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

Myocardial preservation for prolonged ischemia has traditionally centered around deep hypothermia with metabolic arrest. This approach is limited in tolerable ischemic time by the state of energy reserves at the onset of ischemia, because anaerobic glycolysis during ischemia is limited by end-product accumulation (lactate, alanine, and H+). In this study we evaluated a novel preservation solution containing the basic amino acid histidine to buffer H+, glucose as substrate, and low sodium and calcium concentrations to mimic the intracellular ionic environment. Isolated rabbit hearts were subjected to hypothermic ischemia for 8 and 16 hours at 4 degrees and 21 degrees C followed by reperfusion. The buffered solution was compared to University of Wisconsin solution (high potassium). Intracellular pH was maintained at preischemic levels in the buffered solution hearts at 21 degrees C, and this was associated with better preservation of high energy stores and recovery of contractile function. Developed pressure recovered to 90% +/- 3% of preischemic values after 16 hours of 21 degrees C ischemia with the buffered solution as compared with 79% +/- 2% in the University of Wisconsin group at 4 degrees C (contracture occurred in the University of Wisconsin hearts at 21 degrees C). The optimal temperature in the buffered solution hearts was 13 degrees C, and with this temperature acceptable recovery of contractile function was seen after 24 hours of ischemia. On the basis of these results, we conclude that promoting anaerobic glycolysis during ischemia achieves superior prolonged preservation of energetic and contractile function of the heart.
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PMID:Evaluation of highly buffered low-calcium solution for long-term preservation of the heart. Comparison with University of Wisconsin solution. 793 14

A 51-year-old male was admitted to our Institution with a complaint of dyspnea on effort. He had undergone coronary artery bypass grafting and mitral valve annuloplasty three years previously. The left ventriculograms showed severe mitral regurgitation. The coronary angiograms revealed an ITA graft and two SVG grafts were fully functioning. Considering the risk of injury of ITA/SVG graft during redo median sternotomy, we approached the heart through right anterolateral thoracotomy. Mitral valve replacement was performed under profound hypothermia without aortic cross clamping. Temporary reduction of perfusion flow was useful in order to obtain a better visual field. His postoperative course was uneventful. Right thoracotomy has an advantage over median sternotomy when reoperation is to be done for patients with a functioning ITA graft.
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PMID:[Mitral valve replacement through right thoracotomy in a patient with a functioning ITA graft]. 796 80

Myocardial preservation has centered around the deep hypothermia with metabolic arrest to save energy loss. We evaluated the efficacy of histidine buffered cardioplegia containing 100 mM histidine formulated to promote anaeraboic energy production in a blood perfused canine heart subjected to 24 hours or 30 hours ischemia. The hearts were flushed with 100 mM histidine containing buffered solution (HBS) in one group and a second group and University Wisconsin solution (UWS) in a third group. The hearts were preserved at 4 degrees C for 24 hours in one and third group, and for 30 hours in a second group, then reperfused with autologous blood in an isolated heart perfusion apparatus. Standardized stroke volume, ejection fraction, developed pressure and end-systolic elastance were measured at 2 hours after reperfusion and compared with control non-preserved hearts. Better recovery of cardiac performance was attained in the hearts preserved with histidine containing cardioplegia for 24 hours or 30 hours than that in UW group. Although cardiac performances in the hearts preserved with histidine cardioplegia for 30 hours was worse than that in 24 hours preserved heart for 24 hour, those were comparable if low dose or high dose cathecolamine was given. We concluded that the histidine containing cardioplegia provides effective preservation of the canine heart with superior recovery of pump performance after 24 hours or 30 hours of preservation by buffering proton and lactate to promote anaerobic glycolysis.
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PMID:[Prolonged preservation due to acceleration of anaerobic glycolysis with histidine buffered cardioplegia in canine heart]. 855 Oct 68

We report herein the case of a 56-year-old man with angina pectoris suspected to be accompanied with aortitis syndrome who underwent coronary artery bypass grafting (CABG). His cerebral blood flow consisted of only that of the right vertebralartery, and the marked collaterals of the bronchial artery anastomosing to the coronary artery. CABG was performed under combined with electrical fibrillation and systemic deep hypothermia, for fear of a bad influence on the cerebral tissue by the influx of high potassium cardioplegic solution. The postoperative course was uneventful and the coronary angiography revealed that the all graft were patent.
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PMID:[Coronary arterial bypass grafting for angina pectoris suspected with aortitis syndrome: a case report]. 884 50

