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

The development of myocardial ischemia is known to elicit the formation and enlargement of collateral vessels. The stimulus for these events is unknown. We have investigated the possibility that cardiac tissue releases a factor that can stimulate endothelial cell proliferation. Hearts from New Zealand rabbits were made progressively ischemic by differential hypothermia. Extracts from these hearts were tested for their growth-stimulating ability and were found to increase the proliferation of fetal bovine aortic endothelial cells as well as DNA synthesis by 3T3 cells. The level of activity in the extracts appears to be related to the degree of ischemia as measured by creatine phosphokinase levels. The liberation of an endothelial cell growth factor by ischemic cardiac tissue may function in the initiation and/or potentiation of coronary collateral formation.
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PMID:Do ischemic hearts stimulate endothelial cell growth? 646 72

The ability of dl-verapamil to enhance myocardial protection when given before, during, or after myocardial ischemia was assessed with the use of an isolated working rat heart model of cardiopulmonary bypass and ischemic cardiac arrest. Under conditions of normothermic ischemic arrest (30 minutes at 37 degrees C), the addition of verapamil enhanced the protective properties of the St. Thomas' Hospital cardioplegic solution. Optimal protection was observed with verapamil concentrations of 0.5 mg/L (1.09 mumol/L) of cardioplegic solution. Under these conditions, postischemic enzyme leakage was reduced by 32.2% and the postischemic recovery of aortic flow was improved by 18.7%. Despite the additional protection at normothermia, the drug at several concentrations appeared unable to improve functional recovery after an extended period of hypothermic arrest (150 minutes at 20 degrees C), although under these conditions its inclusion in the cardioplegic solution could substantially reduce enzyme leakage. In other studies, the ability of various doses of verapamil alone as a substitute for the cardioplegic solution was examined. At the optimal dose (again 0.5 mg/L), and under normothermic conditions, verapamil alone was a good protection against ischemic injury, although this protection did not match that afforded by the St. Thomas' Hospital cardioplegic solution. In similar studies under hypothermic conditions, the drug failed to afford tissue protection, perhaps indicating some common modality between hypothermia and verapamil-induced protection. Pretreatment with verapamil (0.1 mg/L) prior to ischemia offered moderate additional protection, but its use during reperfusion failed to enhance overall recovery.
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PMID:Cardioplegia and slow calcium-channel blockers. Studies with verapamil. 687 61

Recent experimental work implicates oxygen free radicals as mediators of ischemia/reperfusion injury. A simple cardioplegic solution was designed to scavenge superoxide anion and hydroxyl free radical with superoxide dismutase (10 micrograms/ml), mannitol (325 mOsm/L), and KCl 25 mEq/L (FRS). Hemodynamic and subcellular functions were studied in seven in situ canine models of hypothermic global ischemia receiving FRS, compared to a group (n = 7) receiving hyperosmolar, hyperkalemic saline (HSK) and to a standard model of topical hypothermia (TH, n = 5). Following 60 minutes of ischemia (10 degrees to 15 degrees C), hearts were reperfused and rewarmed. After 45 minutes of reperfusion, left ventricular peak systolic pressure (LVPSP), developed pressure (LVDP), dP/dt max, -dP/dt max, compliance, and elastic stiffness constant (K) were improved in the FRS group and not significantly different from control. Sarcoplasmic reticulum (SR) calcium transport in the FRS group was significantly improved (control = 1.077 +/- 0.022, TH = 0.754 +/- 0.018, HSK = 0.725 +/- 0.05, and FRS = 0.966 +/- 0.05 mumol/mg-min). Calcium adenosine triphosphatase (ATPase) activity did not differ significantly from control at pH 7.0. In this model of hypothermic global ischemia and reperfusion, free radical scavengers provide significant protection of mechanical and subcellular function. These findings support the hypothesis that oxygen free radicals are important mediators of myocardial ischemia and reperfusion injury.
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PMID:Inhibition of surgically induced ischemia/reperfusion injury by oxygen free radical scavengers. 687 62

