Gene/Protein Disease Symptom Drug Enzyme Compound
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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 hypothermia and hyperpotassium on alveolar fluid clearance in the resected human lung was examined by instilling an isosmotic albumin solution with a potassium concentration of 0.3 mEq/l or 20 mEq/l into one segment of a resected lobe within 10 min of surgical removal for bronchogenic carcinoma. The experiments were carried out at 37 degrees C, 25 degrees C, and and 8 degrees C over 4 hr, after which the alveolar fluid was aspirated. Alveolar fluid clearance was calculated by a simple equation using the changes in the albumin concentration of the alveolar fluid. It was found that although hypothermia at 8 degrees C abolished alveolar fluid clearance completely, alveolar fluid clearance at 25 degrees C was not different from that at 37 degrees C. Moreover, although the potassium concentration increased in the alveolar fluid at 37 degrees C and 8 degrees C, hyperpotassium did not affect the alveolar fluid clearance. These findings indicate that the net transport of potassium leans to influx from the alveolar epithelial cells into the alveolar spaces when the alveolar potassium concentration is low, and to efflux from the alveolar spaces when the alveolar potassium concentration is high. Thus, we conclude that hypothermia abolishes alveolar fluid clearance in resected human lungs, but that the potassium concentration in alveolar fluid does not affect alveolar fluid clearance.
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PMID:Effects of hypothermia and hyperpotassium on alveolar fluid clearance in the resected human lung. 852 Jan 63

Little information is available regarding the effect of ion transport agonists and antagonists on ion transport in the human lung. Therefore, we studied ion transport in lungs resected from patients with lung cancer. A test solution of 45 ml of isosmotic albumin was instilled into one segment of a resected lobe within 10 min of resection. Because protein leaves the air space very slowly, the concentration of alveolar protein over 4 h was used to quantify the volume of alveolar fluid. Ion transport was measured from the changes in ion concentrations and the volume of alveolar fluid. In the basal condition, the net efflux of Na+ and Cl- were 4.66 +/- 0.83 mEq/l/h and 3.52 +/- 0.84 mEq/l/h, respectively. In contrast, the net influx of K+ was 0.44 +/- 0.07 mEq/l/h. Amiloride (10(-5) M), an inhibitor of apical Na+ uptake, ouabain (10(-3) M), an inhibitor of Na(+)-K+ ATPase, and hypothermia (8 degrees C) reduced the efflux of Na+ and Cl-. Ouabain and hypothermia increased the net influx of K+. Terbutaline (10(-3) or 10(-4) M) increased the efflux of Na+ and Cl-, but did not affect the influx of K+. Propranolol (10(-4) M) and amiloride (10(-5) M) inhibited the terbutaline-induced increase in the transport of Na+ and Cl-. Alveolar fluid clearance was closely correlated with Na+ transport and with Cl- transport. However, the values of Na+ transport were greater than those of Cl- transport. These data suggest that Na+ transport is accompanied by Cl- transport and fluid movement out of the alveolar space in resected human lungs.
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PMID:[Transport of ions across alveolar epithelial cells in resected human lungs]. 853 92

Although hypothermia abolishes alveolar fluid clearance in the in situ goat lung and in the ex vivo human lung, it is unknown whether alveolar fluid clearance resumes in lungs that are rewarmed after severe hypothermia. An isosmolar albumin solution was instilled into resected human lungs that were rewarmed to 37 degrees C after hypothermia (7 +/- 3 degrees C), and then alveolar fluid clearance was measured by the concentration of albumin in the alveolar fluid sample after 4 h. In control experiments in lungs that had not been cooled and rewarmed, alveolar fluid clearance was 11 +/- 2% over 4 h. In separate experiments, hypothermia completely abolished alveolar fluid clearance. However, alveolar fluid clearance resumed to a normal level of 12 +/- 1% over 4 h in the lungs that were rewarmed after hypothermia. Amiloride decreased alveolar fluid clearance by 47% in the rewarmed lungs. Terbutaline increased alveolar fluid clearance by nearly 300% in 2-h experiments in the rewarmed lungs (P < 0.05). The results of this study indicate that alveolar sodium-channel transport mechanisms are preserved in resected human lungs that are exposed to rewarming after hypothermia.
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PMID:Preservation of alveolar epithelial fluid transport mechanisms in rewarmed human lung after severe hypothermia. 872 55

Forty patients undergoing CPB for coronary artery surgery, using a standardized technical setting, were randomized to receive either Ringer's acetate, dextran 70 (Macrodex), polygeline (Haemaccel) or albumin 4% for volume replacement during and after surgery. The choice of fluid did not affect early complement activation (C3 activation products). Higher values of the terminal complement complex (TCC) were found only at the end of the operation in patients receiving polygeline. There were no differences between any two of the four groups during the postoperative course. The use of blood transfusion or autotransfusion and the degree of haemodilution and hypothermia did not affect complement activation. We conclude that complement activation in association with open-heart surgery is only marginally affected by the choice of fluid for volume replacement.
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PMID:Complement activation during and after open-heart surgery is only marginally affected by the choice of fluid for volume replacement. 888 61

