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

Nifedipine, a slow-channel calcium blocker, is thought to provide useful myocardial protection during prolonged total ischemia and reperfusion. An isolated, isovolumic, feline heart model was used to asses the effectiveness of nifedipine in both cardioplegic (100 microgram/10 ml) and noncardioplegic (10 microgram/10 ml) doses for providing myocardial preservation during 90 minutes of hypothermic ischemic arrest and 45 minutes of normothermic reperfusion. Use of nifedipine was compared to hypothermia (27 degrees C) alone and to hypothermia with potassium cardioplegia. Ventricular function was assessed by recovery of isovolumic left ventricular developed pressure and dP/dt. Myocardial carbon dioxide tension (PCO2) and myocardial oxygen tension (PO2) were measured by mass spectrometry. Potassium cardioplegia and the higher dose of nifedipine resulted in immediate asystole. The rates of rise of PCO were greatest in the group receiving 10 microgram nifedipine and in the control group. The rates of rise in the two cardioplegic groups were significantly lower. Recovery of ventricular function was significantly lower with low-dose nifedipine than with potassium cardioplegia. Higher dose nifedipine resulted in a return of function, which was no different than with potassium cardioplegia. Morphologic protection was better with higher dose nifedipine and potassium cardioplegia than with either low-dose cardioplegia or hypothermia alone. These results demonstrate that nifedipine in a cardioplegic dose results in preservation of myocardial structure and function that is similar to that obtained with potassium cardioplegia. In lower noncardioplegic dose, nifedipine does not appear to offer additional protection compared to hypothermia alone. Whether persistent depression of ventricular contractility will limit nifedipine's clinical usefulness as a myocardial protection agent will require further study.
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PMID:Comparison of myocardial protection with nifedipine and potassium. 44 71

The effect of d-amphetamine-induced hypothermia among rats maintained at a cold ambient temperature is related to its ability to release dopamine in the dopaminergic neurons in the mesolimbic pathway. However, the physiological mechanisms which mediate the hypothermia (heat loss or a decrease in heat production) are not known. Since we have failed to demonstrate effects induced by d-amphetamine on food intake or on heat sensors on the rat's tail we conclude that these are not the mechanisms involved in hypothermia. Effects of d-amphetamine on O2 consumption and CO2 production of rats kept at various ambient temperatures were investigated in order to find out if there is any relation between a decrease in body temperature and a decrease in the Basal Metabolic Rate. Neither such relations nor any relations between levels of body temperatures and levels of motor activity were found. The problem of the peripheral mechanisms involved in d-amphetamine-induced hypothermia remain as yet unidentified.
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PMID:D-Amphetamine thermal effects, metabolic rate and motor activity in rats. 59 Nov 93

Experiments were conducted on dogs; cranio-cerebral hypothermia (a reduction of body temperature from 38 to 28 degrees C) led to increase of oxygen and to reduction of carbon dioxide tension in the blood. In case of marked hypothermia (24 degrees C) the blood gaseous concentration became less than at 28 degrees C, but remained above the initial level. This indicates prolonged preservation of adequate lung ventilation in the hypothermic organism.
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PMID:[Blood gases in craniocerebral hypothermia]. 67 45

Acute oral and inhalation toxicity of dichloromethane was investigated in both male and female Sprague-Dawley rats. Oral LD50 was found to be 1.72 ml/kg for males and 1.06 ml/kg for females. LC50 was found to be 18 100 PPM (1 X 6 hours) for both male and female rats. Acute oral intoxication is characterized by severe vascular changes and depression of the central nervous system accompanied by gastro-intestinal hemorrhagy. A similar CNS depression is also found in acute intoxication by inhalation. The nature of the symptoms as well as the sequence of physiological (hypotension, hypothermia) and biochemical events observed (high COHb level, etc.) indicate that the combined action of dichloromethane and its metabolite, carbon monoxide, are responsible for the development of vascular and CNS disturbances and subsequently the sudden death of the animals.
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PMID:[Toxicological studies on dichloromethane, a solvent simulating carbon monoxide poisoning (author's transl)]. 74 72

1 Noradrenaline (0.2 to 20 micrograms) and carbachol (0.1 to 1 microgram) injected into the preoptic/anterior hypothalamic area, evoked dose-dependent falls in core temperature at all sites tested, followed in most experiments by delayed increases that were not dose-related. Muscarine (0.1 to 10 microgram) produced effects similar to those evoked by carbachol. 2 These falls in core temperature were associated with increases in tail temperature, locomotor activity and CO2 elimination (a measure of metabolic rate). 3 The temperature responses to noradrenaline (10 microgram) and to carbachol (1 microgram) were antagonized by intrahypothalamic injections of phentolamine (10 microgram) and atropine (1 microgram), respectively. 4 Analysis of the temperature responses and their respective latencies indicates that carbachol-induced hypothermia was mediated by cholinoceptors in the anterior hypothalamus, whereas hypothermia after noradrenaline was mediated by adrenoceptors throughout the preoptic/anterior hypothalamic area. 5 Vasodilatation of the tail blood vessels contributed significantly to the hypothermia evoked by carbachol, and to that evoked by injections of noradrenaline into the anterior hypothalamus. 6 Hypothermia induced by noradrenaline injection into the preoptic area, was mediated by effector mechanisms additional to non-evaporative heat loss.
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PMID:Effects of noradrenaline and carbachol on temperature regulation of rats. 76 Aug 90