After cardiac catheterization a 53-year old patient developed widespread myocardial ischemia that produced electromechanical dissociation and cardiogenic shock. The administration of methylprednisolone, the initiation of cardiopulmonary bypass and hypothermia within 40 min of the onset of ischemia, and reperfusion within 90 min of the onset of ischemia were sufficient to salvage a major portion of the ischemic myocardium.
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PMID:Salvage of acutely ischemic myocardium by emergency coronary artery bypass grafting. 696 63

Postoperative graft patency and thirteen perioperative variables were evaluated as potential risk factors for perioperative myocardial infarction (MI) in 102 consecutive patients undergoing coronary artery bypass grafting. Also, the incidence of perioperative MI and the amount of CK-MB released in the postoperative period were compared in three groups of patients selected according to the myocardial preservation technique employed: (1) topical hypothermia with and (2) without aortic cross-clamping and (3) cardioplegia. A perioperative MI as detected by electrocardiogram, enzymes, and myocardial scintigraphy with technetium 99 developed in 15 patients. Most important predictors of perioperative MI were found to be (1) left main and triple-vessel coronary artery disease, (2) a left ventricular end-diastolic pressure greater than or equal to 15 mm Hg, (3) a decreased ejection fraction (p < 0.05), and (4) cardiopulmonary bypass time > 120 minutes (p < 0.01). The incidence of perioperative MI was 50% in patients with three or more risk factors and 7% in those with less than three risk factors (p < 0.001). Graft patency was similar in patients with or without perioperative MI. Differing myocardial preservation techniques did not influence CK-MB release or the incidence of perioperative MI. Thus, the severity of ischemic heart disease and the length of the cardiopulmonary bypass time were important predictors of perioperative MI while graft patency and myocardial preservation technique did not appear to be related to its incidence in this study.
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PMID:Predictors of perioperative myocardial infarction in coronary artery operation. 697 16

Fifty patients undergoing isolated coronary artery bypass grafting procedures using a clear, cold cardioplegic solution, topical hypothermia, and reduced systemic flow for intraoperative myocardial protection were evaluated for myocardial injury by serial plasma creatine kinase-MB isoenzyme (CK-MB) measurements and electrocardiograms. Forty-one (82%) of the patients had three-vessel disease. Preoperative left ventricular contractility determined angiographically was normal in 13 patients (26%), mildly abnormal in 26 (52%), and moderately or severely abnormal in 11 (22%). The number of arteries grafted ranged from 2 to 6 (mean, 3.5). The mean duration of aortic clamping was 38.6 +/- 1.6 minutes. There were no hospital deaths. Enzymatic and electrocardiographic (ECG) evidence of myocardial infarction occurred in 1 patient. Nonspecific ECG changes occurred in 16 patients (32%), and th electrocardiograms were unchanged in the remaining 33 patients (66%). In the 49 patients without ECG evidence of infarction, the mean peak plasma CK-MB value, which occurred 6 hours after the onset of cardiopulmonary bypass, was 7.9 +/- 0.8 IU/L (standard error of the mean) and the mean integrated area 158 +/- 19.5 IU/L X hours. There was no correlation between these CK-MB values and the extent of disease, number of arteries grafted, or the duration of myocardial ischemia. These data document a low incidence of perioperative myocardial injury with this technique, and can serve as a baseline for comparison with other techniques for intraoperative myocardial protection in this setting.
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PMID:Detection of myocardial injury after coronary artery bypass grafting using a hypothermic, cardioplegic technique. 697 14

The dynamics of the content of insulin, somatotropic hormone, glucose and the free fatty acids were studied in 32 male patients with ischaemic heart disease subjected to direct revascularization on the myocardium under neuroleptanalgesia and artificial circulation with moderate hypothermia and haemodilution. It is established that during operations on the coronaries under these conditions insulin secretion is not depressed, despite stable increase of the somatotropic hormone in the blood. High concentrations of glucose and insulin in the blood prevent the rise of the free fatty acids.
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PMID:[Dynamics of the insulin, somatotropic hormone, glucose and free fatty acid content in the blood during a direct myocardial revascularization operation under neuroleptanalgesia]. 703 32

