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

After induction of left ventricular hypertrophy by supravalvar constriction of the ascending aorta in mini pigs (ATP and lactate) were measured under different cardioplegic conditions. In normothermia and plain anoxic arrest ATP decrease and lactate increase were significantly slower in hypertrophied myocardium compared to normal myocardium. Injection cardioplegia using magnesium-aspartate-procaine at 37 degrees C did not influence the ATP decrease and lactate increase in the hypertrophied ventricle, whereas in the normal heart it showed some protection according to these parameters. Optimal ATP preservation and the lowest lactate increase rate were achieved in left ventricular hypertrophy by combined application of magnesium-aspartate-procaine and hypothermia of 25 degrees C. We conclude that normothermic injection cardioplegia has no protective effect on the hypertrophied left ventricle, whereas additional hypothermia can improve magnesium-aspartate-procaine cardioplegia significantly.
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PMID:[The protective effect of magnesium-aspartate-procaine cardioplegia on the hypertrophied left ventricle of the mini-pig (author's transl)]. 15 67

Myocardial high-energy phosphate and glucose-6-phosphate levels were determined in the in vivo pig heart model during ischemic arrest and reperfusion to determine the effectiveness of potassium cardioplegia in myocardial protection. Thirty-five pigs were divided into six experimental groups consisting of 2-hour normothermic arrest, 2-hour hypothemic arrest, 2-hour normothermic cardioplegic arrest, and 1-, 2-, and 3-hour hypothermic cardioplegic arrest. Myocardial biopsies from the left ventricle were obtained prior to arrest, every 30 minutes during the arrest interval, and at 30 and 60 minutes of reperfusion. The measurement of adenosine triphosphate and creatine phosphate showed that (1) cardioplegic arrest requires hypothermia to preserve high-energy phosphate levels in myocardial tissue; (2) hypothermia, while not completely protective alone, is more effective than potassium cardioplegia alone in providing myocardial preservation during 2-hour ischemic arrest; (3) the combination of potassium cardioplegia and hypothermia is additive in providing an effective means of maintaining myocardial high-energy phosphate stores during 1, 2, and 3 hours of ischemic arrest; (4) myocardial reperfusion does not allow a return to preischemic adenosine triphosphate (ATP) levels after 2 hours of arrest, except following hypothermic cardioplegia; and (5) extension of the duration of ischemic arrest to 3 hours using hypothermic cardioplegia prevents recovery of high-energy phosphate stores to preischemic levels during reperfusion. Optimal preservation can be achieved during 2 hours of ischemic arrest by using hypothermic potassium cardioplegia. The effects of myocardial reperfusion, however, prevent full ATP and creatine phosphate (CP) recovery following 3 hours of arrest. No other technique studied was as effective in providing myocardial preservation.
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PMID:The time course of myocardial high-energy phosphate degradation during potassium cardioplegic arrest. 57

Techniques for organ preservation generally use hypothermia to retard metabolic requirements. However, excessive hypothermia may also produce injury. Using a canine left lung allotransplantation procedure, we compared two preservation temperatures (4 degrees and 10 degrees C) in terms of subsequent lung function measured by temporary occlusion of the right pulmonary artery after implantation of the preserved left donor lung. The lungs were flushed with low-potassium dextran electrolyte solution, inflated with 100% oxygen, and preserved for 18 hours. To investigate possible changes of energy stores at different temperatures, we performed phosphorus 31-nuclear magnetic resonance analyses of lung samples. Sequential determinations of adenosine triphosphate levels in lung tissue preserved at 4 degrees, 10 degrees, and 22 degrees C were studied. After transplantation, lungs preserved at 10 degrees C (n = 6) provided significantly better arterial oxygen tension than those preserved at 4 degrees C (n = 6), 451 +/- 46 mm Hg versus 243 +/- 86 mm Hg (p less than 0.05), and lower pulmonary vascular resistance, 581 +/- 68 dynes.sec.cm-5 versus 1006 +/- 157 dynes.sec.cm-5 (p less than 0.05). Adenosine triphosphate levels at 4 degrees and 10 degrees C were stable and did not differ from each other at the end of the 18-hour preservation period: 0.86 +/- 0.04 mumol/gm wet weight for control versus 0.86 +/- 0.07 mumol/gm wet weight for 4 degrees C and 0.93 +/- 0.06 mumol/gm wet weight for 10 degrees C after 18 hours of preservation. Preservation at 22 degrees C caused a 28% depression of adenosine triphosphate after 18 hours of preservation. These results lead us to conclude the following: (1) Optimal temperature for lung preservation is in the vicinity of 10 degrees C, and (2) lung dysfunction caused by excessive hypothermia is not due to a failure to maintain adenosine triphosphate levels. We suspect that adenosine triphosphate is generated by oxidative phosphorylation during lung preservation.
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PMID:In a canine model, lung preservation at 10 degrees C is superior to that at 4 degrees C. A comparison of two preservation temperatures on lung function and on adenosine triphosphate level measured by phosphorus 31-nuclear magnetic resonance. 154 20

