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

Anesthetized dogs were cooled to a core body temperature of 26 degree C. or maintained at a body temperature of 37 degree C. during periods of 5 and 10 hours of LAD coronary artery occlusion. Subsequent macroscopic dehydrogenase enzyme mapping showed that ischemic injury was 25 per cent less after 5 hours of coronary occlusion and 20 per cent less after 10 hours of occlusion in hypothermic dogs than in normothermic controls. The heart rate and left ventricular minute work in hypothermic dogs decreased to roughly half the levels measured in normothermic animals, while left ventricular contractility was 10 to 40 per cent lower in hypothermic dogs than in normothermic dogs. However, cardiac index and left ventricular end-diastolic pressure were unchanged by whole-body cooling. Thus, hypothermia appeared to diminish the oxygen requirements of the ischemic myocardium without reducing the performance of the heart as a pump. Hypothermia may be useful as a therapeutic adjunct to myocardial revascularization or pharmacologic interventions.
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PMID:Protection of ischemic myocardium by whole-body hypothermia after coronary artery occlusion in dogs. 71 40

The effect of ischemic cardiac arrest on intramyocardial oxygen tension (MpO2) in hearts of dogs under normothermia, moderate hypothermia as well as in heart in deep local hypothermia and in hearts subjected to deep local hypothermia combined with Bretschneider cardioplegia was examined. In the last mentioned condition the myocardial oxygen depletion was slowest and even at the end of 30 minutes of anoxia MpO2 was significantly higher in comparison with the other groups. Release of myocardial ischemia resulted in an immediate rise of MpO2 to overshoot levels in animals in normothermia and with deep local hypothermia alone, while in animals in moderate hypothermia and with combination of local hypothermia with cardioplegia reversed only to preanoxic values. On the basis of MpO2 measurements and of postischemic recovery of cardiac function the authors conclude that the combination of deep local hypothermia with cardioplegia is superior for myocardial protection to other used techniques.
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PMID:Influence of moderate hypothermia and deep local hypothermia with or without cardioplegia on intramyocardial oxygen tension during ischemic cardiac arrest. 73 59

Subendocardial ischemia develops in hearts that are fibrillated during cardiopulmonary bypass when: (1) the normal ventricle is fibrillated with a sustained electrical stimulus, (2) the hypertrophied ventricle is allowed to fibrillate spontaneously, (3) the fibrillating heart becomes distended, or (4) the perfusion pressure is reduced to approximately 50 mm Hg. Myocardial hypothermia reduces cardiac oxygen requirements during fibrillation but does not prevent ischemia when perfusion pressure falls to levels frequently attained during clinical open-heart operations. The ischemia occurs because flow cannot rise sufficiently to meet the metabolic demands of ventricular fibrillation. The forces interacting to impede adequate flow to the subendocardium during ventricular fibrillation are: (1) the compressive forces exerted on subendocardial muscle by the strength of fibrillation, (2) the compressive forces resulting from raised intracavitary pressure due to occlusion or malfunction of the ventricular vent, and (3) the evolution of myocardial edema as ischemia is prolonged. We have abandoned the use of ventricular fibrillation in clinical open-heart operations and now allow the heart to beat continually with adequate perfusion pressure. We have not needed to use inotropic drugs postoperatively after aortic or mitral valve replacement since adopting this technique.
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PMID:Ventricular fibrillation. Its effect on myocardial flow, distribution, and performance. 80 60

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

This study compares the effects of normothermic and hypothermic spontaneous fibrillation at perfusion pressures of 100 and 50 mm. Hg on the adequacy and distribution of coronary blood flow. During normothermia (37 degrees C.), subendocardial oxygen delivery decreased 45 per cent ( p less than 0.01) and left ventricular flow became redistributed away from the subendocardium (endo-epi flow ratio fell from 1.2 to 0.8) when perfusion pressure was lowered to 50 mm. Hg; abnormal glycolysis (lactate washout) became evident when perfusion pressure was raised to 100 mm. Hg and ischemia was demonstrated by histochemical stains. Hypothermia (28 degrees C) reduced myocardial oxygen uptake 52 per cent (p less than 0.01) at 100 mm. Hg perfusion pressure; left ventricular flow, distribution, and metabolism did not change from control values. Lowering perfusion 50 mm Hg caused a pronounced reduction in subendocardial oxygen delivery (63 per cent, p less than 0.01); abnormal glycolysis developed and histochemical ischemia was seen. These studies show that lowering perfusion pressure in normothermic fibrillating hearts impairs oxygen delivery to the left ventricular subendocardium. While hypothermia significantly reduces left ventricular oxygen requirements, the ventricle is not protected against subendocardial ischemia if perfusion pressure falls to levels frequently used during clinical open-heart surgery.
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PMID:Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. III. Effects of temperature, time, and perfusion pressure in fibrillating hearts. 83 Sep 99

The effects of hypothermia (32 degrees, 28 degrees, and 22 degrees C.) on left ventricular flow distribution (microspheres) and oxygen uptake in adequately perfused, beating, empty, fibrillating, and arrested hearts were studied. Minute left ventricular oxygen uptake fell progressively as myocardial temperature was reduced under all conditions. In beating hearts, however, left ventricular oxygen uptake per beat increased significantly due to the inotropic effect of hypothermia and diastolic compliance fell. Cold fibrillating hearts consumed slightly less oxygen per minute than beating hearts at comparable temperatures as fibrillation became less forceful with hypothermia. Myocardial wall tension, however, was always higher in fibrillating than beating hearts at each level of hypothermia. The lowest myocardial oxygen requirements were always found in arrested hearts (70 to 80 per cent less than either beating empty or fibrillating hearts) at any myocardial temperature. Left ventricular coronary flow remained distributed evenly across the beating heart at all myocardial temperatures and in fibrillating hearts at 28 degrees, and 22 degrees C. Left ventricular flow became redistributed toward the subendocardium in fibrillating hearts at 37 degreegs and 32 degrees C. and in arrested hearts at all myocardial temperatures.
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PMID:Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. I. The adequately perfused beating, fibrillating, and arrested heart. 83 Oct 12

