Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

University of Wisconsin and modified Euro-Collins solutions for pulmonary preservation were compared in a rat orthotopic left lung isotransplant model. Heart-lung blocks of donor rats were flushed with and preserved in one of the preservation solutions at 0 degrees C. After 6 or 12 hours of cold ischemia, the left lungs were transplanted into recipient rats and reperfused for 1 hour. Pulmonary function was assessed by measuring oxygen and carbon dioxide tensions in arterial blood after removal of the right lung. Lipid peroxide concentrations were measured as thiobarbiturate acid-reactive substances. The ratios of wet to dry weight of grafts after ischemia and after reperfusion were calculated. Histologic changes of ischemia-reperfusion injury of the lung tissue were evaluated using a graded scale. Oxygen tension after 6 hours of preservation followed by reperfusion was significantly higher with University of Wisconsin solution (308.8 +/- 81.1 mm Hg) than with Euro-Collins solution (50.8 +/- 17.8 mm Hg; p less than 0.001). Carbon dioxide tension in the University of Wisconsin solution group was also significantly lower than in the Euro-Collins solution group (28.2 +/- 2.3 versus 46.0 +/- 4.5 mm Hg; p less than 0.05). Lipid peroxide concentration after 6 hours' preservation in University of Wisconsin solution was significantly lower (0.88 +/- 0.07 mumol/g) than that in Euro-Collins solution (1.26 +/- 0.12 mumol/g; p less than 0.05). After 12 hours of preservation only lipid peroxide concentration with University of Wisconsin solution was significantly lower (1.30 +/- 0.09 mumol/g) than with Euro-Collins solution (1.71 +/- 0.15 mumol/g; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:University of Wisconsin solution for pulmonary preservation in a rat transplant model. 153 Oct 7

We studied changes in myofibrillar function and protein profiles after complete global ischemia with anoxia in rat hearts. Hearts were exposed to global ischemia and anoxia (CGI) for 30 or 60 minutes at 37 degrees C, and myofibrils were prepared for measurement of Ca(2+)-dependent Mg(2+)-ATPase activity at pH 7.0 and 6.5. Hearts incubated in cold saline (1 +/- 1 degrees C) and nonincubated hearts served as controls. Maximum ATPase activity was unchanged at pH 7.0 and pH 6.5 in myofibrils from hearts treated with 30 or 60 minutes of CGI. At pH 7.0, the Hill coefficient, which is an index of cooperative interactions among thin-filament proteins, was unchanged after 30 minutes of CGI but was significantly increased after 60 minutes of CGI. A similar trend for increased cooperativity was observed when myofibrillar ATPase activity was measured at pH 6.5 in myofibrils from rat hearts made ischemic for 30 or 60 minutes. Both 30 and 60 minutes of CGI resulted in increased pCa50 values (half-maximally activating free [Ca2+]) at pH 7.0 and pH 6.5. Densitometric analysis of myofibrillar proteins separated with sodium dodecyl sulfate-polyacrylamide gel electrophoresis indicated that troponin I and troponin T were degraded during 60 minutes of CGI. Two new protein bands appearing in ischemia-treated myofibrils were identified as partially degraded troponin I and troponin T with Western blots. The troponin I fragment could be phosphorylated by cAMP-dependent protein kinase. In addition, we observed phosphorylation of a protein band that corresponded to myosin light chain-2 in myofibrils from CGI-treated hearts. These results suggest that degradation of thin-filament proteins may contribute to the changes in cooperativity of Ca2+ regulation of ATPase activity observed in the myofibrils from rat hearts exposed to CGI.
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PMID:Alterations in myofibrillar function and protein profiles after complete global ischemia in rat hearts. 153 Nov 86

We evaluated the hemodynamic effects of amiodarone on left ventricular (LV) function after global ischemia. Amiodarone was administered orally at 15 mg/kg/day for an average of 28 days to a group of 10 dogs. The concentration of amiodarone in serum and LV myocardium was 0.40 +/- 0.24 micrograms/ml and 44 +/- 27.0 micrograms/g, respectively. This experimental group and a control group of 10 dogs each underwent 120 min of aortic cross-clamping with cold crystalloid cardioplegia resulting in an average myocardial temperature of 15 degrees C. LV function measurements by pulse-transit sonomicrometry and Millar solid-state micromanometers were processed by a minicomputer. Compared to the nontreated control group, oral amiodarone for 28 days produced depression of LV contractility which was reflected by lower slope of the end-systolic pressure-volume relation (Evmax), percentage shortening of segment length, left ventricular pressure-segment length loop area, and slope of the end-systolic pressure-segment length relation (Esmax). After ischemia, percentage recovery of LV global function (Evmax and mean velocity of circumferential fiber shortening) and regional function (Esmax) was significantly better in the amiodarone group than in the control group. We conclude that oral amiodarone for 28 days results in a depression of LV contractility but the combination of amiodarone and ischemia does not act synergistically to further depress postischemic LV function.
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PMID:Hemodynamic effects of oral amiodarone on left ventricular function before and after global ischemia. 153 5

