Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study investigates the influence of inadequate oxygen supply on CK and CK-MB release rate in congenital cyanotic heart disease in fourteen patients. Eleven patients had Tetralogy of Fallot and 3 Transposition of great vessels. Their age ranged between 10 days and 10 years (mean 50.48 +/- 31.82 months). The corrective repair was carried out under CPB with systemic hypothermia (20 degrees-25 degrees C) and intermittent St. Thomas Cardioplegia perfusion in the aortic root until the septal temperature was below 16 degrees C. Three blood samples were taken before, during and 10 minutes after CPB to quantitate the CK and CK-MB. In 6 cases of Fallot, two simultaneous biopsies, one from the right and another from the left ventricular walls were taken at the end of the 10 first minutes of reperfusion to evaluate the ATP, CP and glycogen contents. CK and CK-MB levels showed an increasing evolution; the CK-MB per cent increased sharply after aortic clamp release and then fell abruptly to low values at the 10th minute after CPB arrest. Comparative evaluation between the 3 values for C K showed significant differences (P less than 0.001) in all, except when the first values were compared to the second (P greater than 0.05) and for CK-MB an overall significant differences were found at P less than 0.025 and P less than 0.001. On the other hand, quantification of ATP, CP and glycogen contents from simultaneous biopsies from the left and the right ventricular walls did not demonstrate significant differences between the two ventricles after the ischemic period.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Profile of creatine phosphokinase (CK) and its isoenzyme MB (CK-MB) during corrective procedures of congenital cyanotic heart disease. 274 16

The purpose of this work was to study the effects of warm (37 degrees C) and cold (4 degrees C) ischemia on different mitochondrial functions in rat brain, liver and kidney. After 10 to 60 minutes of ischemia at 37 degrees C the energy coupled respiration as well as the ADP-induced malate-aspartate shuttle activity in brain and liver mitochondria or the rate of mitochondrial ATP synthesis in kidney were significantly decreased. However, the respiratory rates and the shuttle activity in the absence of ADP remained unchanged. These data suggest that ischemia primarily affects electron transport in the respiratory chain rather than the hydrogen shuttle and the energy coupling system. When the temperature during the indicated ischemic periods was decreased to 4 degrees C, in brain and liver no significant alterations of these mitochondrial functions were found in comparison with the non-ischemic controls. When rat kidneys were stored for 36 hours at 4 degrees C according to Collins mimicking transplantation conditions, the mitochondrial respiration and ATP synthesis were only slightly decreased. It therefore appears that hypothermia can prevent effectively mitochondrial dysfunction due to ischemia.
 ...
PMID:Effects of warm and cold ischemia on mitochondrial functions in brain, liver and kidney. 277 Jul 17

The purpose of this study was to assess the degree, time sequence, and biochemical correlates of hypothermic protection against ischemic acute renal failure. Rats subjected to 40 minutes of bilateral renal artery occlusion (RAO) were made mildly hypothermic (32 degrees-33 degrees C, by cold saline peritoneal lavage) during the following time periods: 1) RAO only, 2) reperfusion only (beginning at 0, 15, 30, or 60 minutes after RAO and maintained for 45 minutes), or 3) during and after (0-45 minutes) RAO. Continuously normothermic (37 degrees C) RAO rats served as controls. The control rats developed severe acute renal failure (blood urea nitrogen [BUN], 95 +/- 4 mg/dl; creatinine, 2.2 +/- 0.1 mg/dl; and extensive tubular necrosis at 24 hours). Hypothermia confined to RAO was highly protective (BUN, 33 +/- 5 mg/dl; creatinine, 0.62 +/- 0.07 mg/dl; and minimal necrosis). Hypothermia partially preserved ischemic renal adenylate high-energy phosphate (ATP and ADP), increased AMP and inosine monophosphate concentrations, and lessened hypoxanthine/xanthine buildup (assessed at end of RAO). Hypothermia confined to the reflow period (beginning at 0, 15, and 30 minutes) was only mildly protective (e.g., BUN, 58-63 mg/dl); the degree of protection did not differ according to the time of hypothermic onset. Lowering reflow temperature to 26 degrees C had no added benefit. Hypothermia that started at 60 minutes after RAO conferred no protection. Combining ischemic and postischemic hypothermia abolished all renal failure (assessed at 24 hours). This study offers the following conclusions: Mild hypothermia can totally prevent experimental ischemic acute renal failure. Hypothermia is highly effective during ischemia, and it is mildly protective during early reflow; these benefits are additive. During early reflow, hypothermic protection is not critically time dependent. By 60 minutes of reflow, no effect is elicited; this absence of effect possibly signals completion of the reperfusion injury process. Hypothermia's protective effects may be mediated, in part, by improvements in renal adenine nucleotide content and, possibly, by decreasing postischemic oxidant stress.
 ...
PMID:Degree and time sequence of hypothermic protection against experimental ischemic acute renal failure. 280 43

