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)

A total of 201 consecutive cadaveric kidney transplantations were performed in 188 patients at the Chinese Great Wall Hospital, Beijing, from October 1977 to May 1990. The overall 1-, 2-, 5-, and 10-year graft survival rates were 75.5%, 64.5%, 37.0%, and 32.9%, respectively. In the last 5 years, these figures have risen to 83.7% at 1 year, 69.5% at 2 years, and 40.8% at 5 years, respectively. The 14 variables correlating to graft survival in the present study were analyzed using the log rank test for univariate analysis and the Cox proportional hazard model for multivariate analysis. The results show that immunosuppressive drug therapy, cold ischemia time, acute tubular necrosis, and infection were significant factors affecting the survival of cadaveric kidney grafts. Triple therapy with low-dose cyclosporin, as compared to conventional immunosuppressive drug therapy, significantly increased the 1-year graft survival rate (90.3% vs 31.3%) but did not influence the long-term graft survival rate after 3 years. The incidence of acute tubular necrosis significantly correlated to the cold ischemia time and influenced the 1-year graft survival. Analysis showed that the lymphocytotoxic crossmatch affected graft survival after 3 years and that most late graft losses were due to chronic rejection, suggesting that histocompatibility is the strongest factor affecting long-term graft survival. A beneficial effect of pretransplant blood transfusions on long-term graft survival was seen in patients treated with conventional immunosuppressive drugs but not in cyclosporin-treated patients.
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PMID:Analysis of prognostic factors affecting renal allograft survival. 141 14

In view of the hypothesis that free radicals induced damage during ischemia and reperfusion is mediated by transition metals, we investigated the effect of the potent metal chelator TPEN (N,N,N'N'-tetrakis(-)[2-pyridylmethyl]-ethylenediamine) on cardiac function after prolonged myocardial ischemia. Isolated working rat hearts were subjected to 12 hours of cold ischemic arrest followed by reperfusion for 1 hour. The study was carried out on five groups (nine hearts in each): (1) St. Thomas' Hospital cardioplegic solution; (2) St. Thomas' Hospital cardioplegic solution with 7.5 mumol/L TPEN; (3) protection conditions as in group 2, but with TPEN administration during preischemic and reperfusion periods; (4) University of Wisconsin solution; and (5) the same conditions as in group 4 with TPEN administration during the preischemic and reperfusion periods. Significant enhancement of hemodynamic recovery was observed in the presence of TPEN throughout the experiment. The recovery of cardiac output was 24% +/- 4% in group 3, as compared to 12% +/- 4% in group 1 (p < 0.01). The postischemic left ventricular pressure recovery was 57% +/- 4% in group 3, as compared to 18% +/- 7% in group 1 (p < 0.005). The hearts in group 5 recovered, reaching 29% +/- 2% of the preischemic cardiac output and at 65% +/- 2% of the left ventricular pressure recovery (p < 0.05 versus group 3). Lactate dehydrogenase was released throughout the reperfusion. TPEN addition to groups 2 and 3 did not significantly reduce lactate dehydrogenase release; however, TPEN in University of Wisconsin solution and throughout the experiment significantly decreased lactate dehydrogenase release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:TPEN, a transition metal chelator, improves myocardial protection during prolonged ischemia. 142 Feb 48

Pain-like sensory disorders lasting several days were observed in rats after transient ischemia in the lumbar region of the spinal cord. The ischemia was induced with a recently developed photochemical technique. Rats exhibited strong allodynia, a pain-like reaction to innocuous stimuli, to mechanical stimulation of the caudal trunk, hind limbs, and hind paws, which were areas innervated by the ischemic spinal segments. The rats also expressed hypersensitivity to cold stimuli. However, no changes in sensitivity to noxious heat could be detected with the hot-plate test. Furthermore, no morphological damage could be observed in the spinal cord at the light microscopic level in the majority of rats after transient spinal cord ischemia. The present results indicate that allodynia-like symptoms to mechanical stimuli after spinal ischemia may be mediated by myelinated afferents and could be associated with dysfunction of inhibitory transmission in the spinal cord. We suggest that this pain-related syndrome after spinal ischemia could be considered as an animal model of painful states of spinal origin.
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PMID:Photochemically induced transient spinal ischemia induces behavioral hypersensitivity to mechanical and cold stimuli, but not to noxious-heat stimuli, in the rat. 142 27

