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

Some of the barriers to successful lung transplantation include the lack of acceptable methods for ischemic protection and the absence of reliable systems for preservation. The lung response to 60 minutes of warm ischemia basically consists of alveolar-capillary edema and disruption, mitochondria swelling, interstitial hemorrhage, significantly depressed pulmonary function, elevation of pulmonary vascular resistance, and considerable drop in levels of glucose, phospholipids, and adenosine triphosphate. The tolerance to warm ischemia increases to several hours with the use of different systems of ventilatory assistance with or without positive end-expiratory pressure. Several methods of preservation have been attempted: hypothermia, hyperbaria, and hypothermic pulsatile or nonpulsatile perfusion. Hypothermic pulsatile perfusion appears to offer longer periods of protection than the other methods. Longer periods of ischemia and extended preservation may be made possible by advances in the use of drug protection during warm ischemia and the utilization of intracellular colloid or noncolloid solutions for hypothermic storage or hypothermic pulsatile perfusion.
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PMID:Lung preservation techniques. 32 20

In an experimental work published in 1973, it was found, that it was possible to preserve pig kidneys with up to one hour of warm ischemia for 24 hours using pretreatment with chlorpromazine and subsequent preservation with simpel hypothermia (Collings C2-solution). Clinical experiences with this method are now presented and confirm, that this method allows preservation of ischaemic damaged kidneys for about 24 hours.
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PMID:Experimental and clinical experiences with long-term kidney preservation by use of simpel hypothermia. 35 12

Dog kidneys were flushed and stored in Collins (n = 30) and Sacks (n = 32) solution under hypothermia. These results were compared with those gained by mechanical perfusion (n = 21). Before preservation, the kidneys were subjected to 15 - 60 min of warm ischemia then stored for 12 - 24 h. It was concluded that 12-h preservation time after 15-min ischemic injury was the limit of hypothermic storage preservation. Sacks' solution gave better results than Collins' solution as regards the immediate function after transplantation. In contrast, mechanical perfusion was well tolerated for 24-h preservation time after a warm ischemia of 30 min. In case of warm ischemic damage, mechanical perfusion should be preferred to hypothermic storage.
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PMID:[Preservation of kidneys with ischemic injury using hypothermic storage and mechanical prolonged perfusion]. 37 5

The efficiency of hypothermic mechanical perfusion and hypothermic storage, resp., for kidney preservation was to be examined. For this purpose dog kidneys were subdued to 0 to 60 min of warm ischemia, then preserved for 12--72 hours and thereafter transplanted. It could be concluded: 1. Hypothermic mechanical perfusion makes a successful 72 hour preservation possible with excellent kidney function immediately after transplantation. After 30 minutes of warm ischemia the preservation period should be limited to 24 hours. 2. Hypothermic storage is inferior to mechanical perfusion concerning the immediate function after transplantation: 24 hours storage time and 15 minutes of warm ischemia should not be exceeded. 3. Kidney function decreases exponentially by the time of preservation. This means that the warm ischemic period and the preservation time, resp., should be as short as possible to get an undamaged kidney after transplantation: the shorter the preservation period the better the kidney function after transplantation.
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PMID:[Kidney preservation by mechanical perfusion or hypothermic storage]. 38 66

There are 2 competing methods for cooling the kidney in situ during surgical ischemia: from without by applying ice to the renal surface and from within by perfusing the renal artery. The latter procedure is said to be superior in protecting renal function. Herein the protective effect on renal function of both methods are compared. Pigs of 15--25 kg weight underwent nephrectomy on one side. The remaining kidney was subjected to cold ischemia during 90 minutes while perfusion- or surface cooling was performed. For perfusion cooling the aorta was punctured and the catheter introduced into the renal artery. The perfusing liquid consisted of a physiologic electrolyt solution (Ringer-Lactate) with heparin kept at a temperature of 3--5 degrees C. The initial perfusion lasted 10 minutes and resulted in a median renal core temperature of 23 degrees C. Then the kidney was put on a cooling pad and every 15 minutes again perfused for one minute. For surface cooling sterile melting ice made of glucose solution 5% was applied directly to the kidney. The renal core temperature could be kept at 15--20 degrees C. The two methods of hypothermia were judged by comparing the serum creatinine levels and the I131-hippuran clearances one month after surgery. There was no difference whatever as analysed by the t-test. Hypothermia by applying ice to the renal surface therefore proved to be equivalent to hypothermia by perfusion. Moreover it is much simpler.
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PMID:[Renal hypothermia in situ. Comparison between surface and perfusion cooling concerning renal function in pigs (author's transl)]. 41 41