Clinical application of hypothermic pharmacologic cardioplegia in pediatric cardiac surgery is less than satisfactory, despite its well known benefits in adults. Protection of the ischemic immature rabbit heart with hypothermia alone is better than with hypothermic St. Thomas' II cardioplegic solution. Control of cellular calcium is a critical component of cardioplegic protection. We determined whether the existing calcium content of St. Thomas' II solution (1.2 mmol/L) is responsible for suboptimal protection of the ischemic immature rabbit heart. Modified hypothermic St. Thomas' II solutions (calcium content, 0 to 2.4 mmol/L) were compared with hypothermic Krebs bicarbonate buffer in protecting ischemic immature (7- to 10-day-old) hearts. Hearts (n = 6 per group) underwent aerobic "working" perfusion with Krebs buffer, and cardiac function was measured. The hearts were then arrested with a 3-minute infusion of either cold (14 degrees C) Krebs buffer (1.8 mmol calcium/L) as hypothermia alone or cold St. Thomas' II solution before 6 hours of hypothermic (14 degrees C) global ischemia. Hearts were reperfused, and postischemic enzyme leakage and recovery of function were measured. A bell-shaped dose-response profile for calcium was observed for recovery of aortic flow but not for creatine kinase leakage, with improved protection at lower calcium concentrations. Optimal myocardial protection occurred at a calcium content of 0.3 mmol/L, which was better than with hypothermia alone and standard St. Thomas' II solution. We conclude that the existing calcium content of St. Thomas' II solution is responsible, in part, for its damaging effect on the ischemic immature rabbit heart.
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PMID:Calcium content of St. Thomas' II cardioplegic solution damages ischemic immature myocardium. 192 65

Twenty-nine female northern sea lions (Eumetopias jubatus) were immobilized using Telazol in dosages ranging from 1.8 to 8.1 mg/kg. Best results were achieved with Telazol dosages ranging between 1.8 and 2.5 mg/kg which resulted in smooth induction and recovery. Optimal injection location was in the muscle mass of the lower back and hip. Dosages greater than 3.5 mg/kg resulted in a tendency toward hypothermia. Six mortalities occurred which were partially caused by the location of drug injection and perhaps the high dosage.
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PMID:Use of Telazol to immobilize female northern sea lions (Eumetopias jubatus) in Alaska. 276 Oct 7

Thirty-six brain-dead children were managed to allow organ harvesting, which was possible in 21 (7 multi-organ). Optimal ventilation allowed for normal PaO2 and PaCO2 (mean +/- SEM FiO2 = 0.50 +/- 0.05). The management of hemodynamics was quite difficult and cardiac arrest may be due to patient transport, electrolyte disorders and dehydration. Vascular filling was of main importance and required standard solutes (5 or 2.5% glucose, normal saline, Ringer lactate) at a rate of 3.0 +/- 0.5 ml/kg/h, adapted for electrolytes (mainly KCl); sometimes, other solutes may be used: blood (17 patients), human 20% serum albumin (17 patients), plasma (9 patients). This filling was sufficient for 15 patients; the others required inotropic agents: dopamine (17 +/- 8 micrograms/kg/min), dobutamine (42 +/- 18 micrograms/kg/min). Diuresis was more than 3 ml/kg/h in 38% of the patients and desmopressin was used in 3 cases. Hypothermia (minimum 31.2 degrees) had no major consequence. No infection was found. Quality of management of brain-dead patients is of main importance; the possibility of organ harvesting must be evoked in such situations and is the first step in organ transplantations.
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PMID:[Resuscitation of children in the brain death state from the view of organ procurement for therapeutic purposes]. 324 51