The orthotopic heart transplantation is an accepted treatment for terminal cardiac disease. The technique of heart procurement and preservation is explained and the primary graft function in 108 subsequent heart transplantations is assessed. The mean ischemia time is 41 +/- 10 min in local, 98 +/- 19 min in distant (< 100 km) and 114 +/- 16 min in distant (> 100 km) organ procurement. Our method of preservation consists of cold cardioplegic arrest with potassium (30 mEq/L) cardioplegic solution. The incidence of the indication for high dose katecholamine-treatment after surgery and the maximal creatininekinase levels rose with ischemia time. All hearts recovered within a few days and the stay in the intensive care unit was not prolonged. We conclude that the heart preservation with cold cardioplegic arrest results in a good primary graft function. It is important to keep the ischemia time as short as possible.
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PMID:[Technique and organization of heart removal from the multi-organ donor]. 142 30

Lazaroids are a class of novel 21 aminosteroids. They have been reported to be potent inhibitors of lipid peroxidation, which is a major contributing factor to ischemia-reperfusion injury in the lung. A Lewis rat orthotopic left lung isotransplant model was used to investigate the effects of the lazaroid U74500A on pulmonary preservation. The heart-lung blocks of donor rats were flushed with and then stored in either standard University of Wisconsin solution or University of Wisconsin solution with 30 mumol/L of U74500A substituted for the dexamethasone. After 6 or 12 hours of cold storage at 0 degrees C, 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 a thiobarbituric acid-reactive substance. Although arterial oxygen and carbon dioxide pressures and water content after 6 hours of preservation followed by reperfusion were similar in both the lazaroid and dexamethasone groups, lipid peroxide concentration was significantly higher in the dexamethasone group (0.88 +/- 0.07 mumol/gm) than in the lazaroid group (0.54 +/- 0.07 mumol/gm) (p < 0.01). After 12 hours of preservation, there were significant differences between the lazaroid and dexamethasone groups in arterial oxygen pressure (339 +/- 70 vs 27 +/- 3 mm Hg, p < 0.01), arterial carbon dioxide pressure (24.3 +/- 2.7 vs 47.7 +/- 7.0 mm Hg, p < 0.001), and lipid peroxide concentrations (0.69 +/- 0.07 vs 1.30 +/- 0.09 mumol/gm, p < 0.001). We conclude that addition of U74500A to the flush and storage solution enhances the preservation of the pulmonary graft in this transplant model.
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PMID:Lazaroid U74500A as an additive to University of Wisconsin solution for pulmonary grafts in the rat transplant model. 143 15

