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

Cardiac biopsies were taken from the hearts of 40 patients undergoing open heart surgery for acquired and congenital disease. Tissue samples were taken prior to aortic cross-clamping, at the end of the ischemic period, and 20 minutes after reperfusion. Cardiac arrest was induced with Kirsch's cardioplegic solution at mild hypothermia (28-30 degrees C). Electron-microscopy of these tissue samples showed that cardioplegic arrest allows safe recovery with a tolerable degree of cellular alterations following ischemic periods of approximately 45 minutes. This period of reversible ischemia agreed well with similar studies in dogs that were completed by metabolic studies. ATP4-time in these dogs was 60 minutes under conditions closely resembling those at operationmin spite of the similarity between ischemia tolerance times, marked discrepancies existed on the ultrastructural level. Human hearts showed, generally, a much more marked degree of cellular alterations. The good correlation between ultrastructural alterations and the metabolic status of the canine heart can, therefore, not be used to predict levels of metabolites from human electron-micrographies.
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PMID:Ischemia-tolerance following cardioplegic arrest in human patients and in experimental animals. 115 Jul 32

Clinical use of profound hypothermia and total circulatory arrest has been accompanied by occasional postoperative neurological abnormalities. In a series of infant baboons, surface cooling to 32 degrees C (brain) followed by perfusion cooling by cardiopulmonary bypass with a membrane oxygenator and heat exchanger to 18 degrees C was carried out, after which the circulation was stopped for 30 minutes. The animal was rewarmed to 35 degrees C. Marked alterations in the regional cerebral circulation were observed during perfusion cooling and rewarming. Regional cerebral ischemia was negatively correlated with jugular outflow (total cerebral blood flow) during rewarming, while regional hyperemia showed positive correlation both following perfusion cooling and after rewarming. A higher degree of ischemia in brain ischemic samples was found during rewarming than during cooling. These alterations in regional cerebral perfusion were associated with lactacidosis and hyperglycemia after rewarming, and may be considered potentially responsible for posthypothermic cerebral dysfunction.
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PMID:Cerebral effects of profound hypothermia (18 degrees C) and circulatory arrest. 115 33

Eighty-eight operations for correction of intracardiac congenital heart defects were performed using local cardiac hypothermia for protection of the ischemic myocardium. Twenty-six patients underwent repair of tetralogy of Fallot, 23 had patch closure of ventricular septal defect, 24 had correction of various types of congenital aortic stenosis, and 15 were operated upon for other complex lesions. The overall operative mortality was 5.6%. Ischemia times ranged from 9 to 119 minutes (mean, 48 minutes). Ischemic arrest protected by local cardiac hypothermia provides an optimal operative field, permitting repair of uncomplicated intracardiac defects in a precise, unhurried manner. No hemodynamic abnormalities attributable to the technique were encountered.
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PMID:Local cardiac hypothermia for myocardial protection during correction of congenital heart disease. 118 May 98

The risk of open heart surgery can be lowered by combination of different methods of myocardial protection. 1. Cardioplegia with a potassium free Mg-1-aspartate and Procaine-solution (Cardioplegin). 2. Coronary perfusion after ischemia longer than 35-40 minutes in case of excessive left ventricular hypertrophy or failure. 3. Hypothermia. Surface cooling gives an additional safety if coronary perfusion is not ideal possible in case of multiple coronary stenoses. For patients with this dispositions a continuous coronary perfusion with cardioplegic solution might be advisable, as it was presented by Gercken in his paper. This method was used three times already in human, but is still in an experimental stage.
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PMID:Induced ischemic cardiac arrest. Clinical and experimental results with magnesium-aspartate-procaine solution (Cardioplegin). 119 31

Isolated perfused working rat hearts were subjected to elective cardiac arrest for 20 or 30 min. Various methods of arrest were studied, either singly or in combination and with or without coronary perfusion. The functional recovery of the heart following the termination of arrest was found to be related to the concentration of ATP and creatine phosphate in the myocardium at the end of the period of arrest. In turn, these concentrations were dependent upon the method used to induce arrest. Normothermic ischemic arrest led to a marked reduction in high energy phosphates and a poor functional recovery. In contrast, coronary perfusion with hypothermic solutions or solutions containing high concentrations of potassium, induced arrest without depleting ATP or creatine phosphate. These procedures conferred considerable protection on the myocardium and thus permitted good recoveries. The energy status and recovery associated with ischemic arrest could be improved by combining the ischemia with hypothermia or potassium arrest. The latter, while increasing recovery significantly, still failed to afford complete protection to the myocardium. Potassium chloride gave greater protection than potassium citrate. When topical hypothermia was combined with ischemia, a time and temperature relationship was demonstrated but effective protection could only be obtained with severe topical hypothermia over a relatively short time period. The results stress the importance of maintaining high energy phosphates during arrest, and this requires the provision of a continuous supply of oxygen and nutrient, which may perhaps be best achieved by ensuring continuous and adequate coronary perfusion.
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PMID:Ischemic damage and metabolism during elective cardiac arrest. 120 80

