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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although a role for free radicals in myocardial damage during cardiopulmonary bypass for open heart surgery has been postulated, direct evidence of free radical production as well as consumption of tissue antioxidants such as vitamin E is still lacking. Twenty patients (age 26-66 yr, mean 48) undergoing elective open heart surgery with moderate hypothermia, and cold crystalloid cardioplegia, were studied. Cardiopulmonary bypass time was 61.4 +/- 31.2 min. The specimens of atrial tissue collection before and after cardiopulmonary bypass, were immediately frozen in liquid nitrogen. Mean vitamin E atrial content, measured by reverse phase HPLC, was 355 +/- 249 pmol/mg of dry weight basally, 135 +/- 85 pmol/mg (p < 0.05) at the end of the ischemic period and 405 +/- 288 pmol/mg after the reperfusion period (p < 0.01). Microscopic examination of right atrial biopsies ruled out differences in fibrosis or cellular damage as the cause of vitamin E changes. Although a great basal variability in atrial vitamin E content was observed, which was independent of age, sex and clinical status, a reproducible and substantial decrease in atrial vitamin E content after cardiopulmonary bypass occurred (mean reduction 45 +/- 17% and 55 +/- 22%, respectively, after ischemia and after reperfusion). This was directly related to the aorta cross-clamping duration and partially to the minimum temperature achieved. In conclusion, apart from the great variability observed in basal vitamin E tissue content, vitamin E was always reduced during cardiopulmonary bypass, suggesting an oxidative stress on the myocardium during open heart surgery.
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PMID:Myocardial vitamin E is consumed during cardiopulmonary bypass: indirect evidence of free radical generation in human ischemic heart. 146 17

The QRS complex in lead V5 was studied during cardiac surgery. R wave amplitude decreased after induction of anesthesia to approximately 50% to 60% of the preanesthetic level before the institution of CPB (P < 0.001). An rS complex appeared immediately after cardioversion and changed in configuration to an Rs complex 15 to 30 minutes after aortic declamping. The R wave continued to recover toward the preanesthetic level at sternal closure. Patients with coronary artery disease had a poorer recovery of the R wave (P < 0.05) than patients with valvular heart disease; the former recovered to only 50% of the preanesthetic level at sternal closure. Nonsurvivors had much smaller R waves (26.1 +/- 20.5%) than survivors (P < 0.001). The R wave peaked 30 to 40 ms after initiation of the QRS complex, which indicates recovery of conductivity and the activation sequence of the left ventricular (LV) free wall, which is easily disturbed by hypothermia, cardioplegia, and ischemia during aortic cross-clamping. Monitoring QRS complex changes in lead V5 appears to be important on weaning from cardiopulmonary bypass to detect regional ischemia, and also to observe electrophysiologic recovery of the LV free wall.
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PMID:QRS complex changes in the V5 ECG lead during cardiac surgery. 147 59

A mild decrease in temperature (2-3 degrees) can result in marked attenuation of ischemic neuronal damage in living animals. We now report the protective effects of hypothermia in an astrocyte with simulated ischemia in cell culture system. Hypothermia when used during ischemia showed significant reduction of damage. Brief episodes of post-ischemic hypothermia were not protective whereas more prolonged post-ischemic hypothermia showed moderate protection. Cell culture systems may prove to be useful tools to study the mechanisms of hypothermic protection during ischemia.
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PMID:Hypothermia protects astrocytes during ischemia in cell culture. 147 52

Numerous and extremely varied conditions (intense muscular activity, ischemia, metabolic and genetic disorders, infections, immunological diseases and toxic causes) may play a role in the genesis of non-traumatic rhabdomyolysis. Over the past years there has been an increased number of reports of forms due to drug or narcotic intoxication. Seven cases of rhabdomyolysis are reported in patients admitted to emergency wards in a state of coma due to heroin overdose (4 cases), cocaine overdose (1 case), carbamazepin (1 case), and tricyclic anti-depressives (1 case). In all cases it was possible to hypothesise a multifactorial pathogenesis of the disease in which other factors, such as acidosis, hypoxia, hypothermia and compression of the muscle mass during coma, were associated with the direct toxic damage caused by the drug. The most frequent complication was acute renal failure. One case of myocardial involvement with non-Q infarction characteristics was also observed.
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PMID:[Rhabdomyolysis during acute poisoning with drugs and narcotics. Experience with 7 clinical cases]. 149 66