It has been suggested that rapid cooling before the induction of arrest may be harmful to the newborn myocardium. The objective of this study was twofold: (1) to evaluate whether prearrest rapid cooling is indeed detrimental to myocardial recovery and (2) if so, to evaluate whether the adverse effect of prearrest hypothermia is dependent on the rate of cooling or the total duration of cold perfusion. After an initial stabilization period isolated Langendorff hearts (n = 5 per group) from neonatal piglets (5 to 7 days old) were randomized to four groups: group 1, 5 minutes of rapid cooling to 15 degrees C; group 2, 20 minutes of slow cooling to 15 degrees C; group 3 and group 4, rapid and slow cooling, respectively, with the addition of St. Thomas cardioplegic solution. All groups were then subjected to 2 hours of ischemia at 15 degrees C followed by 30 minutes of reperfusion at 38.5 degrees C. Post-ischemic recovery of left ventricular developed pressure was significantly greater in group 1 versus group 2 (80% +/- 3% versus 61% +/- 2%; p less than 0.05) and in the presence of cardioplegia, group 3 versus group 4 (72% +/- 3% versus 57% +/- 3%; p less than 0.05). The increase in left ventricular end-diastolic pressure was significantly less in group 1 versus group 2 (8% +/- 5% versus 33% +/- 7%; p less than 0.01). Myocardial adenosine triphosphate content recovery correlated with ventricular recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse effect of prearrest hypothermia in immature hearts: rate versus duration of cooling. 154 65

The influence of ischemia and reperfusion on nucleotide concentration in human myocardium was investigated during heart and heart-lung transplantation. Myocardial preservation during heart transplantation was achieved by infusion of cold St. Thomas' Hospital cardioplegic solution followed by storage in Ringer's solution at 4 degrees C during transport. In contrast, the hearts of heart and lung donors were preserved by core cooling using cardiopulmonary bypass and infusion of cold blood cardioplegia containing 26 mM potassium. The heart-lung block was transported in cold donor blood. Nucleotides and their catabolite concentrations were measured in donor tissue specimens taken before organ collection, before commencement of implantation and 30 min after aortic clamp removal. During reperfusion, samples of coronary sinus and arterial blood were collected and analysed for nucleotide catabolite concentration. Myocardial ATP and total nucleotide pool remained almost unchanged during the ischemic transport of the donor organs with only very small increases in myocardial inosine and hypoxanthine concentrations. However, a significant decrease of total adenine nucleotide pool by 10%-20% was demonstrated between the start of implantation and 30 min post-reperfusion. A release of inosine + hypoxanthine was greatest in the 1st minute (15-25 microM), but was still substantial after 10 min of reperfusion (5-15 microM). Metabolic changes tended to be more pronounced during heart-lung transplantation than during heart transplantation.
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PMID:Adenine nucleotide catabolism in human myocardium during heart and heart-lung transplantation. 154 98

A number of case reports and series have reported successful replantation after prolonged periods of ischemia. However, the acceptable range of normothermic and hypothermic ischemic storage remains controversial. There is little question that the tolerance of composite tissue for ischemia is dependent on the quantity of contained skeletal muscle. We report a successful hand replantation after 54 hours of cold ischemia. We believe that this case documents the longest anoxic period yet reported for successful hand replantation. We further believe that the functional results obtained confirm the value of hand replantation even after such a prolonged ischemic interval.
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PMID:Hand replantation after 54 hours of cold ischemia: a case report. 156 65

The prognostic significance of early malfunction or delayed function after cadaveric renal transplantation is controversial. This study examines the influence of intraoperative management in 438 cadaveric renal transplant recipients on seven posttransplant outcome measures: (1) time of onset of urine output, (2) urine volume, (3) renal function, (4) incidence of delayed function, (5) never-functioning kidney, (6) graft survival, and (7) patient survival. Delayed function, defined as the need for hemodialysis during the first posttransplant week, decreased from 46% in 1982 to 15% in 1990 and was associated with a 25% lower 1-year graft survival rate and a mortality rate of 10% at 3 months, compared with 3% when immediate function was present. The most important factors influencing the outcome were cold ischemia time (P = 0.007), intraoperative administration of albumin (P = 0.0027), duration of surgery (P = 0.020), and recipient age (P = 0.041). A high albumin dose (1.2-1.6 g/kg bodyweight) induced urine output within 30 min in 75% of patients and induced larger urine volumes (7.3 L/24 hr), as compared with the effects of a low dose (0-0.4 g/kg), which induced urine output within 30 min in 39% and only 3.7 L/24 hr. Serum creatinine at 1 week was 3.4 and 5.8 mg/dl for the high and low albumin doses, respectively (P less than 0.0001). Similarly, mean glomerular filtration rates at 1 and 7 days were 33 and 21 ml/min, compared with 47 and 28 ml/min, for the high and low albumin doses, respectively (P less than 0.01). The incidence of delayed function and of never-functioning kidneys declined from 34% and 9% for the low dose to 12% and 1% for the high dose, respectively. Finally, with increasing albumin dose, the graft survival rate at 1 year improved from 59 to 78% (P less than 0.002), and the patient mortality rate at 3 months dropped from 6% to 2%. For albumin dose intervals between the high (1.2-1.6 g/kg) and low (0-0.4 g/kg), the effect on all seven outcome measures was intermediate, generally describing a linear relationship. Weighted least-squares analysis of the relationship of delayed function with high vs. low doses of albumin, mannitol, furosemide, and volumes of crystalloid solutions showed significance only for the albumin effect. High-dose albumin infusion likely produces intravascular volume expansion and achieves a prompt restoration of blood flow, minimizes hypoxic injury, and helps preserve renal tissue. The possibility of other beneficial effects of albumin unrelated to intravascular volume also exists.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intraoperative albumin administration affects the outcome of cadaver renal transplantation. 156 43