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 effects of pentobarbital on survival times of mice exposed to oxygen, 5 per cent, were studied over a large dosage range in normal mice and in mice made tolerant to the effect of barbiturates. Tolerance was induced by pretreatment with phenobarbital, 210 mg/kg, for three days, which increased the median anesthetic dose (AD50) for pentobarbital from 34 to 53 mg/kg. In nontolerant mice there was a dose-related increase in mean survival times for doses between 35 and 60 mg/kg, with a maximum increase to 303 per cent above control. At doses of more than 60 mg/kg survival times progressively decreased toward control. For tolerant mice survival time as a function of pentobarbital dosage was shifted to the right, i.e., protection necessitated higher doses. This shift was not explained by lower brain concentrations of pentobarbital in tolerant animals, but rather parallelled the increased tolerance to the anesthetic effect of the barbiturate. The authors conclude that in this model the protective effect of barbiturate is a function of the anesthetic effect rather than the barbiturate concentration in brain per se. Hypothermia (29 C) resulted in an increase in mean survival time comparable to that in barbiturate-treated animals. This supports the hypothesis that protection is ultimately a function of decreased cerebral metabolism, whether produced by anesthesia or by hypothermia. This model measures only the effect on spontaneous respiration during hypoxia. It is possible that other mechanisms are involved if barbiturates protect in other situations, such as during or after periods of complete ischemia.
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PMID:Barbiturate protection in tolerant and nontolerant hypoxic mice: comparison with hypothermic protection. 45 57

The present study reports on the epicardial spread of excitation during premature beats and during the initial stages of ventricular fibrillation, both of which were induced by single-test stimuli during regional ischemia or local hypothermia. Simultaneous recording of the activity at 48 epicardial sites on the right ventricle of dog hearts enabled us in some instances to demonstrate a circus movement.
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PMID:Circus movement in canine right ventricle. 45 4

To determine the protective effects of different methods of cardioplegia, studies on ATP/lactate levels and ultrastructure were performed in human papillary muscles obtained during mitral valve replacement. In group I (n = 5), plain ischemic arrest in hypothermia (systemic venous temperature = 24 degrees C) was accomplished. In group II (n =12), the heart was arrested by injection cardioplegia using magnesium-aspartate-procaine at systemic venous and myocardial temperatures of 24 degrees C. In group III (n = 12) Bretschneider infusion cardioplegia at systemic venous and myocardial temperatures of 26 degrees C and 19 degrees C respectively was applied. With regard to ultrastructural changes there were no clearcut differences in the three methods of hypothermic cardiac arrest after 60 minutes of ischemia. Ischemic changes tended to be slightest in group III (infusion cardioplegia). ATP decay and lactate increase were significant in group I and moderate to minimal in groups II and III after the same period of time. It is concluded that for aortic cross-clamp times up to 60 minutes, body hypothermia and injection cardioplegia using magnesium-aspartate-procaine at a myocardial temperature of 24 degrees C provide adequate protection of the myocardium. For ischemia times beyond 70 minutes, profound myocardial hypothermia below 20 degrees C is preferred.
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PMID:Ultrastructural and biochemical changes of human papillary heart muscle during different methods of induced cardiac arrest. 49 22

Potassium (34 mEq/L) cardioplegia was induced with cold blood (CBK) in three groups of six dogs undergoing 60 minutes of myocardial ischemia at a systemic temperature of 27 degrees +/- 2 degrees and a myocardial temperature of 7 degrees +/- 2 degrees C (crushed ice). Group 1 (CBK) animals were reperfused initially with 400 ml cold blood over 8 to 10 minutes at increasing pressures of up to 75 mm Hg. Group II (CBK-K) dogs were reperfused in the same manner as Group I with the addition of potassium chloride, 30 mEq/L. In Group III (CBKG-KG) glutathione, 30 mg/100 ml, was added to both the pre- and postischemic perfusions with CBK. After 30 minutes of reperfusion control studies were repeated. Heart rate, peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of contractile element, pressure-volume curves, coronary flow distribution, muscle stiffness, and heart water were not significantly different from control values. Total coronary flow and myocardial uptake of oxygen, lactate, and pyruvate did not serve to separate the three groups; the same was true for right ventricular creatine phosphate, adenosine triphosphate, and adenosine diphosphate during ischemia and recovery. Ultrastructural myofibrillar lesions were noted in all groups. thus, postischemic cardioplegia and use of a physiological reducing agent do not enhance CBK cardioplegia with topical and systemic hypothermia.
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PMID:Cold-blood potassium cardioplegia: evaluation of glutathione and postischemic cardioplegia. 50 72


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