorphin levels were unchanged. In the warmer dogs, naloxone significantly improved hemodynamic function and myocardial perfusion as indicated by the increased mean arterial pressure, cardiac output, stroke volume, dP/dt, and coronary blood flow. Furthermore, naloxone reduced plasma beta-endorphin levels and corrected the metabolic derangements of shock in this group. Our data indicate hypothermia significantly diminished the beneficial effects of naloxone treatment in canine hemorrhagic shock.
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PMID:Effect of temperature on naloxone treatment in canine hemorrhagic shock. 609 39

A marked increase in left ventricular diastolic pressure ( PLVD ) relative to volume is regularly observed during angina pectoris and may contribute to further deteriorations of myocardial perfusion in the ischemic myocardium and to pulmonary congestion as well. A possible simultaneous increase in myocardial oxygen consumption (MVO2) due to a reversible diastolic tone during transient ischemia has not been taken into consideration in previous studies on alterations in ventricular diastolic properties. 13 closed-chest experiments were carried out in clinical catheterization technique with situations of high PLVD (18-50 mm Hg) relative to volume induced by right ventricular pacing (n = 19; 172 +/- 5 beats/min) and catecholamine-induced reversible diastolic tone (n = 17) in moderate hypothermia (31 degrees C). MVO2 was directly measured and indirectly calculated from its hemodynamic determinants using Bretschneider's equation (Et) that does not consider ventricular diastolic pressure. In addition, an energy demand for maintenance of active diastolic wall tension (E5) was calculated from PLVD , mean ventricular diastolic volume estimated from endsystolic and stroke volume, diastolic time and heart rate in ml O2/min X 100 g. During pacing tachycardia with high PLVD (27.4 +/- 1.8 mm Hg) the MVO2 (12.49 +/- 0.50 ml O2/min X 100 g) exceeds Et (10.11 +/- 0.25 ml O2/min X 100 g) (p less than 0.001), partly due to neglect of E5 (1.39 +/- 0.11 ml O2/min X 100 g). During catecholamine-induced high PLVD (31.1 +/- 2.5 mm Hg) the MVO2 (12.29 +/- 0.83 ml O2/min X 100 g) increases significantly (p less than 0.001) over Et (10.43 +/- 0.81 ml O2/min X 100 g). Addition of E5 (1.76 +/- 0.14 ml O2/min X 100g) to Et abolishes the differences between MVO2 and Et yielding non-significantly different values. Results indicate by means of indirect energetic evidence the occurrence of a diastolic tone of the heart under unphysiologic conditions. Acute increases in PLVD during angina pectoris are supposed to increase MVO2 markedly due to an additional energy demand for maintenance of reversible active diastolic wall tension.
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PMID:Increase of myocardial oxygen consumption due to active diastolic wall tension. 614 4

Dorsal aortic blood flow was measured with a pulsed-Doppler meter in Hamburger-Hamilton stage 18, 21, and 24 chick embryos, and stroke volume index was calculated by dividing mean blood flow per minute by heart rate. These parameters were measured at baseline temperature 34.7 degrees C after cooling to 31.1 degrees C and subsequent rewarming to 34.2 degrees C. In stage 21 embryos, after environmental cooling, heart rate decreased from 170 bpm to 118 bpm (P less than 0.01), mean dorsal aortic blood flow decreased from 0.38 mm3/sec to 0.24 mm3/sec (P less than 0.01) but stroke volume index did not change [baseline, 0.13 mm3/beat; after cooling, 0.12 mm3/beat; after rewarming, 0.15 mm3/beat (P = N.S.)]. Similar results were observed in stage 18 and 24 embryos. The bradycardic response to environmental hypothermia was independent of functional autonomic innervation and probably mediated by a direct suppression of cell action potential dv/dt. Myocardial cell function was not adversely affected by an acute change in environmental temperature as the index of stroke volume was not altered, and all parameters returned rapidly to baseline with rewarming.
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PMID:Effect of environmental hypothermia on dorsal aortic blood flow in the chick embryo, stages 18 to 24. 622 76