Using an isolated rat heart preparation (Langendorff perfusion, perfusion pressure 100 cm H2O) the response of the hypertrophied heart (spontaneous hypertensive rats lv/bw ratio 3.6 +/- 0.5) to global normothermic (30 min) and hypothermic (25 degrees C, 120 min) ischemic and cardioplegic arrest and reperfusion (30 min) was examined and compared with normal hearts (Wistar rats lv/bw ratio 2.0 +/- 0.3). St. Thomas solution and verapamil (2 mg/l Ringer solution) were used as cardioplegic agents. Before ischemia hypertrophied hearts had a significantly higher pressure-rate product, a lower myocardial perfusion/g myocardium and a lower myocardial ATP and adenine nucleotide content. Unmodified ischemia reduced myocardial function in the hypertrophied hearts to a greater degree than in normal hearts in both normo- and hypothermia. St. Thomas solution and verapamil protected significantly the myocardial function in the normal and hypertrophied heart after normothermic ischemia in a similar manner (60-70% of the initial value). In the hypertrophied ventricle ATP decay and adenine nucleotide loss was greater in verapamil than in St. Thomas solution treated hearts. In hypothermic ischemia only St. Thomas solution protected left ventricular function and adenine nucleotide loss in both normal and hypertrophied hearts. Verapamil was ineffective in the normal ventricle and protected left ventricular function but not the ATP and adenine nucleotide decay in the hypertrophied heart.
 ...
PMID:Function and energy-rich phosphate content of the hypertrophied ventricle after global ischemia and reperfusion. 294 60

The effect of captopril on energy-rich phosphates and pH during normothermic ischemic arrest, hypothermic cardioplegic arrest and subsequent reperfusion was investigated in the isolated rat heart using 31P-nuclear magnetic resonance. The hearts remained in the probe during all perfusion procedures and captopril (80 ml.l-1) treatment was started directly after cannulation. After normothermic ischemic arrest (15 min), the ATP content of captopril-treated hearts was not significantly different from that of untreated hearts (53 +/- 9% and 52 +/- 8%, respectively). Accumulation of inorganic phosphate at the end of ischemia was significantly less in treated hearts, suggesting a higher end-ischemic nucleotide content in treated hearts. Hypothermic cardioplegic arrest (St. Thomas' Hospital solution, 4 degrees C) lasted for 3 h at 10 degrees C. Adenosine triphosphate in untreated hearts was significantly lower at the end of ischemia; 36 +/- 6% compared to 53 +/- 9% for untreated hearts. Adenosine triphosphate in untreated hearts recovered to 76 +/- 9% after normothermic ischemia and to 72 +/- 7% after hypothermic ischemia at the end of 30 min reperfusion. Captopril significantly improved adenosine triphosphate recovery in both treated groups; 89 +/- 4% after normothermic and 83 +/- 4% hypothermic ischemia. We conclude that captopril has a beneficial effect on recovery of adenosine triphosphate both after normothermic and after hypothermic ischemia.
 ...
PMID:Captopril improves recovery of adenosine triphosphate during reperfusion of the ischemic isolated rat heart; a 31-phosphorus-nuclear magnetic resonance study. 306 91

Currently, for practical clinical purposes, the preservation of donor hearts is limited to about 4 h. Transplantation must be finished within this period to assure complete functional recovery upon reperfusion. From the clinical setting it is well known that hypothermia results in a better myocardial preservation during ischemia. During ischemia, rapid catabolism of high-energy phosphates (e.g., ATP and creatine phosphate) occurs. The purpose of this study was to investigate the influence of temperature during a 24-h preservation period on the rate of catabolism of ATP and on the rate of accumulation of breakdown products (ADP, AMP, adenosine, inosine, hypoxanthine, and xanthine). For this purpose, hearts were excised and stored for 24 h at 0.5 degrees, 12 degrees, or 18 degrees C. In addition, the effect of initial cardioplegic arrest was compared with simple normothermic excision of the heart followed by 24 h in cold storage. It was found that the higher the storage temperature, the higher the rate of catabolism of high-energy phosphates and, hence, after 24 h, the lower the final ATP level and the higher the level of breakdown products, mainly nucleosides. It was also found that the initial cardioplegic arrest strongly benefits the preservation of high-energy phosphates as a result of the ATP-sparing effect.
 ...
PMID:Optimal storage temperature and benefit of hypothermic cardioplegic arrest for long-term preservation of donor hearts: a study in the dog. 307 13