The present experiments were designed to assess whether brain hypothermia can reduce the behavioral and histopathological deficits associated with global forebrain ischemia. Animals were subjected to 12.5 min of four vessel occlusion (4VO) with moderate hypotension, and brain temperature maintained at either 37 degrees C (4VO-37) or 30 degrees C (4VO-30). Behavioral tests designed to assess forelimb reflexes and sensorimotor function were given on post-operative weeks 2 and 4. Beginning in week 5, the rats were trained on a variety of navigation problems in the Morris water maze. Histopathological examination of the tissue 2 months following reperfusion revealed that 4VO-37 animals sustained substantial cell death in hippocampal region CA1 and moderate damage to the dorsolateral neostriatum. 4VO-30 animals showed minimal cell death in CA1 and neostriatum. There were no group differences for any of the sensorimotor measures, or for acquisition performance on either the simple place task or visible platform version of the water maze. In contrast, during acquisition of the learning set task, the performance of 4VO-37 animals was impaired relative to either of the other groups, whereas the performance of 4VO-30 animals was not significantly different from the sham controls. These data suggest that moderate intra-ischemic brain hypothermia provides long-lasting protection from behavioral deficits as well as neuronal injury following transient global ischemia.
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PMID:Protective effects of brain hypothermia on behavior and histopathology following global cerebral ischemia in rats. 150

In the present study, a rat hindlimb tourniquet model was used to investigate the effect of moderate hypothermia on ischemic muscle necrosis. Complete circulatory arrest was maintained for 4.5 h. During the ischemic period the animals were kept in an infant incubator at different temperatures. After 72 h survival the percentage of necrosis in the anterior tibial muscle was measured morphometrically on histological slides. At an ambient temperature of 24 degrees C there was 80% necrosis in the anterior tibial muscle. At 22 degrees C the necrosis was reduced to 29%. This reduction corresponds to more than 30 min shortening of the ischemia time. Differences in tissue temperature may explain some of the discrepancies reported in tolerance limits for muscle ischemia. To achieve consistent results in experimental muscle ischemia, it is necessary to control the ambient temperature.
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PMID:Protective effect of low-grade hypothermia in experimental skeletal muscle ischemia. 150 97

The methodological requirements for accurate measurements of brain and body temperature during brain ischemia have been validated in Wistar rats submitted to 30 min of four-vessel occlusion. During ischemia, brains were exposed to three different temperature profiles: spontaneous cooling from 36 to 31 degrees C (n = 10), constant hypothermia at 30 degrees C (n = 19), and constant normothermia at 36 degrees C (n = 21). Direct and indirect brain temperature recordings were carried out by placing fine thermocouples (200 microns diameter) into the striate nucleus, the temporal muscle, and the epidural space. Body temperature was measured with a flexible thermocouple inserted at various depths into the rectum. Accurate measurements of body temperature required insertion of the rectal probe to a depth of at least 6 cm; lesser insertion resulted in an underestimation of up to 6 degrees C. Accurate estimates of brain temperature were obtained in all three experimental conditions by recording of the epidural temperature. The temperature in the temporal muscle, by contrast, differed from the brain temperature by up to 2 degrees C, depending upon the experimental condition and the duration of ischemia. We therefore suggest that indirect measurements of brain temperature during ischemia are carried out in the epidural space in order to avoid misinterpretations of temperature-sensitive pathological changes.
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PMID:Methodological requirements for accurate measurements of brain and body temperature during global forebrain ischemia of rat. 150 46

