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

The concept of pretreatment of the myocardium with a pharmacological agent protecting the cell against ischemic and reperfusion injury is very attractive. Lidoflazine, a calcium overload blocker, predominantly membrane stabilizing, is able to prevent cell damage during ischemic arrest and reperfusion. The purpose of this study was to determine whether the combination of lidoflazine pretreatment and St. Thomas' Hospital cardioplegia can provide, in clinical practice, better myocardial protection in aorto-coronary bypass grafting than St. Thomas' Hospital cardioplegia alone. As indices for myocardial protection, recovery of cardiac function, enzyme release, and clinical outcome were registered. Ninety-three patients undergoing aorto-coronary bypass surgery were studied. These patients were randomized into two groups in a double blind fashion. Patients in group A (n = 48) received lidoflazine 1 mg/kg intravenously over a period of 20 min before initiation of cardiopulmonary bypass. Group B (n = 45) receiving placebo, acted as a control group. Myocardial protection consisted of intermittent infusion of cold 4 degrees C St. Thomas' Hospital cardioplegia, topical slush ice, and systemic hypothermia (28 degrees C rectal). No significant differences between the two groups were noted in terms of recovery of cardiac function, enzyme release, incidence of myocardial infarction, low cardiac output, rhythm, and conduction disturbances. In conclusion, our data suggest that the combination of intravenous pretreatment with lidoflazine and St. Thomas' Hospital cardioplegia did not provide significant additional myocardial protection in the clinical situation.
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PMID:Evaluation of myocardial protection by combination of lidoflazine pretreatment and St. Thomas' Hospital cardioplegia in aorto-coronary bypass grafting. 149 31

The effect of almitrine bimesylate or the solvent malic acid on pulmonary vascular perfusion pressure was assessed in isolated rat lungs and on the contractile behavior of rat aorta and main pulmonary artery rings. Addition of almitrine to the lung perfusate during normoxia caused a dose-dependent, transient increase in pulmonary artery pressure with no change of the lung microvascular pressure. In systemic or pulmonary conduit arteries, the contractile tension was unaffected by almitrine. This indicates a precapillary locus of drug action. We also examined almitrine's effect on hypoxic pulmonary vasoconstriction (HPVC) in isolated lungs perfused with blood or with physiological salt solution (PSS). Low-dose almitrine potentiated hypoxic vasoconstriction in blood- but not in PSS-perfused lungs. However, a high dose of almitrine reduced hypoxic vasoconstriction dose dependently. When almitrine was added to the lung perfusate during hypoxia- or cyanide-induced (NaCN, 5 x 10(-5) M) pulmonary vasoconstriction, almitrine caused no further vasoconstriction. However, when the pulmonary perfusion pressure was elevated by KCl (20 mM) to the same magnitude as by alveolar hypoxia or cyanide, almitrine elicited a pressor response comparable to that observed during normoxia. Almitrine-induced pulmonary vasoconstriction resembled hypoxic vasoconstriction in that agents known to enhance hypoxic vasoconstriction (phorbol myristate acetate, vanadate, and 4-aminopyridine) enhanced, and known inhibitors of HPVC (the Ca2+ entry blocker nifedipine and hypothermia) inhibited, the almitrine-induced vasoconstriction. These findings lead us to speculate that almitrine also affects the oxygen-sensing limb of the hypoxic pressor response, not simply the effector (contractile apparatus of the vascular muscle cell).
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PMID:Almitrine mimics hypoxic vasoconstriction in isolated rat lungs. 151 Jan 35

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

Isometric contraction of isolated guinea-pig taenia caeci was induced with acetylcholine (ACh) and 5-hydroxytryptamine (5-HT) at 37 and 30 degrees C to investigate the effect of hypothermia on the response of smooth muscle to neurotransmitters. Lowering the temperature increased the amplitude of contraction in response to 10(-6) M ACh. Contraction in response to 10(-6) M 5-HT was also greater at 30 degrees C. 5-HT-contraction was not inhibited by atropine, but was inhibited by ketanserin. Calcium-contraction was also induced in an isosmotic high potassium solution. The amplitude of the contraction elicited by 5 x 10(-3) M Ca was significantly greater at 30 degrees C, and was inhibited by verapamil. The amplitude of the contractile response to 5 x 10(-3) M caffeine was also greater at 30 degrees C than at 37 degrees C. The finding that both calcium- and caffeine-contraction were enhanced at low temperature raises the possibility that intracellular calcium participate in cold-induced enhancement of contraction.
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PMID:Hypothermia enhances contractile responses of the guinea pig taenia caeci to acetylcholine, 5-hydroxytryptamine, caffeine and calcium. 157 74