The effect of halothane-100% oxygen anesthesia on oxygen consumption was studied in 10 dogs subjected to surface-induced deep hypothermia with 30 minutes of circulatory arrest. The results were compared with previous oxygen consumtion data under ether-100% oxygen anesthesia. Low cardiac output, especially during the rewarming period, low PaO2, and a large arteriovenous oxygen difference during rewarming were significantly different in the halothane group, despite identical oxygen consumption in both groups. These differences could not elucidate the exact cause of postoperative motor disturbances associated with 30 minutes of circulatory arrest in the halothane group. The possibility that there was higher oxygen consumption under halothane anesthesia is discussed.
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PMID:Oxygen consumption during surface-induced deep hypothermia under halothane anesthesia. 83 45

This study compares (1) the effects of slowing heart rate by topical hypothermia in hearts perfused at 37 degrees C. with bradycardia produced by perfusion hypothermia (28 degrees C.) and (2) the consequences of counteracting the bardycardic effects of perfusion hypothermia by atrial pacing. Topical atrial hypothermia (myocardial temperature 37 degrees C.) produced a level of bradycardia comparable to perfusion hypothermia (82 vs. 71 beats per minute), but reduced myocardial oxygen requirements 25 per cent more than perfusion with 28 degrees C. blood. Myocardial oxygen uptake per beat did not change with topical atrial hypothermia but increased 40 per cent with perfusion hypothermia. Counteracting the bradycardic effects of perfusion hypothermia with atrial pacing (to 130 beats per minute) reduced subendocardial flow 25 per cent, caused a redistribution of flow away from the subendocardium, and produced evidence of ischemia on the intracavitary electrocardiogram. This study shows that (1) topical atrial hypothermia with systemic normothermia reduced myocardial oxygen demands as effectively as perfusion hypothermia and (2) subendocardial ischemia develops in beating empty hearts when the expected bradycardia of hypothermia does not occur.
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PMID:Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. IV. Topical atrial hypothermia in normothermic beating hearts. 83 58

This study compares the effects of 60 minutes of ischemic arrest with profound topical hypothermia (10 dogs) on myocardial (1) blood flow and distribution (microspheres), (2) metabolism (oxygen and lactate), (3) water content (wet to dry weights), (4) compliance (intraventricular balloon), and (5) performance (isovolumetric function curves) with 180 minutes of cardiopulmonary bypass with the heart in the beating empty state (seven dogs). Studies performed before and 30 minutes after 1 hour of ischemic arrest with profound topical hypothermia showed: (1) total left ventricular blood flow increased 50 per cent but became redistributed away from the subendocardium (endocardial/epicardial flow ratio fell from 1.13 to 0.77,(2) left ventricular oxygen consumption fell 30 per cent while left ventricular oxygen extraction fell from 51 to 29 per cent; (3) lactate extraction fell from 15 to 4 per cent (two dogs produced lactate); (4) left ventricular endocardial (papillary muscle) water content rose 2.4 per cent; (5) left ventricular compliance decreased from 1.68 to 1.01 ml. H2O/mm. Hg (at 25 ml.); (6) left ventricular performance was depressed 49 per cent below control values. In contrast, 3 hours of cardiopulmonary bypass in the beating empty heart produced only minimal changes in these variables.
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PMID:Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. V. Profound topical hypothermia during ischemia in arrested hearts. 83 59

Isolated rat liver was studied before, during, and after hypothermic perfusion at 5 C for 24, 48, or 72 hr with an acellular perfusate consisting of 7% bovine serum albumin in Kreb-Ringer buffer containing glucose, penicillin, and streptomycin. Bile production ceased at 5 C but resumed when the temperature was raised to 35 C. The rate of flow and the total amount produced was unaffected by 24 hr of hypothermia but decreased when the cooling period was extended to 48 and 72 hr. The data of other workers was used to show a correlation between bile flow and oxygen consumption by the liver. Cooling also caused the release of potassium into the perfusate but it was quickly reaccumulated after rewarming; however, the extent and rate of reaccumulation decreased as the cooling period increased, as did the ability of the livers to retain the ion. Urea synthesis did not cease after cooling and after rewarming, the rate of synthesis increased as the period of hypothermia was lengthened. The maximum concentration of urea in the perfusate was found when rewarmed livers had produced 200 mumol of urea but at this point, control livers had produced 280 mumol. The concentration of glucose in the perfusate of livers maintained at 35 C showed peaks at 2 and 9 to 10 hr after the start of perfusion. After cooling for 24 hr these peaks arose at 2 and 7 hr after rewarming, but with 48 hr of hypothermia, these peaks were higher and appeared at 2 and 4 hr. When the cooling period was extended to 72 hr, only a single peak was seen 2 hr after rewarming. These results suggest that rat liver can be cooled to 5 C for 24 hr with little effect on its functional characteristics but a marked decline becomes apparent when the cooling period is extended beyond 24 hr. None of the livers studied was transplanted after perfusion and it remains to be seen how the functional tests conducted in vitro correlate with the ability of the livers to support life.
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PMID:Maintenance of the functional state of isolated rat liver by hypothermic perfusion with an erythrocyte-free medium. 83 68


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