Effects of intracerebroventricular injection of histamine and its related compounds on rectal temperature were studied in mice. Histamine (0.1-1.0 mu g) and histidine (500-1,000 mg/kg) caused a dose-related hypothermia. H1 agonist, 2-methylhistamine and 2-thiazolylethylamine also displayed a dose-dependent hypothermia. In addition, H2 agonists, 4-methylhistamine and dimaprit elicited a decrease in body temperature. Preinjection of not only H1-antagonists (diphenhydramine and chlorpheniramine) but also H2 antagonists (cimetidine and ranitidine) abolished histamine-induced hypothermia. Either intracerebroventricular or intraperitoneal injection of thioperamide, a histamine H3 antagonist, showed hypothermia. The hypothermic effect produced by intracerebroventricular injection of thioperamide was significantly blocked by (R)-alpha-methylhistamine, a selective H3 agonist. In addition, the effect induced by thioperamide was inhibited by H1 and H2 antagonists, indicating that the H3 receptor also participates in histamine-induced hypothermia.
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PMID:Effects of intracerebroventricular injection of histamine and its related compounds on rectal temperature in mice. 905 87

Cyclo(His-Pro) (CHP) has been shown to facilitate cold-induced hypothermia in the desert rat Mastomys natalensis. In the present study, we examined the role of endogenous CHP in hyperthermia induced by hot ambient temperature (40 degrees C) in the above rodent species. The results of these studies show that housing rodents at 40 degrees C resulted in a altered distribution of CHP in the brain, with a rise in hypothalamic content accompanied by an increase in rectal temperature. While administration of exogenous CHP decreased hyperthermia, immunoneutralization of endogenous CHP increased hyperthermia. The results of these studies show that changes in endogenous CHP levels may affect body temperature regulation.
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PMID:Cyclo (His-Pro) modulation of body temperature at hot ambient temperature in the desert rat (Mastomys natalensis). 921 62

A 14-year-old boy presented with a 1-week history of hypothermia and obtundation. His medical history included surgical resection of craniopharyngioma with postoperative visual impairment and panhypopituitarism. The patient's rectal temperature remained persistently lower than 35 degrees C during the first 3 days of hospitalization. His blood pressure was 90/56 mmHg on admission. The peripheral blood leukocyte count was 2.7 x 10(10)/L with 18% neutrophils, 19% band forms, 44% metamyelocytes, 3% myelocytes, and 16% lymphocytes. The C-reactive protein concentration was 133.9 mg/L. Two separate blood cultures both yielded Pseudomonas putida. The patient was treated with amikacin and ceftazidime along with aggressive fluid therapy. Replacement therapy directed at his hormonal deficiencies was initiated as soon as his hemodynamic status was stabilized. The patient responded well to therapy with a gradual rise in body temperature and improvement in general activity. A growth experiment carried out on the P. putida isolate showed that the bacteria grew more rapidly at 30 degrees C than at 37 degrees C. The clinical course of the patient, as well as the results of the laboratory study, suggest that hypothermia may predispose human infection with P. putida.
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PMID:Hypothermia predisposing to Pseudomonas putida sepsis in a child with panhypopituitarism. 958 82