The management of 23 patients with traumatic pseudoaneurysms is presented. A pulsatile mass associated with pain was the usual presentation. Hypertension and hypovolemic shock from rupture are uncommon presentations but potential hazards of this lesion. Twenty-one pseudoaaeurysms were treated surgically. Resection with end-to-end anastomosis (eight patients), with graft replacement (one patient), with lateral repair (seven patients) was done. Hypothermia with circulatory arrest and external Dacron shunt were used to prevent visceral ischemia during high aortic occlusion. There were no mortalities or significant postoperative complications.
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PMID:Traumatic pseudoaneurysms: a review of 32 cases. 124 98

Many renal lesions that were once treated by nephrectomy now lend themselves to surgical correction. The value of in situ hypothermia and ischemia produced by occlusion of the renal artery is detailed. This technique has proved to be a simple, safe and effective surgical approach to the management of most difficult renal lesions.
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PMID:Surgical management of renal lesions using in situ hypothermia and ischemia. 124 4

Drugs that dissolve clots, such as streptokinase and rTPA, and drugs that promote vasodilation are undergoing clinical testing for the treatment of hyperacute stroke, but an adjuvant therapy that either prolongs temporal thresholds before irreversible injury occurs or actually protects the brain from ischemia would transform these trials. Mild hypothermia, either intraischemically or at the onset of reperfusion, provides us with a gold standard for cytoprotection against which new pharmacologic strategies can be measured. The cytoprotective effects of the voltage-sensitive calcium channel blockers and the NMDA antagonists have been relatively less compelling than more recent findings with non-NMDA or AMPA antagonists. Their ability to inhibit SINN or reduce neocortical infarction is remarkable. Future randomized clinical trials for both resuscitated cardiac arrest victims and patients sustaining embolic stroke are predicted by this major advance in the field of stroke medicine.
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PMID:Advances in cerebral ischemia: experimental approaches. 131 34

The effect of opioids on delayed neuronal death was evaluated in the gerbil hippocampus. Male Mongolian gerbils were subjected to transient forebrain ischemia and neuronal density was evaluated in the hippocampus 7 days following ischemia. When hypothermia during and after ischemia was prevented, treatment with morphine, U-50488H, or naloxone provided no significant protection. In contrast, a spontaneous drop in rectal temperature to 32 degrees C at the end of ischemia produced near-complete protection of CA1 pyramidal neurons. No opioids modulate the protective effect of hypothermia.
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PMID:Effect of opioids on delayed neuronal death in the gerbil hippocampus. 131 87

We examined the ability of phenyl-t-butyl-nitrone (PBN), an electron spin trapper, to attenuate ischemia-induced forebrain edema and hippocampal CA1 neuronal loss in gerbils, and to protect rat cerebellar neurons in primary culture from glutamate-induced toxicity. PBN, given i.p. at 75 or 150 mg/kg 30 min before ischemia (5 min occlusion), increased survival (at 7 days) of CA1 neurons from 60 +/- 14 (vehicle-treated, n = 17) to 95 +/- 15 (P less than 0.05, n = 15) and 145 +/- 3 (P less than 0.01, n = 15), respectively. When gerbils were treated with PBN (50 mg/kg, i.p.) immediately and 6 h after reperfusion, followed by b.i.d. for an additional 2 days, CA1 neurons survival improved from 35 +/- 9 (vehicle, n = 20, 6 min occlusion) to 106 +/- 17 (P less than 0.01, n = 13). In gerbils exposed to a more severe ischemia (10 min), pretreatment with 150 mg/kg PBN increased the survival of CA1 neurons from 6 +/- 6 (vehicle) to 27 +/- 10 (P less than 0.05, n = 11). Pretreatment with PBN, at 150 mg/kg, reduced forebrain edema (following 15 min ischemia) by 24.7% (P less than 0.01, n = 16). PBN at 50 mg/kg, i.p. had no hypothermic effect and at 75 or 150 mg/kg caused a transient hypothermia. The presence of PBN in the brain was confirmed in microdialysis samples and brain tissue extract using HPLC. In vitro, PBN protected rat cerebellar neurons against 100 microM glutamate-induced toxicity with an EC50 value of 2.7 mM. Our results further support the concept that free radicals contribute to brain injury following ischemia and suggest the potential therapeutic application of electron spin trappers in stroke.
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PMID:Neuroprotective effects of phenyl-t-butyl-nitrone in gerbil global brain ischemia and in cultured rat cerebellar neurons. 135 99


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