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

The effect of preserving the heart and lungs with hypothermia and Collins solution was studied in 13 mongrel dogs undergoing combined heart-lung transplantation. The five control animals who underwent an immediate transplant following Collins solution perfusion had small increases in extravascular lung water when measured 2.5 hours posttransplant as seen in a previous study. The eight animals who had hypothermic preservation following Collins solution perfusion had significantly higher extravascular lung water than controls (16.3 +/- 1.8 ml/kg in preserved animals; 11.2 +/- 1.7 ml/kg in controls p less than 0.05). The level of lung water reached at 2.5 hours postoperatively was similar to that reached with a previously reported, unacceptable preservation technique. Survival beyond this point was poor due to severe pulmonary edema. We conclude that the use of this solution, given under the experimental conditions which we describe, is not acceptable for hypothermic preservation of the heart and lungs for combined transplantation.
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PMID:Hypothermic preservation of the heart and lungs with Collins solution: effect on cardiorespiratory function following heart-lung allotransplantation in dogs. 308 3

The significance of dynamic changes in energy state during lung harvesting and preservation has not been extensively studied. Phosphorus 31 nuclear magnetic resonance spectra at 81 MHz were obtained from degassed rabbit lungs. Changes in the adenosine 5'-triphosphate-to-inorganic phosphate peak-intensity ratios were used to measure changes in energy state. Two groups of rabbit preparations were studied to evaluate the effect of hypothermia during the initial 120 minutes of harvesting (n = 8 at 36 degrees C and n = 5 at 4 degrees C). The significance of these changes was assessed in a second experiment in which lungs were reperfused in vitro at selected intervals of hypothermia (5, 12, and 24 hours) and assessed for injury. Hypothermic preservation sustained a significantly higher energy state. The depletion of energy state was correlated with injury, particularly as measured by lung edema (r2 = -0.715). Short periods of warm ischemia (30 minutes) result in a significant depletion of energy state, which may be a component of pulmonary injury during harvesting and preservation.
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PMID:31P nuclear magnetic resonance determination of changes in energy state in lung preservation. 318 Apr 8

With methylprednisolone as a chemical inhibitor of leukocytes, extended preservation was conducted with an isolated rabbit lung model. The heart-lung blocks of 39 New Zealand white rabbits were flushed in situ with 100 ml of Euro-Collins' solution, harvested, inflated (70%), and preserved at 4 degrees C. Lungs immediately reperfused with whole blood (control lungs, group 1) were compared with lungs preserved without methylprednisolone for 5, 12, and 24 hours (groups 2 to 4) and those preserved with methylprednisolone for 12 and 24 hours (groups 5 and 6, respectively). Methylprednisolone (30 mg/kg) was administered before harvest and was used as an additive to the flush and in the blood reperfusate. Hypothermia and Euro-Collins' flush alone provided adequate preservation for up to 5 hours; however, lung edema was evident by 12 hours of cold ischemia and became severe by 24 hours. By all measured parameters, the lungs in group 5 (treated with methylprednisolone) demonstrated values equal to or better than control lungs. By 24 hours of preservation the beneficial effects of the steroid treatment were no longer evident. Histologic evaluation revealed mild to moderate injury after 5 hours of cold ischemia; progressive edema and hemorrhage were found after 12 and 24 hours of preservation. This injury was significantly ameliorated by methylprednisolone treatment at 12 hours but not at 24 hours. This study suggests that static preservation for up to 5 hours is possible with hypothermia and a Euro-Collins' flush and that extended preservation to 12 hours is possible with pharmacologic dosages of methylprednisolone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved static lung preservation with corticosteroids and hypothermia. 319 47