A large number of clinical conditions are associated with a transient or permanent disturbance of brain function. Common to all of them is that, in some way, brain metabolism is changed from the normal. These changes cover a vast spectrum, ranging from the subtle alterations of metabolism encountered in mental disease to those underlying death and dissolution of cells in conditions of oxygen lack. This communication is concerned with brain metabolism in the critically ill with emphasis on conditions of hypoglycemia, hypoxia, and ischemia. We begin by briefly recalling the salient features of brain metabolism in the healthy individual. Since clinicians caring for critically ill patients take an interest in factors that may aggravate the primary disease and in measures that may prevent or minimize its final effect on the brain, we will also briefly consider how brain metabolism is influenced by potentially harmful factors (hyperthermia, anxiety and stress, and tissue acidosis due to CO2 retention) as well as by measures that are often instituted to ameliorate the effects of hypoxia and ischemia (hypothermia, administration of anesthetics and sedatives). We refer the reader to selected references with preference to recent articles reviewing previous literature.
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PMID:Brain metabolism in the critically ill. 80 79

The lethality of 187 patients with severe carbon monoxide intoxication was investigated in relation to body temperature. 22 per cent of the normothermic, but 36 per cent of hypothermic or hyperthermic patients did not survive the carbon monoxide poisoning. The lethality increases following enhancement of degree and duration of hypothermia. Pretreatment of rats with chlorpromazine producing a decrease of body temperature of 4 degree C induces a small reduction of toxicity after subcutaneous carbon monoxide injection. However, the CO-DL50 decreases from 17 to 11,5 mmol/kg following administration of the same dose of chlorpromazine after carbon monoxide injection. Changes in carboxyhemoglobin levels are consistent with alterations of CO toxicity. On the basis of these results, it appears that it is not advisable to maintain a spontaneous hypothermia during carbon monoxide intoxication.
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PMID:[Hypothermia and carbon monoxide poisoning]. 84 68

Manifestations of carbon monoxide poisoning are mostly attributable to acute hypoxic insult. In the absence of immediately available hyperbaric oxygen chamber, 100% oxygen should be delivered to the patient until carboxyhemoglobin levels in the blood are less than 5%. Presence of abnormal motor activity or prolonged abnormal consciousness are indications for proceeding with hypothermia and mechanical ventilation. Reversal of these manifestations was achieved in 3 reported cases though induction of hypothermia was delayed for as long as 24 hours. However, no beneficial effects were obtained in a fourth patient who did not receive hypothermia until 5 days after exposure. The duration of hypothermia varied between 60-70 hours in patients who showed near-complete recovery.
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PMID:Management of carbon monoxide poisoning in the absence of hyperbaric oxygenation chamber. 93 3

Changes in intramyocardial carbon dioxide tension (Pco2) and arterial oxygen tension (Po2) were recorded in dogs with a mass spectrometer after temporary occlusion of the aorta and the proximal part of the anterior descending coronary artery at normothermic and hypothermic levels. Patterns of hypoxic and hypercapnic changes and their recovery were favorably modified with moderate hypothermia. Deep levels of hypothermia seemed to enhance this protective effect and progressively slow the myocardial metabolism. Occlusion of the proximal part of the anterior descending coronary artery for 30 minutes had a regional effect similar to the general myocardial changes recorded after aortic clamping, while the posterior myocardial probe showed stable control values. These data support previous studies showing that moderate hypothermia halves the oxygen consumption and doubles the "safe" period of anoxic arrest.
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PMID:Myocardial perfusion and metabolism at normothermic and hypothermic levels. 111 22

The influence of halothane, ether, carbon dioxide, and perfusion rewarming on the electrocardiogram was studied in 37 dogs subjected to surface-induced deep hypothermia. Significant anesthetic-related differences in P-R, QRS, Q-T and R-R intervals during cooling were not apparent; however, reduced arterial pressure, ventricular fibrillation, and a greater tendency for bradycardia requiring supportive measures were noted at low temperatures with halothane anesthesia. The use of 95% O2/5% CO2 significantly reduced the QTc at low temperatures; Other phenomena, including the occurrence and significance of J waves, are discussed. The relationship of the electrocardiogram to clinical and pathological results was evaluated and indicates that (1) properly managed resuscitation (manual massage and defibrillation) is not a serious hazard, (2) ether in 100% oxygen is the agent of choice for surface-induced deep hypothermia with prolonged circulatory arrest, and (3) halothane may be used in a procedure combining surface cooling and perfusion rewarming if given in a mixture of oxygen and carbon dioxide.
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PMID:Electrocardiographic changes during surface-induced deep hypothermia. The influence of ether, halothane, carbon dioxide, and perfusion rewarming. 112 62


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