For clinical use of bioartifical liver devices a constant supply of primary liver cells has to be provided. Hypothermic storage of isolated pig hepatocytes could support large-scale stocking of cells. Freshly isolated pig hepatocytes from slaughterhouse livers were stored at 4 degrees C for 24, 48, and 72 h three different solutions: Leibovitz L-15 + 5% polyethylene glycol (PEG), University of Wisconsin (UW) solution, and a simplified UW solution. After storage, cells were cultured for 2 weeks in the collagen sandwich configuration. Viability of hepatocytes was 65, 85, and 83% after 24 h storage, 21, 74, and 70% after 48 h, and 5, 65, and 59% after 72 h in Leibovitz L-15 medium, UW, and the simplified UW, respectively. After storage in L-15 medium, cells attached poorly to collagen matrices and exhibited ultrastructural lesions. Functional performance in this group, as judged by albumin secretion and cytochrome P450-dependent activity in subsequent culture, decreased rapidly as a function of storage time, with zero values after 48 h storage. In contrast, hypothermia of hepatocytes in both UW solutions resulted in well-preserved cells with respect to ultrastructural appearance, attachment rates, and functional performance during culture. No significant differences were observed between the original and the simplified UW solution. Higher cell concentrations up to 5 x 10(7) cells/ml improved viability of hepatocytes on warmup. In terms of cell supply for hybrid artificial liver support, hypothermic storage of hepatocytes at 4 degrees C could mean an alternative to the cryopreservation of cells, which usually results in a substantial loss of cells and vital function of cells. Thus, pig hepatocytes could be stored at 4 degrees C for several days and meet the logistical need of bioartificial liver devices while avoiding the hazards of cell freezing.
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PMID:Hypothernic storage of pig hepatocytes: influence of different storage solutions and cell density. 889 13

1. We have studied the components of the metabolic acidosis that accompanies urethane anaesthesia in rats, both with and without the hypothermia that results from this anaesthesia. 2. Acid-base disturbances were analysed with an approach based on Stewart's analysis of acid-base chemistry. 3. The pH fall in the blood of normothermic anaesthetized rats (body temperature Tb) = 37 degrees C) was related to increases in plasma anions (lactate and [Cl-]), which decreased the strong ion difference ([SID]), as well as to increase the weak acid buffers due to increases in albumin. 4. A stronger metabolic acidosis was found in the blood of rats with hypothermia induced by urethane (Tb = 32 degrees C). Although plasma lactate was unchanged in hypothermic rats, [SID] decreased due to alterations in the plasma ionic balance. The metabolic acidosis found in hypothermia was also associated with increased weak acid buffers due to increases in albumin and inorganic phosphate. Further to hyperphosphataemia, signs of acute renal disfunction, such as increases in plasma [Mg2+] and blood urea nitrogen were found. Plasma retention of endogenous acids together with the retention of acid end-products of the metabolism of urethane because of acute renal failure may have contributed to strengthening the fall in pH and [HCO3-] found in urethane-induced hypothermic rats.
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PMID:Components of the blood acid-base disturbance that accompanies urethane anaesthesia in rats during normothermia and hypothermia. 924 67

This study was conducted to determine whether hypothermia inhibited alveolar epithelial injury in the resected human lung during preservation. Hyposmotic albumin solution, 248 mOsm/kg, was instilled into the alveolar spaces of resected human lungs which were inflated with an airway pressure of 7 cmH2O and stored at either 37 degrees C or 8 degrees C for 4 h. Alveolar fluid was aspirated and the influx of lactate dehydrogenase (LDH) and globulin into the alveolar spaces, as markers of alveolar epithelial injury, was measured. Ion transport and fluid clearance across the alveolar epithelium were calculated by the changes in electrolyte and albumin concentrations in the alveolar fluid, respectively. While the LDH levels and globulin concentrations increased significantly in the hyposmotic experiments at 37 degrees C, hypothermia inhibited these increases. Alveolar fluid clearance at 37 degrees C increased to 20% in the hyposmotic experiments compared with 12% in the control isosmotic experiments; however, sodium and chloride transport in the hyposmotic experiments was not significantly different from that in the isosmotic experiments. Thus, we conclude that hypothermia at 8 degrees C inhibits alveolar epithelial injury caused by the hyposmotic solution in resected human lungs. Moreover, alveolar ion and fluid clearance mechanisms were preserved across the injured alveolar epithelial cells.
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PMID:Hypothermia inhibits the alveolar epithelial injury caused by hyposmotic albumin solution during preservation of the resected human lung. 930 46