Open heart surgery was performed without perfusion under deep hypothermia in 343 patients with congenital heart defects aged from 1 year 3 months to 44 years. Cooling to a temperature of 26-25 degrees C in the oesophagus was achieved by covering the body with crushed ice. The patients were maintained under superficial ether narcosis and they were given morphine (0.5 mg/kg) and tubocurarine (0.5-1.0 mg/kg). The duration of circulatory arrest was 30 minutes in 190 and longer in 153 patients--60-77 minutes in 10 patients. It took an average of 7.6 minutes for resumption of normal cardiac activity after circulatory arrest prolonged beyond 60 minutes. Of the 343 patients operated on 32 (9.3%) died. Analysis of the mortality pattern showed that patients with acute cardiac insufficiency contributed most to the total number of deaths (19 patients, 5.5%); those with pulmonary oedema ranked second (4 patients, 1.2%) and those with brain oedema third (3 patients, 0.9%). Neurological complications were observed in 13 patients (3.8%). Their frequency was significantly related to the duration of circulatory arrest. Circulatory inadequacy in patients with poor myocardial function who had undergone extensive repair appeared to be a contributory factor. The results obtained without perfusion under deep (26-25 degrees C) hypothermic protection suggest that 75 minutes is a safe time, in terms of brain damage, for circulatory arrest. Under these conditions complex cardiac defects can be repaired.
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PMID:Hypothermic protection (26-25 degrees C) without perfusion cooling for surgery of congenital cardiac defects using prolonged occlusion. 340 6

Groups of male and female Fischer 344 rats, B6C3F1 mice, and Hartley guinea pigs were exposed once for 6 hr to mean concentrations of 10.5, 5.4, 2.4, 1.0, or 0 (control) ppm of methyl isocyanate (MIC) vapor. Rats and mice were also exposed to 20.4 ppm of MIC. No deaths occurred in animals exposed to 2.4 or 1.0 ppm. The majority of deaths for the 20.4- and 10.5-ppm groups occurred during postexposure Days 1 through 3, while at 5.4 ppm deaths were observed throughout the 14-day postexposure period. The 6-hr LC50 values (with 95% confidence limits) were 6.1 (4.6 to 8.2) ppm for rats, 12.2 (8.4 to 17.5) ppm for mice, and 5.4 (4.4 to 6.7) ppm for guinea pigs. Notable clinical observations during and immediately following MIC exposure were lacrimation, perinasal/perioral wetness, respiratory difficulty (e.g., mouth breathing), decreased activity, ataxia, and hypothermia. The frequency of clinical signs decreased during the second postexposure week. Body weight losses were common in all species following MIC exposures of 2.4 ppm or greater. At 1.0 ppm, only female mice had body weight depression. Recovery of body weight loss was observed in the 5.4- (guinea pigs only), 2.4- and 1.0-ppm concentration groups. The lungs of all animals that died were discolored. Following microscopic examination of the respiratory tract, deaths were attributed to pulmonary edema and congestion. In a separate study, Fischer 344 rats and Hartley guinea pigs were exposed once for 4 hr to mean concentrations of 36.1, 25.6, 15.2, or 5.2 ppm of MIC vapor. In general, the results were similar to those of the single 6-hr exposure study.
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PMID:Acute inhalation studies with methyl isocyanate vapor. I. Methodology and LC50 determinations in guinea pigs, rats, and mice. 371 40

Excessive numbers of moderator bands bridging the left ventricular septum and free wall and entangling papillary muscles were associated with heart failure and death in 21 cats. Clinical findings included dyspnea, anorexia, hypothermia, cardiomegaly, pleural effusion, plumonary edema, heart murmurs, gallop rhythm, electrocardiographic abnormalities (especially conduction disturbances), increased left ventricular end-diastolic pressure, angiocardiographic evidence of left ventricular restriction, and aortic thromboembolism. Pathologic changes included a morphologically distinct network of abnormal numbers of moderator bands in the left ventricle, left ventricular hypertrophy (younger cats--mean age, 4 years) or dilatation (older cats--mean age, 8.7 years), left atrial enlargement and hypertrophy, and pulmonary edema with heart failure cells in the alveoli. Heart weights of affected cats were significantly less than those of cats with congestive, hypertrophic, and restrictive cardiomyopathy (endocardial fibrosis), but were not significantly less than heart weights of clinically normal cats. Pathologic changes were characteristic of the syndrome grossly and histologically, but clinical findings were not clearly definable.
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PMID:Excessive moderator bands in the left ventricle of 21 cats. 621 23