The combined action of phosphatidylcholine preferring phospholipase C (PC-PLC) and intracellular lipases has recently been shown to cause glycerol output in energy deprived rat cardiomyocytes. In the present study we examined the effect of hypothermia and rewarming on PC-PLC evoked glycerol output in freshly isolated, calcium-tolerant myocytes. The cells were preincubated for 60 min at hypothermic (5 degrees C) or normothermic (37 degrees C) conditions in Krebs-Henseleit bicarbonate buffer (pH 7.4) supplemented with 1 mM DL-carnitine, 1% B.S.A. and 5 mM glucose. Addition of PC-PLC resulted in a significantly higher (P less than 0.05) output of glycerol in myocytes undergoing rewarming than in myocytes kept constantly at 5 degrees C or 37 degrees C. The values obtained for PC-PLC induced glycerol output (difference in glycerol output between incubations with and without PC-PLC) were 6.77 +/- 2.6 (37 degrees C), 4.54 +/- 1.7 (5 degrees C) and 22.85 +/- 5.9 (5-37 degrees C) nmol/10(6) cells.h. Rewarming in addition caused a significantly higher (P less than 0.05) leakage of lactate dehydrogenase (LDH) from the rewarmed cells as compared to cells at constant temperatures (5 degrees C or 37 degrees C). However, there was no additional effect of PC-PLC on LDH leakage. The elevated PC-PLC induced glycerol output in rewarmed myocytes was not related to a fall in the percentage of rod-shaped cells or a reduced cellular content of ATP, since no differences could be detected between the various myocyte preparations with respect to these parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of hypothermia and rewarming on phospholipase C-evoked glycerol output in rat myocardial cells. 163 71

During cardiac surgery, the heart is infused with cold crystalloid cardioplegic solutions such as St. Thomas' Hospital (StT) solution, which contains high concentrations of K+ and Mg2+. The high K+ and Mg2+ block impulse conduction and inhibit Ca2+ influx, thereby arresting the heart and reducing cardiac oxygen consumption. Nevertheless, myocardial edema and post-operative abnormalities have been noted after cardioplegia and attributed to ischemia and reflow or to hypothermia. We found, however, that cold StT (9 degrees C) was hypotonic and induced cell swelling in the absence of ischemic injury. Cell swelling in cold StT was not due to hypothermia alone, but rather was caused by KCl influx and was prevented by partially replacing Cl- with an impermeant anion. After exposure to cold StT, cells transiently shrank to less than control volume on rewarming in physiological saline (Tyrode's solution, 37 degrees C). The transient shrinkage was blocked by ouabain suggesting that Na+ loading of depolarized hypothermic cells and Na(+)-K+ pump activation on rewarming were responsible. Hypothermic ventricular cells seem to follow Donnan equilibrium, and the product of [K+] x [Cl-] in cardioplegic solutions affects cell volume in the absence of ischemic injury.
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PMID:Prevention of myocardial intracellular edema induced by St. Thomas' Hospital cardioplegic solution. 166 12