It was the aim of the present study to investigate the influence of Bretschneider's cardioplegia on norepinephrine (NE) release [determined by high pressure liquid chromatography (HPLC) and electrochemical detection] in isolated perfused guinea-pig hearts. The following resulted were noted. (1) Calcium-dependent exocytotic NE release evoked by electrical field stimulation (12 Hz, 1 min) was completely suppressed after only 3 min of normothermic (37.5 degrees C) Bretschneider's cardioplegia. (2) Stop-flow ischemia is associated with a substantial calcium-independent, non-exocytotic NE release, which is regarded as a sodium-dependent carrier-mediated process. Accordingly, it is inhibited by blockers of the sodium/proton-exchanger (e.g. amiloride) and the neuronal uptake1-carrier (e.g. desipramine). Compared with stop-flow ischemia alone, cardioplegia with 3 min of Bretschneider's histidine-tryptophan-ketoglutarate (HTK)-solution preceding stop-flow enhanced NE release at all stop-flow durations (10-90 min) investigated (e.g. after 30 min of normothermic Bretschneider's cardioplegia: 1070+/-41 pmol/g, n = 45, v stop-flow alone: 764+/-48 pmol/g, n = 27, P<0.05). The NE concentrations determined in the cardiac effluent upon reperfusion followed a typical first order kinetic indicating that the transmitter release had already occurred during stop-flow. Hypothermia reduced NE release in a temperature-dependent manner down to intramyocardial temperatures of 2 7.5 degrees C. NE release evoked by Bretschneider's cardioplegia still exceeded that induced by stop-flow ischemia alone by up to 60%. The NE release evoked by Bretschneider's cardioplegia and stop-flow ischemia was calcium-independent. However, it was significantly reduced by desipramine and amiloride, but both agents had a more pronounced inhibitory effect on NE release evoked by stop-flow ischemia alone. (3) This difference may be due to an intrinsic effect of Bretschneider's HTK-solution, as continuous administration of normothermic Bretschneider's HTK-solution induced a substantial NE release which was neither calcium-dependent nor inhibited by blockade of either uptake1 or sodium/proton-exchange. It is concluded that Bretschneider's cardioplegia is not neuroprotective, as it even augments the stop-flow ischemia-induced nonexocytotic NE release.
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PMID:Influence of Bretschneider's cardioplegia on norepinephrine release from isolated perfused guinea-pig hearts. 1007 18

The introduction of open-heart surgery more than 4 decades ago signaled a new era in medicine. For the 1st time, previously untreatable cardiac anomalies became amenable to surgical therapy. The use of the heart-lung machine seemed to grant the surgeon unlimited time in which to operate inside the heart. Still frustrated by poor operating conditions and the threat of air embolism, Denis Melrose introduced elective cardiac arrest in 1955. His use of a potassium citrate solution seemed to offer a safe method to effect a quiet, bloodless field. However, a few years after its inception, numerous reports began to question the safety of this approach, and the Melrose technique was abandoned in the early 1960s. Nearly 15 years elapsed before potassium-based cardioplegia regained popularity. During this period, topical hypothermia, coronary perfusion with intermittent aortic occlusion, and normothermic ischemia were evaluated and discarded. A few European investigators like Hoelscher, Bretschneider, and Kirsch had maintained their interest in chemical cardioplegia, and it was through their efforts that future researchers like Hearse and Gay spearheaded the return to potassium-based cardioplegia, which today forms the core of the cardiac surgeon's myocardial protective armamentarium and has contributed towards lowering operative mortality rates.
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PMID:Myocardial protection: the rebirth of potassium-based cardioplegia. 1021 72

The ability of brief hypothermic reperfusion (HtR) to restore hepatic energy metabolism following periods of cold hypoxic preservation was studied in isolated rat livers after storage times of 5, 10, and 24 h. In addition, investigations were performed on the effects of HtR used to restore liver oxidative metabolism in the middle of a prolonged (24 h) hypoxic preservation period. A histidine-lactobionate-raffinose solution was used for the initial cold portal flush in all groups. Results showed that cold hypoxia for either 5 or 10 h yielded livers capable of similar recoveries of ATP, energy charge, and total adenine nucleotides, but that HtR after 24 h cold preservation resulted in reduced regeneration of ATP, a lower energy charge, and a fall in tissue adenine nucleotides. When livers were stored for 24 h but subjected to brief HtR after either 5 or 10 h before return to hypoxic storage, improved recoveries of the energy metabolites were seen over those recorded after 24 h hypoxia alone. The fact that these improvements were not due to an improved supply of adenine nucleotide precursors was demonstrated by studying groups which were given HtR with perfusate containing precursors of adenine nucleotides (adenosine, adenine, and inosine) after 24 h cold hypoxia. These data are consistent with the hypothesis that poor metabolic recovery after long-term hepatic cold preservation results more from decreased mitochondrial oxidative phosphorylation than from a lack of precursors for adenine nucleotide resynthesis. In addition, restoring oxidative metabolism at hypothermia for brief periods can to some extent protect final metabolic status after prolonged storage.
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PMID:Energy metabolism following prolonged hepatic cold preservation: benefits of interrupted hypoxia on the adenine nucleotide pool in rat liver. 1052 5


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