The effect of hypothermia on neuronal injury following permanent middle cerebral artery (MCA) occlusion in the rat was examined. Moderate hypothermia (body temperature 24 degrees C) was induced before MCA occlusion (0-minute delay group) in six rats, at 30 minutes in eight rats, and at 1 (seven rats), 2 (seven rats), and 3 (nine rats) hours after occlusion. The rats were kept at a 24 degrees C body temperature for 1 hour, then allowed to rewarm over 90 minutes. The animals were sacrificed 24 hours after MCA occlusion, and infarction was visualized by staining of coronal sections with 2,3,5-triphenyltetrazolium chloride. Infarct volumes were compared to matched normothermic control rats (body temperature 36 degrees C). Additional groups of 0-minute delay hypothermic (10 rats) and control animals (nine rats) were sacrificed 72 hours after MCA occlusion to examine the effects of prolonged survival. A significant reduction in the percentage of infarcted right hemisphere was seen in the animals sacrificed after 24 hours with 0-minute, 30-minute, and 1-hour delays in inducing hypothermia (mean +/- standard error of the mean: 2.2% +/- 0.7%, 4.4% +/- 0.9%, and 3.6% +/- 1.1%, respectively) as compared to normothermic control rats (10.8% +/- 1.5%, p less than 0.01 by Student's t-test). In the 2- and 3-hour delay groups, the percentage of infarcted right hemisphere was 17.1% +/- 2.4% and 12.0% +/- 2.7%, respectively, and no decrease in infarct volume was observed. The 0-minute delay hypothermia group sacrificed after 72 hours also displayed a significant reduction in right hemisphere infarct compared to their respective controls (4.8% vs. 11.7%, p less than 0.05). These findings indicate that, in the setting of permanent MCA occlusion, hypothermia markedly decreases brain injury even when its induction is delayed for up to 1 hour after the onset of ischemia. Ischemic damage does not appear to be merely retarded but permanently averted.
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PMID:Reduction by delayed hypothermia of cerebral infarction following middle cerebral artery occlusion in the rat: a time-course study. 150 91

Difficulties persist in providing optimum myocardial protection to neonatal hearts undergoing congenital cardiac repair. Controversy on actual ischemic sensitivity of neonatal hearts compared to adult hearts may depend on species, age selected, and conditions of the experimental protocol. In 1985, our laboratory began to investigate this area using the time to ischemic contracture (TIC) model popularized by Hearse and Wechsler and reported that neonates developed TIC in a significantly shorter time than adult hearts. The neonatal heart had rapid lactate accumulation and early rapid decline in glycogen that was not sustained. This led to ATP decline and triggered TIC. The adult heart had a more gradual lactate accumulation with complete glycogen utilization. As a result ATP stores were maintained longer, which prolonged TIC. Neonatal hearts demonstrated sensitivity to alterations in extracellular calcium and only minimal additional detrimental effects of ventricular fibrillation (VF) on TIC. More complete glycogen utilization and a greater tolerance to ischemia was noted in the neonates when constant washout was provided by removing tissue metabolites (Lactate). In neonates moderate hypothermia (25 degrees C) and deep hypothermia of varying levels (19 degrees C, 12 degrees C) demonstrated that lactate accumulation was significantly less than normothermia and ATP decline was slowed. A subgroup of hearts had 40%-50% lower ATP stores before ischemia and significantly shorter TIC. These "at risk" hearts do not have the same safe time for surgical repair. Further developments will result in improved outcomes for this young patient population.
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PMID:Age-related differences in myocardial metabolism affects response to ischemia. Age in heart tolerance to ischemia. 152

The protective effect of mild hypothermia was studied in rodent models of both permanent and transient focal cerebral ischemia. In Expt. 1, Wistar rats were exposed to 6 h permanent ischemia by bilateral occlusion of both common carotid arteries and right middle cerebral artery. In Expt. 2, animals were exposed to 3 h transient ischemia followed by 21 h reperfusion, and in Expt. 3, 3 h transient ischemia was followed by 69 h of reperfusion. Expt. 4 used 3 h transient ischemia followed by 3 h reperfusion. In Expt. 1, animals maintained at 37 degrees C rectal (normothermia) suffered a mean infarct volume (+/- S.D.) of 142 +/- 44 mm3 (n = 6), which was reduced for those exposed to permanent hypothermic (32 degrees C) ischemia to 56 +/- 64 mm3 (n = 10) (P less than 0.05). In Expt. 2, normothermic ischemia and reperfusion resulted in an infarction of 211 +/- 35 mm3 (n = 6). Intra-ischemic hypothermia (32 degrees C) followed by 21 h of normothermic reperfusion resulted in 17 +/- 12 mm3 of infarction (n = 9) (P less than 0.001). Hypothermia for either the first or second 1.5 h of the 3 h ischemic insult reduced the infarct volume to 116 +/- 76 mm3 (n = 6) (P less than 0.05) or 108 +/- 73 mm3 (n = 7) (P less than 0.01), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immediate or delayed mild hypothermia prevents focal cerebral infarction. 152 50


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