Many antidepressants reverse arylpiperazine-induced hypothermia after acute treatment by a mechanism that does not seem to implicate monoamine uptake inhibition. Activity is found in reversing 1-(m-trifluoromethylphenyl)piperazine (TFMPP)-induced hypothermia by desipiramine 5 and 10 mg/kg and not by maprotiline 10 and 20 mg/kg. Clomipramine and fluoxetine with comparable serotonin uptake blocking potential do not have comparable TFMPP-reversing effects. A dibenzothiadiazepine compound (IM/P/3/4), hypothesized to have antidepressant activity though devoid of uptake blocking properties, was active at 10 and 20 mg/kg. Other classes of tricyclics such as neuroleptics (clozapine 5 and 10 mg/kg) and chlorpromazine (2 and 10 mg/kg) and the H1 antihistamines, promethazine (20 mg/kg) and cyproheptadine (10 mg/kg) are active, as well as the calcium antagonists nifedipine (10 mg/kg) and verapamil (10 mg/kg). We hypothesize that properties other than monoamine-uptake block which these compounds share (such as calcium-uptake inhibition) could be involved. Activity was also seen with the 5-HT1A agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, at 0.05 and 0.25 mg/kg), and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT at 3 mg/kg) as well as with the muscarinic agonist oxotremorine (0.1 mg/kg).
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PMID:m-trifluoromethylphenylpiperazine and m-chlorophenylpiperazine-induced hypothermia in mice is reversed by tricyclic antidepressants and other drugs. 168 12

The influence of calcium, resting force and temperature on the contractile behaviour in isolated demembranized ("skinned") pig papillary muscle fibers (n = 36) was analysed. Demembranisation excludes the influence of any membrane related processes on the contractile response as the myofilaments are in direct contact with the bathing medium. Resting force (1 mN-9 mN), temperature (22 degrees C or 32 degrees C) and pCa 7.0-4.3 were varied and the contractile response was analyzed by studying the time constant and the extent of post vibration force recovery (PVFR) of the activated preparations (the vibration method). Additional constant-load experiments and detection of sarcomere-length were carried out. There was an inverse-linear relationship between time constants of post vibration force recovery and maximum shortening velocity as estimated by constant load experiments. Resting force affected the extent of force development but not the time constant of post vibration force recovery and modulated the pCa-force relationship without altering the calcium concentration required for half-maximal activation (calcium sensitivity). In contrast lowering the bath temperature from 32 degrees C to 22 degrees C caused a significant leftward shift of the pCa-force relationship potentially due to changes of the contractile filaments' calcium sensitivity. The effect of temperature on the myocardial contractile system is of special interest as hypothermia is frequently used in cardiac surgery. Analysis of alterations of the contractile proteins' calcium sensitivity during the rewarming period of the patient may provide further insight in the pathophysiology of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analyzing contractile responses in demembranized pig papillary muscle fibres: the influence of calcium, resting force, and temperature. 178 37

Microfluorometry was used to investigate temperature dependence of hypoxia-induced intracellular calcium accumulation in gerbil hippocampal slice. When slices were superfused with hypoxic medium at 37 degrees C, 35 degrees C, 33 degrees C or 31 degrees C, latencies of acute increase of calcium accumulation, which was accompanied by a large negative shift of extracellular DC potentials, were delayed in a dose-dependent manner: mean latencies in field CA1 were 130 s, 182 s, 232 s and 277 s after hypoxia, respectively. This retardation in calcium accumulation may be involved in the mechanisms by which hypothermia diminishes ischemic injury.
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PMID:Temperature dependence of hypoxia-induced calcium accumulation in gerbil hippocampal slices. 179 68

Caffeine induces a dose-dependent decrease in core body temperature in mice and the hypothermia induced by a 100 mg/kg dose of caffeine was seen to persist for greater than 160 min. Other alkylxanthines including theophylline, enprophylline, isbutylmethylxanthine and 1,3-dipropyl-7-methylxanthine also showed dose-dependent reductions in body temperature. The dose of these drugs required to reduce body temperature by 2 degrees C was calculated and correlated with the affinities for the compounds at adenosine A1 and A2 receptors and their activities in inhibiting calcium dependent and independent phosphodiesterases. Significant relationships were found between the 2 degrees C hypothermic dose (HD2) and soluble and membrane calcium-independent phosphodiesterase inhibiting activity (r2s = 0.950 and 0.940, respectively). No significant relationship was seen between HD2 and soluble calcium-dependent phosphodiesterase inhibiting activity or with A2 adenosine receptor affinity. The relationship between HD2 and A1 adenosine receptor affinity (r2 = 0.739) did however almost reach statistical significance. These results would suggest that phosphodiesterase inhibition, instead of or in addition to adenosine receptor blockade, may play an important role in the effects of alkylxanthines on body temperature.
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PMID:Hypothermic effects of alkylxanthines: evidence for a calcium-independent phosphodiesterase action. 180 62


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