The reduced thiol pool of myocardial tissue represents an important defense mechanism against oxygen toxicity. Since the ischemia-induced depletion of this pool might favor the cytotoxicity of oxygen-derived free radicals produced during reperfusion, we assessed the effects of the thiol group donor N-acetylcysteine in an isolated buffer-perfused rat heart model of ischemia/reperfusion. Fifty hearts were studied. A first series of experiments that consisted of two groups (n = 10) was designed to simulate the conditions of standard cardioplegic arrest. Hearts were subjected to 180 minutes of cold (15 degrees to 18 degrees C) global ischemia and 1 hour of reperfusion. The control group received crystalloid hyperkalemic cardioplegic solution given every 30 minutes during arrest, and the treated group received the same solution supplemented with N-acetylcysteine (0.04 mol/L). On the basis of comparisons of postreperfusion left ventricular developed pressure, maximal dP/dt, and diastolic pressure, N-acetylcysteine-containing cardioplegic solution afforded significantly better protection. A second series of experiments was then undertaken to assess the effects of N-acetylcysteine in hearts subjected to the sequence of ischemic events that is inherent in transplantation procedures. Hearts were cardioplegically arrested, stored for 5 hours at 2 degrees C, subjected to 1 additional hour of ischemic arrest at 15 degrees to 18 degrees C, and reperfused for 60 minutes. Three groups (n = 10) were studied that differed by the modalities of cardioplegic preservation used during the poststorage ischemic interval. One group received multidose unmodified cardioplegic solution. A second group received multidose cardioplegic solution supplemented with N-acetylcysteine (0.04 mol/L), and the third group was given only a single dose of N-acetylcysteine-enriched (0.07 mol/L) cardioplegic reperfusate at the end of arrest. Multidose N-acetylcysteine-containing cardioplegic solution resulted in a significantly better hemodynamic recovery than unmodified cardioplegic solution. The protection afforded by N-acetylcysteine was lost when the drug was given only at the time of reperfusion. We conclude that supplementation of cardioplegic solution with N-acetylcysteine markedly improves postarrest recovery of function, presumably through an enhancement of the reduced thiol pool, which increases the capacity of reperfused myocardium to handle the postischemic burst of free radical production. The clinical relevance of these findings stems from the fact that thiol-containing drugs are available for human use.
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PMID:Maintenance of the myocardial thiol pool by N-acetylcysteine. An effective means of improving cardioplegic protection. 156 75

In order to find out if puerarin could protect the hearts from myocardial reperfusion injury after cardiac arrest, twelve dogs divided into two equal groups were placed on moderately hypothermic cardiopulmonary bypass and their hearts were subjected to 140 min of cold cardioplegic arrest and 60 min of reperfusion. In the control group, the hearts were perfused with a crystalloid cardioplegic solution (CPS) through the aortic root every 20 min during arrest. In the treated group, the hearts received CPS containing puerarin (2 mg/kg). Cardiac hemodynamic variables were monitored throughout the experiments. Left ventricular function curves were formed before ischemia and after 60 min of reperfusion. The results showed that the recovery of left ventricular function in the treated group was significantly better than that in the controls (81 +/- 11% versus 39 +/- 7%, P less than 0.01). Compared with preischemic values, the increase of coronary blood flow (CBF) at cardiac arrest in the puerarin-treated group was higher than that in the control group (214 +/- 11 versus 177 +/- 4 ml/min, P less than 0.01). The data indicate that puerarin has protective effects on the cardiac function after prolonged arrest and reperfusion.
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PMID:The protective effect of puerarin against myocardial reperfusion injury. Study on cardiac function. 157 64

This study was carried out to investigate the proportion of the 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha) and thromboxane B2 (TXB2) alteration that is due to ischemia in pancreas transplantation against the proportion due to reperfusion. For this purpose, Lewis rats were divided in three experimental groups: Group I = Control, Group II = Donor pancreas subjected to 15 minutes of cold ischemia, Group III = Same as group II but pancreas were transplanted to the recipient individual and then subjected to reperfusion. The results indicate that increases in pancreas 6-keto PGF1 alpha occur as a consequence of cold ischemia while TXB2 remains unchanged. When blood flow was restored, 6-keto PGF1 alpha remained unchanged compared to the ischemic group while pancreatic levels of TXB2 were significantly increased. These results suggest a different induction of prostanoid metabolism during ischemia and reperfusion in pancreatic tissue.
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PMID:Pancreas prostanoid production in ischemia and reperfusion. 158 98


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