Age-dependent differences in the effects of ischemia and reperfusion on ATP breakdown were studied in perfused adult and newborn (10 days old) rat hearts. No-flow ischemia (15 min at 37, 30, or 23 degrees C) was applied and reperfusion (20 min at 37 degrees C) was studied after ischemia at 23 or 37 degrees C. Hypothermia during ischemia protected both age groups to a similar degree against ATP decline, which was linear with temperature. Reperfusion after normothermic ischemia resulted in higher ATP levels in newborn hearts with less release of ATP catabolites (purines). We found no age-related differences in lactate release but large differences in purine release. During normoxia, adult hearts released mainly urate (80% of total) and inosine (7%), but newborns released hypoxanthine (64%) and inosine (15%). Early during reperfusion adult hearts released inosine (58%) and adenosine (18%), but newborns released inosine (53%) and hypoxanthine (38%). These data suggested a lower activity of the potentially deleterious enzyme xanthine oxidoreductase in newborn hearts, which was confirmed by enzymatic assay. ATP-catabolite release during reperfusion was less in newborn than adult hearts, and this coincided with lower xanthine oxidase activity.
 ...
PMID:Different ATP-catabolism in reperfused adult and newborn rat hearts. 316 69

As whole organisms, most mammals have a poor tolerance for hypothermia. But their cells may have a capacity for a far wider cold tolerance, which may be expressed in peripheral tissues, sporadically in core tissue and in cultured cells. Against this background the cold resistance of cells of deep hibernators may be seen as the extreme of a continuum and is complicated by the consideration that the voluntary hypothermia of hibernation is probably in most cases a metabolic adaptation to forestall starvation. Similarly, cold resistance of peripheral tissues may in diving animals be confounded by the need to be adapted to hypoxia as well. Hence, attempts to analyse cold resistance by comparisons of absolute rates of arbitrarily chosen reactions may be misleading. A more useful approach is analysis of maintenance of balance: balance between ATP synthesis and utilization, balance between macromolecule synthesis and degradation and balance between pumps and leaks. Cation pumps and leaks constitute a major component of energy utilization and are central to other cell functions, even during minimal metabolism. Hence, the maintenance of ion gradients is a central issue in understanding adaptation not only to hypothermia but also to starvation and hypothermia. Of the three hypometabolic states, hypothermia has been best studied in this regard. In most cases, passive permeability is more reduced at low temperature in cold-tolerant cells than in cold-sensitive ones. In some cases there is also a difference in Na-K pump activity and perhaps in ATP dependent Ca-pump activity. Pump activities and probably the maintenance of minimal leak require ongoing metabolism. The question of whether, in cold-sensitive cells, energy supplies are adequate at low temperature was once the focus of this field, but has been ignored for a decade without having been fully resolved. There are many instances of less temperature sensitivity of specific metabolic activities (mitochondrial respiration, etc.) in hibernators than in non-hibernators, without any verification of whether this is essential for survival at low body temperature. Certainly, robust pumping has been found in some failing cold-sensitive cells at low temperature, suggesting no shortage of ATP in these cases, but in other cases the issue may be a more complex one than just that of ATP availability.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Cold tolerance in mammalian cells. 333 88

Myocardial energy metabolism during deep general hypothermia (20 degrees C) and multidose crystalloid cardioplegia, and also during subsequent reperfusion, was studied in eight patients undergoing isolated aortic valve replacement. Six serial transmural biopsy samples from the left ventricular apex were analyzed for high-energy phosphates and their degradation products. Reductions in ATP, total adenine nucleotide content and energy charge were insignificant during cardioplegia, as were changes in adenosine and uric acid concentrations. During reperfusion, however, there was slight but significant reduction in total adenine nucleotide content, despite adequate oxygenation as indicated by reversal of lactate accumulation. These observations suggest that the reperfusion phase is accompanied by metabolic aberrations which are not overcome by good oxygenation in relation to the metabolic rate.
 ...
PMID:Preservation of myocardial high-energy phosphates in open-heart surgery with deep general hypothermia and multidose crystalloid cardioplegia. 343 22

This study was designed to test the hypothesis that infusion of ATP-MgCl2 during reperfusion following a prolonged period of hypothermic global ischemia would result in enhanced functional recovery of cardiac function. Two groups of dogs (n = 6 each) were placed on cardiopulmonary bypass (CP) with systemic hypothermia to 28 degrees C and subjected to 150 min of aortic cross-clamping. Crystalloid cardioplegia was infused every 20 min during ischemia. Reperfusion and rewarming were carried out for 20 min before discontinuation of CP bypass. During reperfusion, the experimental group received ATP-MgCl2(1.0 mg/kg/min ATP, 0.33 mg/kg/min magnesium). At 15 and 45 min following bypass, hemodynamic assessment was carried out for each animal by constructing Starling curves over a range of filling pressures at constant heart rate and comparing each animal to its own prebypass control level. The results indicated that ATP-treated animals exhibited complete functional recovery whereas control animals showed marked reduction in hemodynamic performance and myocardial compliance and had a higher myocardial water content (P less than 0.05). We conclude that infusion of ATP-MgCl2 during reperfusion following hypothermic ischemia may help ameliorate reperfusion injury.
 ...
PMID:Reperfusion with ATP-MgCl2 following prolonged ischemia improves myocardial performance. 349 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>