To study the mechanisms responsible for ischemia-reperfusion lung injury, we developed an anesthetized rabbit model in which the effects of lung deflation, lung inflation, alveolar gas composition, hypothermia, and neutrophils on reperfusion pulmonary edema could be studied. Rabbits were anesthetized and ventilated, and the left pulmonary hilum was clamped for either 2 or 4 h. Next, the left lung was reperfused and ventilated with 100% oxygen. As indexes of lung injury, we measured arterial oxygenation, extravascular lung water, and the influx of a vascular protein (131I-labeled albumin) into the extravascular space of the lungs. The principal results were that 1) all rabbits with the deflation of the lung during ischemia for 4 h died of fulminant pulmonary edema within 1 h of reperfusion; 2) inflation of the ischemic lung with either 100% oxygen, air, or 100% nitrogen prevented the reperfusion lung injury; 3) hypothermia at 6-8 degreesC also prevented the reperfusion lung injury; 4) although circulating neutrophils declined during reperfusion lung injury, there was no increase in interleukin-8 levels in the plasma or the pulmonary edema fluid, and, furthermore, neutrophil depletion did not prevent the reperfusion injury; and 5) ultrastructural studies demonstrated injury to both the lung endothelium and the alveolar epithelium after reperfusion in deflated lungs, whereas the inflated lungs had no detectable injury. In summary, ischemia-reperfusion injury to the rabbit lung can be prevented by either hypothermia or lung inflation with either air, oxygen, or nitrogen.
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PMID:Ischemia-reperfusion lung injury in rabbits: mechanisms of injury and protection. 988 66

Since the first successful replacement of the aortic arch with perfusion of the head, various methods have been employed to preserve cerebral function during aneurysm operations. Although deep hypothermia was used for surgery of the aortic arch, as early as 1963, the introduction of prolonged circulatory arrest has simplified replacements of the aortic arch. Between October 1990 and September 1993, 69 patients underwent aortic arch replacement for aneurysmal disease at the Dept. of Cardio-Thoracic Surg., University of Vienna. 52 patients had an acute dissection Type A, 17 patients were operated on electively. The patients age (48 male, 21 female) ranged between 16 and 81 years. Primary diagnosis was hypertension (n=44), marfan (n=14), unknown (n=10) and trauma (n=1). Total cardiopulmonary bypass was established via femoral artery cannulation. All patients received Cortison and Thiopental for added cerebral protection. Deep hypothermia (12 degrees C), confirmed by 0-EEG, and circulatory arrest were induced in all patients. The aneurysm was opened longitudinally and a full thickness single patch or "island" of aortic wall, containing the origins of the three arch vessels, was constructed and anastomosed in a continuous fashion to an albumin coated graft. 68 patients survived the operation (intraoperative mortality 1%). The 30-day mortality was 23% (n=16). Twelve patients died of multiorgan failure, two patients of a stroke and two due to myocardial infarction. The mean cerebral circulatory arrest time was 32 minutes (range 11-61 min.). Our experience with aortic arch replacements using profound hypothermia and circulatory arrest supports our contention, that it is the method of choice in this very difficult surgical field.
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PMID:Operative management of aortic arch aneurysm using profound hypothermia and circulatory arrest. 1006 52

Systemic hypothermia has neuroprotective effects in experimental models of central nervous system ischemia caused by vascular occlusions. The present study addresses the question as to whether systemic hypothermia can influence the extravasation of plasma proteins following severe spinal cord compression trauma using immunohistochemistry to identify the plasma proteins albumin, fibrinogen and fibronectin. Fifteen rats were assigned to one of three groups and received either thoracic (T) laminectomy or severe spinal cord compression trauma of the T8-9 segment. One group comprised laminectomized animals without compression trauma submitted to a hypothermic procedure in which the core temperature was reduced from 38 degrees to 30 degrees C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were killed 24 h following the surgical procedure. The normothermic and hypothermic trauma groups had indications of marked extravasation of albumin, fibrinogen and fibronectin at the site of the injury (T8-9). There was also pronounced extravasation in the cranial and caudal peri-injury zones (T7 and T10) of normothermic injured rats but, with few exceptions, not in the hypothermic ones with the same degree of compression. By measuring the cross-sectional area of the peri-injury zones we found in the hypothermic trauma group a significant reduction of the expansion compared with that present in normothermic injured rats. Our study thus indicates that hypothermia reduces the extravasation of the plasma proteins albumin, fibrinogen and fibronectin following spinal cord compression in the rat. Such a reduction may contribute to neuroprotective effects exerted by hypothermia.
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PMID:Systemic hypothermia following compression injury of rat spinal cord: reduction of plasma protein extravasation demonstrated by immunohistochemistry. 1041 96


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