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

A number of methods have been used to protect organ systems and cells from the ravages of ischemia and hypoxia. Some have attempted to reduce the metabolic needs, such as by hypothermia, cardioplegia, and slow calcium channel blockers. Others have attempted to provide the metabolic needs, such as by cold blood cardioplegia and solutions of readily metabolized substrates. Our work has centered on the use of fructose 1-6-diphosphate, which can be used anaerobically after glycolysis has been stopped by the effects of anoxia and acidosis. Fructose diphosphate has proved effective experimentally in ameliorating the effects of local and global ischemia of the heart. It has also been found to be of value in many hypoxic or ischemic states including traumatic, septic, endotoxic, and hypovolemic shock. The rationale and a survey of preliminary results are presented.
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PMID:Metabolic effects of fructose diphosphate in hypoxic and ischemic states. 623 13

Using an isolated rat heart preparation under both aerobic and ischemic conditions we have characterized the temperature dependency of the slow calcium channel-blocking drug verapamil. In the first series of studies, isolated working rat hearts were subjected to global ischemia at 37 degrees, 34 degrees, 31 degrees, 29 degrees, 27 degrees, 25 degrees, and 20 degrees C. The duration of ischemic arrest was adjusted so that in the control group the postischemic recovery of function (aortic flow) was approximately 50% of its preischemic value. Ischemic times were therefore 35, 50, 55, 60, 80, 100, and 130 min, respectively. In all cases hearts were subjected to 3 min preischemic infusion with St. Thomas' cardioplegic solution with or without added verapamil (1.1 mumol/liter). At 37 degrees C verapamil increased recovery by 36.6 +/- 4.8%; this increased to 57.4 +/- 6.0% at 34 degrees C. Below 34 degrees C, however, additional protection was progressively lost, so that at 27 degrees C or below verapamil contributed no significant additional protection. In separate aerobic perfusion studies with paced Langendorff-prepared hearts with intraventricular balloons, verapamil (0.2 mumol/liter) was shown to depress pressure development by up to 76% at 37 degrees C; this increased to 92% at 34 degrees C, but thereafter the drug's negative inotropic effects declined, so that at 24 degrees C and below there was no significant difference in developed pressure between the control and drug-treated groups. On the basis of these and other studies, the argument is advanced that by some mechanism common to both hypothermia and verapamil, the anti-ischemic and negative inotropic effects of verapamil are rendered redundant under conditions of hypothermia.
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PMID:Calcium antagonists and hypothermia: the temperature dependency of the negative inotropic and anti-ischemic properties of verapamil in the isolated rat heart. 674 70

This study was designed to investigate whether the calcium channel blocker diltiazem affects the threshold for ventricular fibrillation during hypothermia in dogs. Ten dogs were cooled from 37 to 25 degrees C and rewarmed to 37 degrees C. The threshold for ventricular fibrillation was determined at body temperatures 37, 34, 31, 28 and 25 degrees C by programmed electrical stimulation using a stimulation protocol which involved application of maximal five extrastimuli. At 25 degrees C, six dogs were given an i.v. bolus dose of 100 micrograms.kg-1 followed by a continuous infusion of 100 micrograms.kg-1.h-1 of diltiazem hydrochloride. The other four dogs, were given no drugs at 25 degrees C and served as a control group. The dogs were rewarmed, and the stimulus protocol was performed at the same temperatures as during cooling. Cooling from 37 to 25 degrees C reduced the threshold for ventricular fibrillation in both groups. Heart rate were reduced, monophasic action potential duration at the apex and base of the heart increased from 167 +/- 5 ms to 469 +/- 17 ms and from 164 +/- 5 ms to 466 +/- 17 ms, respectively, when the temperature was reduced. The ventricular effective refractory period increased from 176 +/- 9 ms at 37 degrees C to 472 +/- 15 ms at 25 degrees C. Cooling increased QRS time on the ECG from 55 +/- 4 ms to 138 +/- 13 ms. Addition of diltiazem at 25 degrees C did not affect the threshold for ventricular fibrillation during rewarming. Further, diltiazem at 25 degrees C did not affect the heart rate or refractoriness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diltiazem does not increase ventricular fibrillation threshold during hypothermia. 757 17