Optimal methods of myocardial preservation in the neonate remain unknown. Hypothermia and cardioplegia have been shown to protect neonatal hearts, but few studies have examined the effects of cardioplegia when administered at normothermia. Accordingly, the role of 37 degrees C St. Thomas' cardioplegic solution in protecting the neonatal heart during 1 hour of ischemia in an isolated working rabbit heart model was examined. Both oxygenated and nonoxygenated cardioplegic solutions (CSs) were evaluated and compared with an oxygenated physiological saline solution (PSS). Following ischemia, control hearts were characterized by severely impaired left ventricular function, whereas all three treatment groups recovered well, indicating that the treatments provided substantial protection. Aortic flow recovered to 62, 63, and 57% of preischemic values for the oxygenated CS, nonoxygenated CS, and oxygenated PSS groups, respectively. Similarly, rate of change of pressure recovered to 76, 80, and 76% of preischemic values for oxygenated CS, nonoxygenated CS, and oxygenated PSS groups. All values were significantly greater than those for the control group. Recovery of developed pressure was significantly improved in all three groups. End-diastolic pressure rose markedly following ischemia in control hearts, was not increased after ischemia in hearts receiving oxygenated and nonoxygenated CS, but was increased in the oxygenated PSS group. These data indicate that crystalloid cardioplegia and oxygenated PSS provide substantial protection in neonatal rabbit hearts, even when delivered at 37 degrees C. No additional benefit was seen when the cardioplegic solution was oxygenated. Therefore, either method of balancing the oxygen supply/demand ratio appears to be beneficial: supplying oxygen intermittently during ischemia (oxygenated PSS group) or decreasing oxygen demand during the ischemic period (cardioplegia groups).
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PMID:Protection of the neonatal heart following normothermic ischemia: a comparison of oxygenated saline and oxygenated versus nonoxygenated cardioplegia. 337 77

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

The isolated perfused organ is more sensitive to the toxicity of oxygen since hypothermia reduces the activities of enzymes responsible for minimizing oxygen toxicity. To protect the organ under these conditions reducing agents must be added to the perfusate. Quantitation of the resulting reduction is best obtained by measurement of the oxidation-reduction potential of the perfusate. A device was designed for this purpose and, by electrochemical principle, controlled reduction of the oxidized form of the oxidation-reduction couple was affected. Kidneys were perfused with cryoprecipitated plasma. With the electrochemical cell in the circuit, the oxidation-reduction potential of the perfusate was adjusted by the addition of ascorbic acid and glutathione and the cell was driven by a battery-powered potentiostat. Kidneys subjected to 60 minutes of warm ischemia had optimal survival at -20 mV. Preservation for six days in a monitored group had no survivors, whereas kidneys with oxidation-reduction support maintained life. Optimal oxidation-reduction support maintained life. Optimal oxidation-reduction was at or near -17 mV. These data show a requirement of an optimal oxidation-reduction potential to reverse warm ischemia damage and to prolong the period of ex vivo preservation of isolated perfused organ.
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PMID:Oxidation-reduction maintenance in organ preservation. 398 89

The cause of endothelial injury during vein harvesting and preservation is complex. Hypothermia is thought necessary to preserve cell viability but has been implicated in morphologic injury to the endothelium. This study explored the effect of temperature on preserving endothelial function using prostacyclin production as a metabolic marker. Canine veins were atraumatically excised and matched segments were stored at three temperatures using either nutrient medium or heparinized saline. After storage, endogenous production of prostacyclin by the luminal surface of each vein was collected in a closed perfusion system at 37 degrees C and assayed by radioimmunoassay. Optimal prostacyclin production was observed in veins stored in tissue culture medium at normothermia. Preservation of normal endothelial function may require revision of traditional vein graft-harvesting techniques.
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PMID:Functional injury of vein graft endothelium. Role of hypothermia and distention. 654 26


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