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

To assess the effects of moderate potassium cardioplegia (37 mEq/l KCl) on the severity of myocardial ischemia during arrest and on post arrest ventricular function, 32 isolated, isovolumic feline hearts were studied before, during and 1 hour after ischemic arrest. Normothermia (37 degrees C) was maintained in the remaining 16 hearts, eight without KCl and eight with KCl. Hypothermia (27 degrees C) was maintained in the remaining 16 hearts, eight with KCl and eight without KCl. Myocardial oxygen (PmO2) and carbon dioxide tensions (PmCO2) were measured by mass spectrometry. Maximum developed intraventricular pressure (max DP) and max dP/dt were used as indices of performance. Compared with normothermic or hypothermic arrest alone, the addition of potassium cardioplegia resulted in a significant reduction in the peak PmCO2 measured during the arrest period. Hypothermia alone resulted in morphologic evidence of improved myocardial preservation and a significant reduction in peak PmCO2 compared with normothermia. Post arrest ventricular function was best with the combination of hypothermic arrest and potassium cardioplegia (max DP = 96 +/- 6% of control and max dP/dt = 99 +/- 5% of control). These data suggest that the beneficial effects of postassium cardioplegia and 27 degrees hypothermia are additive, and that reduction in myocardial ischemia as evidenced by a reduction in peak PmCO2 correlated with improvement in ventricular performance in the post arrest period and with preservation of myocardial structure.
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PMID:Effect of potassium cardioplegia on myocardial ischemia and post arrest ventricular function. 30 60

The authors analyze the results of 220 applications of internal cold cardioplegia in 136 patients with ischaemic heart disease, treated surgically by aortocoronary bypass. The operation was performed under neuroleptanalgesia and artificial circulation with hypothermia (27.9 +/- 0.2 degrees C) and haemodilution (24.9 +/- 0.3%). On the basis of clinical examination, electron microscopy of the myocardial ultrastructure, and investigation of the myocardial metabolism (contents of glucose, lactate, pyruvate, free fatty acids, catecholamines, and oxygen in arterial and venous blood flowing out of the myocardium), they come to the conclusion that internal cold cardioplegia efficiently protects the myocardium during aortocoronary bypass and secures favourable conditions for the development of anastomoses between coronary arteries and venous shunts.
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PMID:Myocardial protection during aortocoronary bypass. 31 79

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

Local hypothermia as a procedure for myocardial protection was utilized in 50 patients; 17 had congenital and 33 aquired heart disease. On patient with diagnosis of A-V canal, previously operated on, died on the 2nd postoperative day after mitral valve replacement and closure of a residual defect. Two other valvular patients died suddenly on the 9th and 20th postoperative days from thrombosis of the prosthesis. The lengths of time of aortic clamping required for correction of these various cardiopathies were analized and correlated with the final results. In comparison with the experience of other authors, a close relationship between the duration of the myocardial ischemia and the figures of morbi-mortality was observed. It is concluded that local hypothermia constitutes an adequate procedure for myocardial protection on the condition that the length of aortic clamping times do not exceed certain limits.
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PMID:[Protection of the myocardium with local hypothermia in open heart surgery]. 55 36

We evaluated the effects of methylprednisolone sodium succinate (MPSS) on 60 minutes of myocardial ischemia during profound (5 degrees C) topical cardiac hypothermia (ice chips) in a canine right heart bypass preparation. The ventricular function curve shifted to the right and downward, but not significantly, after ischemia, and stroke work declined significantly for both control and treated dogs. Contractility (rate of rise of left ventricular pressure and maximum velocity of the contractile element) declined for both groups but not significantly. Total coronary flow, oxygen consumption, and metabolism of lactate and pyruvate were not different for control and treated dogs. Ultrastructure of the outer and inner myocardium did not demonstrate benefit from MPSS. Intracellular and extracellular edema of moderate severity was slightly worse in the subendocardium, and reversible mitochondrial injury of a mild to moderate degreee was symmetrically present. Ice-related injury was not noted. We were unable to deomonstrate that pretreatment with MPSS favorably alters cardiodynamics or ultrastructure after 60 minutes of profound topical cardiac hypothermia.
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PMID:Topical cardiac hypothermia: the effect of methylprednisolone sodium succinate. 65 47