Coronary bypass performed with moderate systemic hypothermia (25 degrees C) and cold-potassium cardioplegia was associated with a fall and subsequent rise in core (pulmonary arterial) temperature. Serial hemodynamic measurements during rewarming and recovery revealed a decrease in cardiac index (CI) without a decrease in the left atrial pressure (LAP) of 17 patients recovering from uneventful coronary bypass surgery. Nuclear ventriculograms performed during rewarming demonstrated a decrease in left ventricular end-diastolic volume index (EDVI, calculated from the thermodilution stroke index divided by the nuclear ejection fraction) without a change in LAP. Volume loading during both mild hypothermia (35 +/- 5[SD]degrees C) and normothermia revealed that myocardial performance (the relation between CI and EDVI) was unchanged, but diastolic compliance (the relation between LAP and EDVI) decreased with rewarming. LAP was a poor indicator of left ventricular preload (EDVI) during rewarming, and volume loading was required to maintain preload and prevent hypoperfusion.
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PMID:Rewarming hypovolemia after aortocoronary bypass surgery. 633 89

This study was undertaken to evaluate the optimal myocardial temperature during a 4-hour ischemia induced by blood potassium cardioplegia (PC). Heart-lung preparations with work load circuit were used as experimental model. 24 mongrel dogs were divided into four groups and two myocardial temperatures (moderate hypothermia, deep hypothermia) and two perfusates (PC with blood, PC without blood) were tested. Parameters used to evaluate the myocardial protection include the coronary sinus blood pH of the initial reperfusion and left ventricular stroke work after resuscitation. In blood PC at moderate hypothermia, deleterious acid metabolites were minimally produced as evidenced by the coronary sinus blood pH (7.221 +/- 0.122) at initial reperfusion, and cardiac function was best recovered in this group. Blood PC at moderate hypothermia allows the heart to tolerate 4 h ischemia without an excessively elevated coronary perfusion pressure during cardioplegic infusion.
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PMID:Effect of temperature on the arrested heart exposed to a 4-hour ischemia during blood potassium cardioplegia. An experimental study. 661 6

To investigate the relationship between neuropathologic damage and cerebral metabolic alterations during hypothermia in the neonatal animal, 7 day old Sprague-Dawley rats were subjected to unilateral common carotid artery ligation and hypoxia at 37 degrees C, 29 degrees C, and 21 degrees C. At 37 degrees C, animals had extensive infarction of tectum and ipsilateral cerebral hemisphere, and marked depletion of brain ATP. At 29 degrees C, there was no significant change in brain ATP; neuropathologic damage was limited to a few areas of necrosis in the deeper layers of cerebral cortex. No histologic injury was seen in the 21 degrees C group of rats. Profound hypothermia may prevent cerebral edema and visible neuropathologic damage associated with hypoxic-ischemic injury by decreasing cerebral metabolic demands. Moderate hypothermia confers a partial, but incomplete degree of protection; whereas during normothermia, the full extent of hypoxicischemic injury is manifest.
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PMID:The effect of graded hypothermia on hypoxic-ischemic brain damage: a neuropathologic study in the neonatal rat. 665 97

It is shown that the amount of ATP in rats under hypothermia up to heat stroke lowers and that of ADP and AMP somewhat rises. Ionol administration normalizes the ATP level and increases the ADP and AMP contents. Inhalation of CO2 and especially administration of ionol contribute to a higher resistance of the animals to hyperthermia.
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PMID:[Influence of hyperthermia and protective effect of ionol and carbon dioxide gas on ATP, ADP and AMP content of the rat brain]. 678 22