Several strategies have been proposed for protecting the brain from ischaemic and hypoxic insults, based on an understanding of the pathophysiological processes involved. They include hypervolaemic haemodilution, anaesthesia, hypothermia, normoglycaemia, calcium channel blockers, adenosine modulators, NMDA- and AMPA-receptor antagonisms and lazeroids. Some have only been shown to be effective in animals and some have clinical relevance. Only hypothermia is protective in a variety of pathological states.
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PMID:Neuroprotection: fact or fantasy? 764 47

1. This study investigated the thermoregulatory effects of cocaine combined with two reported antidotal treatments for acute cocaine overdosage, calcium channel blocker therapy and cold ambient temperatures. 2. Cocaine and nicardipine alone lowered the core temperature of female guinea-pigs (ambient temperature, 5 degrees C) which resulted in a drop in core temperature of approximately 2 degrees C at their highest respective doses (40 mg/kg and 50 mg/kg). 3. Nicardipine administration 30 min prior to cocaine caused an almost 2-fold drop in temperature (3.75 degrees C) relative to either drug alone. 4. The data suggest that cocaine and nicardipine produce hypothermia by different, but additive, mechanisms.
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PMID:Additive hypothermic effects of cocaine and nicardipine in guinea-pigs. 772 Oct 32

Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. The incidence of postoperative neurologic deficits varies from 4% to 38%. Factors associated with a greater risk for injury include the presence of dissection or extensive thoracoabdominal disease, and a prolonged cross-clamp time. Spinal cord ischemia initiates a deleterious cascade of biochemical events that ultimately result in an increased intracellular calcium concentration. Calcium-activated proteases, lipases, and nucleases mediate the processes that cause cell injury. The accumulation of oxygen-derived free radicals and the occurrence of hyperemia during reperfusion are also contributing causes of spinal cord injury. Increasing the spinal cord blood flow with shunts, oxygenated bypass circuits, cerebrospinal fluid drainage, the intrathecal administration of vasodilators, and the reattachment of intercostal arteries has been tried in an effort to increase spinal cord perfusion. Pharmacologically based measures to prevent spinal cord injury have been pursued, and these have consisted of hypothermia, anesthetic agents, calcium channel blockers, free radical scavengers, and immune system modulation. However, no single technique has proved to be consistently effective in preventing ischemia-induced spinal cord injury.
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PMID:Prevention of spinal cord injury after repair of the thoracic or thoracoabdominal aorta. 781 42

Several amphetamine analogs, when administered in high-dose regimens, have been shown to cause long-lasting depletions of central serotonin (5-HT), which are indicative of neuronal toxicity. These depletions and the resulting toxicity can be attenuated pharmacologically or by lowering ambient temperature. The noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (DZ) blocks depletion of 5-HT induced by methamphetamine (METH) and p-chloroamphetamine (PCA), but not fenfluramine (FEN). This study investigated whether the effects of DZ and another calcium channel antagonist, dextromethorphan (DEX), are due to induction of hypothermia. Male Sprague-Dawley rats were injected with either saline (SAL), DZ (1 or 2 injections of 2.5 mg/kg), or DEX (75.0 mg/kg) followed by either SAL, METH (4 injections of 10.0 mg/kg), PCA (1 injection of 10.0 mg/kg) or FEN (2 or 4 injections of 12.5 mg/kg). Core body temperature (TEMP) was monitored for 4 h or longer with radiotelemetry. Base-line TEMP was between 37.0 and 37.6 degrees C. SAL/METH caused a significant increase in TEMP which peaked at 40.8 +/- 0.50 degrees C after the last injection. Coadministration of DZ with METH caused TEMP to decrease to 33.8 +/- 0.30 degrees C within 2 h of the first injection and lasting more than 3 h, and protected against depletion of 5-HT. SAL/PCA caused a small increase in TEMP to 37.7 +/- 0.36 degrees C, whereas coadministration of DZ with PCA decreased TEMP to 35.2 +/- 0.50 degrees C, lasting 2 h, in a dose regimen which has been shown to be neuroprotective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of hypothermia in the mechanism of protection against serotonergic toxicity. II. Experiments with methamphetamine, p-chloroamphetamine, fenfluramine, dizocilpine and dextromethorphan. 785 5