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

Recent studies have shown that after total coronary artery occlusion, there is impaired "reflow" of blood accompanied by myocardial and capillary endothelial cell swelling. To investigate the effect of prolonged low flow myocardial ischemia on coronary vascular resistance, regional hypoperfusion of the distal left anterior descending coronary artery was studied in 31 autonomically blocked dogs on right heart bypass. Heart rate, aortic pressure, and, during ischemia, left ventricular end-diastolic pressure were held constant. The distal left anterior descending coronary artery was perfused at a substantially reduced perfusion pressure which resulted in an antegrade coronary blood flow that usually was between 3% and 7% (0.5-1 ml/min) of control. When relative hypothermia (33-34 degrees C) was induced in nine dogs, left anterior descending coronary artery vascular resistance did not change during 2.5-3 hours of low flow ischemia. Under euthermic conditions (37-40 degrees C) in 17 dogs there was a consistent progressive increase in distal left anterior descending coronary artery vascular resistance starting at 90 minutes (median) after onset of ischemia. By 110-140 minutes ischemic antegrade flow decreased by 35 +/- 4% (SEM) (P less than 0.01). Directionally similar flow changes were observed in six euthermic experiments using the krypton-85 washout technique. Light microscopy did not reveal hemorrhage as a cause of the increased vascular resistance. The perfusion impairment did not occur in two euthermic, nonischemic hearts. In five dogs elevation of serum osmolality by 23 +/- 11 mOsmol/liter with mannitol attenuated the progressive decrease in flow. Thus, a progressive perfusion defect exists in the ischemic low flow state in the heart which presumably contributes to the extent of eventual necrosis.
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PMID:Progressive perfusion impairment during prolonged low flow myocardial ischemia in dogs. 93 13

An isolated perfused working rat heart model was used to investigate the extent to which various protective agents, used either singly or in combination, were able to increase the resistance of the heart to periods of transient ischemia. The aim of the studies was to develop a solution which, if infused into the coronary vessels just prior to the onset of ischemia, would rapidly induce arrest and would also counteract several of the deleterious cellular changes known to occur during myocardial ischemia. Agents with induce cardiac arrest, modify cellular ion loss, affect substrate utilization, energy production and energy stores, affect coronary vessel diameter and cell swelling, prevent dysrhythmias, and affect metabolic rate were investigated. The additive effects of these agents were evaluated. An aqueous solution was formulated which contained high concentrations of potassium and magnesium, in combination with adenosine triphosphate, creatine phosphate and procaine. This solution increased the recovery of the ischemic (37 degrees C for 30 min) rat heart from 0% to 93%. The safe period of ischemia could be further increased by the use of hypothermia.
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PMID:Cellular protection during myocardial ischemia: the development and characterization of a procedure for the induction of reversible ischemic arrest. 93 20

Four patients are reported in whom the aortic arch and variable portions of the ascending and descending aorta were replaced with a prosthesis. In three patients the preoperative diagnosis was dissecting aneurysm of the aortic arch and in one an arteriosclerotic aneurysm of the aortic arch was present. A combination of surface cooling and cardiopulmonary bypass was utilized to produce total body hypothermia. Arch replacement was carried out during a period of total circulatory arrest. Cardiopulmonary bypass was then utilized to warm the patient and resuscitate the heart. The average duration of cerebral ischemia was 43 minutes and the average duration of myocardial ischemia was 74 minutes. The average lowest esophageal temperature was 14 degrees C., and the average lowest rectal temperature was 18 degrees C. Three patients are alive and well 4 to 13 months following surgery. One patient died 4 days postoperatively of pulmonary insufficiency. This experience indicates that by utilizing total body hypothermia and circulatory arrest aortic arch replacement can be carried out with an acceptable mortality rate. Corrective surgery could be offered to patients with life-threatening enlarging aneurysms of the aortic arch.
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PMID:Prosthetic replacement of the aortic arch. 118 83

Causes of death in 8 of 235 drunkenness offenders each followed up for two years, have been described. The subjects followed up were a heterogenous population of alcohol abusers. The majority were alcohol dependent irregular heavy drinkers. The main causes of death were suicide, road traffic accident, domestic accident, liver cirrhosis, hypothermia (from exposure) and ischaemic heart disease. More than one cause of death was listed in all cases. Chronic alcoholism was frequently listed. Depression was another sub-ordinate cause of death. The overall observed rate of mortality was 30 times the expected rate which was many times higher than those reported by earlier workers for alcoholics generally. These findings were discussed and it was concluded that drunkenness offenders are a particular at risk sub group of alcoholics. In view of the appreciable post mortem blood alcohol levels, it was further concluded that chronic alcoholism and the actual state of being drunk were the two major causes of death in this group of alcohol abusers.
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PMID:Causes of mortality in drunkenness offenders followed-up for 2 years. 130 84


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