The effectiveness of the University of Wisconsin solution on extended myocardial preservation was examined in this study using phosphorus 31-nuclear magnetic resonance spectroscopy. Isolated perfused rat hearts were arrested and stored in four preservation solutions: group 1, modified Krebs-Henseleit solution; group 2, modified St. Thomas' Hospital solution; group 3, oxygenated modified St. Thomas' Hospital solution containing 11 mmol/L glucose; and group 4, University of Wisconsin solution. The changes in myocardial high energy phosphate profiles and the intracellular pH values were measured during 12 hours of cold (4 degrees C) global ischemia and 90 minutes of normothermic reperfusion. Following ischemia, the hearts were assessed for hemodynamic recovery and myocardial water content. During ischemia, adenosine triphosphate depletion was observed in all groups; however, after 5 hours of ischemia, the adenosine triphosphate levels were significantly higher in group 3 compared with the other groups (adenosine triphosphate levels at 6 hours in mumol/gm dry weight: group 3, 7.6; group 4, 3.2; group 2, < 1; p < 0.025). The tissue water content at the end of ischemia was lower with the University of Wisconsin solution compared with the modified St. Thomas' Hospital solution or the oxygenated modified St. Thomas' Hospital solution (in ml/gm dry weight: group 4, 3.0; group 2, 4.4; group 3, 3.9; p < 0.05). The adenosine triphosphate repletion during reperfusion was greater with the University of Wisconsin solution compared with the modified St. Thomas' Hospital solution or the oxygenated modified St. Thomas' Hospital solution (12 mumol/gm dry weight in group 4; 8.1 in group 2; 9.0 in group 3; p < 0.05). Similar findings were obtained for the recovery of left ventricular pressure (in percent of preischemic control: group 4, 70%; group 2, 42%; group 3, 52%; p < 0.01) and coronary flow (group 4, 61%; group 2, 49%; group 3, 49%; p < 0.05). These data suggest that preservation with the University of Wisconsin solution affords improved hemodynamic recovery, enhanced adenosine triphosphate repletion, and reduced tissue edema upon reperfusion; however, oxygenated St. Thomas' Hospital solution with glucose is associated with the preservation of higher myocardial adenosine triphosphate levels during prolonged cold global ischemia. In conclusion, these data indicate that the University of Wisconsin solution might improve graft tolerance of ischemia in clinical heart transplantation.
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PMID:The effectiveness of University of Wisconsin solution on prolonged myocardial protection as assessed by phosphorus 31-nuclear magnetic resonance spectroscopy and functional recovery. 143 17

We hypothesized that ischemic insult to the lung allograft may render it more susceptible to rejection. Left canine single-lung allografts were subjected to usual periods of cold and warm ischemia (4 hours and 1 hour, respectively). Bronchoalveolar lavage and open lung biopsies were performed at 0, 1, 4, and 24 hours and 1 week after transplantation. Bronchoalveolar lavage fluid was examined for cellular phenotypes, lymphocyte lectin-mediated cytotoxicity, and natural killer cell cytotoxicity. Open lung biopsy specimens were examined for severity of injury/rejection and MHC class II expression. Within 1 to 4 hours of reimplantation, we observed marked influx of polymorphonuclear leukocytes and lymphocytes and an increase in lectin-mediated cytotoxicity (25.6% +/- 14.8% and 50.6% +/- 20.1% versus 5.4% +/- 7.5% preoperatively; p < 0.05). In addition, natural killer cell cytotoxicity increased from 10.2% +/- 13.5% before transplantation to 20.5% +/- 8.6% 4 hours after transplantation (p < 0.03). By 24 hours MHC class II expression became evident and continued to increase while subtle histologic evidence of rejection appeared by 1 week. We conclude that ischemia-reperfusion injury can alter the local bronchopulmonary milieu, thus rendering it more susceptible to the development of rejection.
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PMID:Early cellular events in the lung allograft. 144 89

To ascertain the beneficial effect of puerarin on the myocardium against reperfusion injury, studies on myocardial metabolism and ultrastructure were made. Twelve dogs divided into two equal groups were placed on moderate hypothermic cardiopulmonary bypass, and their hearts were subjected to 140 minutes cold cardioplegic arrest and 60 minute reperfusion. In the control group, the hearts were perfused with crystalloid cardioplegic solution (CPS) every 20 minutes during arrest. In the treated group, the hearts received CPS containing puerarin (2 mg/kg). Myocardial oxygen consumption, lactate production, creatine phosphokinase (CPK) release, water content and ultrastructural alterations were determined before ischemia, during cardiac arrest and at reperfusion. The results showed that intermittent infusion of CPS containing puerarin significantly decreased myocardial lactate production during ischemia, as well as myocardial oxygen consumption, CPK release and water content during reperfusion. Under electronmicroscopy, the degree of ischemic damage judged by a scoring method was less pronounced in the puerarin group than in the control. The authors conclude that puerarin has protective effects on the function of hearts that have undergone long periods of arrest and reperfusion.
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PMID:Protective effect of puerarin against myocardial reperfusion injury. Myocardial metabolism and ultrastructure. 145 45