Recent studies in neonatal animals have shown that hypoxic-ischemic brain damage can be reduced by interventions initiated after the hypoxic-ischemic insult. In this article, the authors focus on potentially new modalities of therapy capable of preventing--or at least reducing--brain damage arising from perinatal cerebral hypoxia-ischemia. Management strategies include oxygen-free radical inhibitors and scavengers, excitatory amino acid antagonists, and calcium channel blocker. Additional information is provided regarding the critical role of glucose in perinatal cerebral hypoxia-ischemia and also the protective effect of hypothermia on preventing brain damage.
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PMID:Potential new therapies for perinatal cerebral hypoxia-ischemia. 810 49

Advances in myocardial preservation have led to improved patient survival after open heart operations. However, few studies have detailed the nature of national or regional patterns of cardioplegia use. To determine the regional pattern, all open heart surgery programs in Missouri were surveyed. During 1 year, it was found that cardioplegia was administered to 8,382 patients by 61 cardiothoracic surgeons at ten academic affiliated hospitals and 16 nonteaching hospitals. All cardioplegic solutions were hospital produced. Of 13 crystalloid solutions, 11 differed from one another and eight were intracellular formulations. Of 28 multidose blood-based cardioplegic solutions, there were 23 different mixtures. Most crystalloid (69%) and blood-based (89%) solutions differed substantially from commonly reported formulations. The incidences of the various additives to crystalloid solutions were as follows: bicarbonate, 92%; glucose, 69%; lidocaine, 54%; mannitol, 46%; magnesium, 31%; calcium, 23%; methylprednisolone, 15%; heparin, 8%; and acetate, 8%. Of the common blood-based cardioplegic solution additives, the following incidences were observed: glucose, 79%; bicarbonate, 43%; trishydroxyaminomethane, 36%; acetate, 29%; magnesium, 29%; procaine (or lidocaine), 25%; citrate-phosphate-dextrose, 18%; mannitol/albumin, 14%; nitroglycerin, 11%; glutamate/aspartate, 11%; calcium, 7%; insulin, 3%; and methylprednisolone, 3%. No calcium channel blocker or high-energy phosphate additives were reported. We conclude that many different cardioplegic admixtures that have not been tested experimentally are used routinely in clinical practice, presumably with acceptable results. Because the salutary effects of induced cardiac arrest and hypothermia may mask suboptimal solutions, further study of customized cardioplegia should be considered, particularly with regard to high-risk patients.
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PMID:Lack of cardioplegia uniformity in clinical myocardial preservation. 814 36

Previous studies have shown that regulation of the cardiovascular system progressively deteriorates with adult aging, limiting cardiovascular adaptive mechanisms to stress such as aerobic exercise or trauma. This present study examined cardiac contractile performance as a function of adult aging in a guinea pig model and secondarily examined the effects of adult aging on cardiac contractile responses to burn injury. In a total of 39 adult and 49 senescent animals, a cutaneous full-thickness burn comprising 45% of the total body surface area was obtained using a template device (Walker model); a sham burn was produced in 38 adult and 35 senescent animals by immersion in room temperature water. Adult aging altered cardiac contraction and relaxation as indicated by significantly lower left ventricular pressure and +/- dP/dt max, as well as diminished left ventricular responsiveness to increases in preload, perfusate calcium, isoproterenol, and calcium channel blockade. Burn injury caused significant hypotension, hypothermia, and a rise in hematocrit regardless of age. Cardiac contractile dysfunction occurred in all hearts after burn injury regardless of age, as indicated by a rightward and downward shift of left ventricular function curves for both burn groups compared with their respective controls. The failure of increasing perfusate calcium to overcome burn-mediated contractile deficits in both age groups suggested that burn injury disrupts sarcolemma-bound calcium. The burn-induced decrease in negative inotropic potency of a calcium channel blocker suggests that burn injury specifically targets the calcium slow channel of the sarcolemma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diminished cardiac contractile response to burn injury in aged guinea pigs. 838 14


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