The initial management of the traumatized cat can be a challenging, but rewarding, task for the veterinarian. The pathophysiology of shock, its clinical presentation, and basic elements of treatment are universal to all species. Special care must be taken when dealing with injured cats, due to their increased susceptibility to stress and tendency toward severe hypothermia in shock. The development of pulmonary edema in response to excessive fluid loads, especially in the face of pulmonary injury, must be borne in mind when establishing treatment regimens. The keys to successful management of the traumatized cat lie in correct assessment of the extent and nature of injuries, rapid institution of rational therapy, and constant re-evaluation of the animal's response throughout the post-traumatic period.
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PMID:Feline trauma and critical care medicine. 633 30

Using infections of Plasmodium berghei in laboratory mice, the following physiopathological changes were observed during the seven days of the infection: reduction in haematocrit, increases in parasitized erythrocytes, pulmonary oedema, hypothermia, formation of prostaglandin-like substances in the central nervous system, increases and decreases in plasma bradykininogen levels and leucocytosis, as evidenced by neutrophilia, lymphocytosis and monocytosis. We found no changes in total plasma protein levels and albumin/globulin ratio.
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PMID:Plasmodium berghei: physiopathological changes during infections in mice. 636 86

Since 1969, 15 patients, ranging in age from 21 to 67 years, with pulmonary hypertension associated with chronic thrombotic obstruction of major pulmonary arteries have had pulmonary thromboendarterectomy. Symptoms compatible with embolism antedated surgery for periods of 8 months to 18 years; several alternative diagnoses were maintained for months to years. Only 2 of 15 were treated for the initial embolic episode. All patients had dyspnea on exertion and were in New York Heart Association class III-IV before surgery. Resting arterial hypoxemia was common. Resting preoperative mean pulmonary artery pressures ranged from 25 to 66 mm Hg; pulmonary vascular resistances, 420 to 1869 dynes/sec X cm-5. Partial or complete thromboendarterectomy was possible in patients using cardiopulmonary bypass with hypothermia and cardioplegia. All patients showed a fall in pulmonary vascular resistance. All developed some degree of "reperfusion" lung edema and arterial hypoxemia that lasted for a few days to several months. Two patients died during hospitalization. The 13 survivors have been followed for 8 to 144 months (mean, 38.3 months). All patients improved after surgery. One patient died of nonembolic causes; none had recurrent embolism.
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PMID:Chronic thrombotic obstruction of major pulmonary arteries. Results of thromboendarterectomy in 15 patients. 661 79

Knowledge of the interrelation of the central nervous system-respiratory axis is crucial to the management of patients with head injuries with or without concomitant pulmonary-thoracic problems. Damage to the central nervous system (CNS) can result in unexplained hypoxemia, noncardiac pulmonary edema, altered patterns of respiration, and an increased risk of aspiration. The damaged thorax and lung can contribute to brain ischemia and rises in intracranial pressure. The treatment of one end of the CNS-respiratory axis is not without effect on the other end of the continuum. Corticosteroids, diuretics, mannitol, iatrogenic hyperventilation, barbiturates, and vasopressors are used in the management of patients with head trauma, but may have an impact on oxygenation and ventilation. When positive end expiratory pressure is used in the management of a pulmonary process, it should be optimized and used with caution while monitoring for its effect on intracranial pressure. Pulmonary toilet, while remaining a necessity, must be performed in a manner so as to minimize potential negative effects on the brain. Hyperoxia and hypothermia should be avoided. Mechanical ventilation should be used as dictated by the desired PaCO2 and not as a mandatory adjunct to endotracheal intubation.
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PMID:Pulmonary effects of head trauma. 679 86


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