We evaluated the viability and energy metabolism of ischemically damaged pancreas during preservation by the two-layer (University of Wisconsin solution (UW)/perfluorochemical (PFC)) cold storage method. The pancreas grafts subjected to 60-120 min warm ischemia were preserved by the two-layer (UW/PFC) cold storage method for 24 hours (group 3), a simple cold storage in UW for 24 hours (group 2) or without preservation (control) (group 1). The tissue concentration of adenine nucleotides (ANs) were determined using high performance liquid chromatography (HPLC) and the viability of the pancreas graft was tested in the canine model of segmental pancreas autotransplantation. The functional success rates of pancreas grafts of groups 1, 2 and 3 after 60 min of warm ischemia were 5/5 (100%), 4/5 (80%) and 5/5 (100%). After 90 min warm ischemia, the success rates of groups 1, 2 and 3 were 0/5 (0%), 0/5 (0%) and 5/5 (100%) respectively. Only the two-layer method (group 3) was effective for functional recovery of the pancreas suffered 90 min warm ischemia. However, after more than 105 min, the result was 0/5 (0%) in group 3. In groups 1 and 2, there was no correlation between the posttransplant viability and tissue concentration of ANs and energy charge potential (ECP) at the end of preservation. However, in group 3, there was an excellent correlation between the posttransplant viability and tissue concentration of adenosine triphosphate (ATP) and total adenine nucleotides (TAN) at the end of preservation. We conclude that tissue concentration of ATP and TAN at the end of 24 hour preservation by the two-layer (UW/PFC) method will predict the posttransplant outcome of pancreas graft subjected to significant warm ischemia.
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PMID:Evaluation of the viability and energy metabolism of ischemically damaged canine pancreas during preservation by the two-layer (University of Wisconsin solution/perfluorochemical) cold storage method. 145 89

Standard methods of myocardial preservation for heart transplantation have generally provided good results. Preservation times beyond 3 hours, however, have been associated with decreased survival. Leukocyte-mediated reperfusion injury is partly responsible for decreased graft function after prolonged graft ischemia. Leukocyte-depleted reperfusion has been shown experimentally to improve cardiac function after cold ischemic arrest. To determine the efficacy and safety of leukocyte-depleted reperfusion, 20 patients were enrolled in a randomized, double-blind clinical trial to be treated with either warm whole blood reperfusion (group I; n = 9) or warm leukocyte-depleted blood reperfusion (group II; n = 11). Reperfusion with leukocyte-depleted blood or whole blood was carried out for 10 minutes, with enriched cardioplegic solution added for the first 3 minutes of reperfusion. The mean donor and recipient age and the ischemic time (142 versus 153 minutes) were not significantly different between the two groups. Coronary sinus release of creatinine phosphokinase-MB 5 minutes after reperfusion was significantly less in group II (1.65 EU/min) than in group I (3.83 units/min; p = 0.05). Thromboxane B2 release was also significantly less (p = 0.05) in group II (33.6 pg/min) than in group I (67.0 pg/min). All hearts functioned adequately in both groups. The duration of inotropic support was shorter in group II than in group I, but the difference was not statistically significant. Postoperative hemodynamics, rejection episodes, and infectious complications were also not significantly different between groups in a mean follow-up of 9 months. Mean ejection fraction 1 month after operation was 65% in both groups. One early death occurred at 66 days secondary to infection; two late deaths occurred in group II, both from rejection. Leukocyte-depleted reperfusion is safe and easily applied in the operating room. Furthermore, leukocyte-depleted reperfusion decreases biochemical evidence of reperfusion injury. Although not influencing postoperative cardiac function when the ischemic time is short, less than 3 hours, leukocyte-depleted reperfusion may prevent significant reperfusion injury and improve posttransplantation graft function when ischemic times are long. Safe extension of the ischemic time would expand the donor pool and allow for better crossmatching.
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PMID:Leukocyte-depleted reperfusion of transplanted human hearts: a randomized, double-blind clinical trial. 145 32


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