The effect of arterial hypotension on cerebral cortical tissue levels of adenosine triphosphate (ATP), phosphocreatine (PGr), lactate, and reduced nicotinamide adenine dinucleotide (NADH) was studied in male Wistar rats with unilateral carotid ligation exposed to arterial by hypoxia (PaO2 25 torr) for 20 min. while the body temperature was maintained at 32 degrees C and 27 degrees C. Brain metabolite levels were normal in normotensive hypothermic animals exposed to hypoxia, but reduction in arterial pressure to 75 torr caused a significant (p less than 0.05) decrease in ATP and PCr values and a significant increase in lactate and NADH levels. These changes were comparable to those of normothermic normotensive, hypoxic animals. Furthermore, there was no significant differences in the brain metabolite levels between the two hypotensive hypoxic groups. These results indicate that arterial hypotension severely alters the cerebral protective effect of hypothermia against injury caused by hypoxia, and that further reduction in body temperature (from 32 degrees C to 27 degrees C) will not prevent the harmful effect of hypoxia upon the brain in hypotensive rats.
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PMID:Reduction of the cerebral protective effect of hypothermia by oligemic hypotension during hypoxia in the rat. 680 24

Circulatory dynamics during surface- induced deep hypothermia using the halothane-diethyl ether azeotrope in 100% oxygen (O2) without circulatory arrest and 95% O2 and 5% carbon dioxide (CO2) with and without 60 minutes of arrest were evaluated in 15 adult mongrel dogs. Mean arterial pressure was lower in animals given 5% CO2 than in animals given 100% O2 during cooling. Cardiac output in the 5% CO2 groups increased until 30 degrees C cooling and then gradually decreased to 29% of control at 20 degrees C. Cardiac output in the 100% O2 group progressively decreased to 16% of control at 20 degrees C cooling and was 51 to 77% of the output in the 5% CO2 animals at comparable temperatures throughout the hypothermia procedure. The differences in cardiac output were attributed primarily to changes in stroke volume since heart rates were not significantly different. These changes were probably secondary to differences in systemic vascular resistance, which had increased sixfold in the animals given 100% O2 and had only doubled in the 5% CO2 groups at 20 degrees C during cooling. Hemodynamic variables in animals given 5% CO2 did not reveal significant differences in arrested versus nonarrested animals during early rewarming. However, with further warming, cardiac output, stroke volume, left ventricular stroke work, and mean pulmonary arterial and pulmonary artery wedge pressures were lower, and systemic and pulmonary vascular resistances were higher in the arrest group. We conclude that the improved results with halothane-diethyl ether azeotrope in 95% O2 and 5% CO2 during surface hypothermia are due to a greater cardiac output and reduced peripheral vascular resistance.
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PMID:Circulatory dynamics during surface-induced hypothermia under halothane-ether azeotrope anesthesia. 680 89

To determine the myocardial temperature that provides maximal preservation of the heart during global ischemic arrest, five groups of dogs were studied (6 per group). In all animals, the aorta was cross-clamped for 120 minutes. Serial biopsies were done for determination of adenosine triphosphate and creatine phosphate, and study by electron microscopy. Starling curves were derived prior to cardiopulmonary bypass and 60 minutes after bypass. Mitochondrial changes were graded on a scale of 0 to 4. In the control group (Group 1), the aorta was clamped when the rectal temperature reached 25 degrees C (myocardial temperature, 18 degrees to 22 degrees C). In Groups 2, 3, 4, and 5, myocardial temperature was maintained at 6 degrees C, 10 degrees C, 14 degrees C, and 18 degrees C (all +/- 2 degrees C), respectively, by the use of systemic and topical hypothermia and repeated injections of cold cardioplegic solution into the aortic root. All groups showed a depression of left ventricular stroke work index, particularly Group 1 (no survivors), Group 2, and Group 3. The high-energy phosphate stores were well preserved in all groups except Group 1. The mitochondrial ultrastructure showed significant changes in all groups, especially Groups 1 and 5. These data indicate that satisfactory preservation of mitochondrial ultrastructure and high-energy phosphates was achieved at myocardial temperatures lower than 18 degrees C. Extreme hypothermia (Groups 2 and 3) was associated with significant reduction in ventricular function under the experimental conditions employed.
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PMID:The optimal temperature for preservation of the myocardium during global ischemia. 686 4


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