The aim of this study was to investigate the protective efficacy of potassium cardioplegia in general moderate hypothermia, in five pigs, after 90 minutes of myocardial ischemia induced by extracorporeal circulation (ECC) and aortic clamping. The behaviour of subendocardial supply demand ratio (DPTI/TTI), of CSBF (coronary sinus blood flow) and numerous hemodynamic parameters was evaluated in addition to lactate myocardial metabolism changes, at rest, after 90 minutes of total ECC and during a 60 minutes reperfusion period. The reperfusion period included two phases: during the first (15-20 minutes) the animals were in ECC with unclamped aorta; spontaneous circulation was instituted during the second one (40 minutes). A marked increase in CSBF was observed at aortic clamp removal during the first phase (post ischemic reactive hyperemia). Coronary sinus lactate release was also noted, probably due to wash-out of previously sequestered acid metabolites during aortic clamping (90 minutes). At the onset of the second phase a depressed left ventricular performance and low DPTI/TTI values were shown. A rapid return (20 minutes) to normal values of this parameter was then noted. DPTI/TTI normalization results strictly correlated to the progressive improvement in myocardial performance. Hypothermic potassium cardioplegia seems therefore to prevent the irreversible myocardial damage and favour a fast recovery of cardiac function.
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PMID:[Importance of metabolic disorders and endocardial viability ratio in the prognosis of open-heart operations. Experimental study of the pig heart protected by potassium cardioplegia in hypothermia]. 712 92

Between 1974 and 1979 nine patients, aged 10 months to 4 years, underwent left ventriculotomy for closure of single or multiple defects in the muscular ventricular septum. The vertical incision paralleled the anterior descending branch of the left coronary artery near the apex of the left ventricle and ranged from 2.5 to 3.5 cm in length. Four patients also had a right ventriculotomy with closure of a high perimembranous ventricular defect in two. Serial electrocardiograms indicated changes of myocardial ischemia or necrosis. Left bundle branch block did not develop in any patient. Three patients died in the early postoperative period. The six surviving patients are living and well 2 to 7 years later. There is apparent complete closure of the ventricular defects, which was documented by cardiac catheterization in four cases. Two patients had cardiomegaly and left ventricular dysfunction as assessed with echocardiographic and angiographic study, whereas four displayed good cardiac function. In three of the latter patients, cardioplegia or deep hypothermia techniques were utilized intraoperatively. The observations indicate that left ventriculotomy of limited size is an acceptable approach to the difficult problem of repair of muscular ventricular defects but may involve some risk of compromise of the coronary circulation.
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PMID:Muscular ventricular septal defects repaired with left ventriculotomy. 730 35

In clinical use cardioplegia is usually combined with local cardiac hypothermia, whose powerful protective effects make it difficult to assess the contributions made by the cardioplegic solution. The additive protective effects of hypothermia and of an experimental cardioplegic infusate were studied in 20 dogs which were subjected to 120 minutes of myocardial ischemia at 20 degrees C. In the hypothermic group 10 hearts were infused with a noncardioplegic solution at 20 degrees C at the onset and after 60 minutes of ischemia. In the cardioplegia plus hypothermia group of 10 hearts identical infusion conditions were followed, with the cardioplegia solution at 20 degrees C. Measurements of ventricular function before and after bypass revealed significantly better recoveries in the cardioplegic group than in the hypothermic group. Recoveries of cardiac output, left ventricular minute work, and dP/dt in the cardioplegia group were 92%, 62% and 91%, respectively, whereas in the hypothermia group the values were 38%, 17%, and 43%, respectively. Parallel biochemical assessments from biopsies revealed that postischemic myocardial adenosine triphosphate (ATP) content was unchanged from control in the cardioplegia group but fell significantly to 56% of control in the hypothermia group. Assessment of myocardial integrity by birefringence showed no change in the cardioplegia group but a deterioration in the hypothermia group. These results demonstrate that chemical cardioplegia when combined with hypothermia affords additional protection to the ischemic heart.
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PMID:The additive protective effects of hypothermia and chemical cardioplegia during ischemic cardiac arrest in the dog. 735 Mar 86


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