Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two types of sinus nodal cells were responsible for the main differences in the literature concerning the ultrastructure of the sinuatrial node: the intercalated clear cells and pale cells. Canine hearts were arrested by (1) aortic cross clamping, (2) coronary perfusion with the cardioplegic solution St. Thomas, and (3) coronary perfusion with the cardioplegic solution HTK (Custodiol(R)). After fixation by immersion or perfusion the sinus node tissue was prepared for electron microscopy. Following cardioplegic arrest and perfusion fixation, three nodal cell types in the non-ischemic sinuatrial node were observed: typical nodal cells, transitional cells, and intercalated clear cells. Less than 1% of the non-ischemic sinuatrial cells were intercalated clear cells, surrounded by typical nodal cells or transitional cells. The contractile apparatus of the intercalated clear cells was extremely poorly developed. Great structural variations in the mitochondria were observed in intercalated clear cells, variations that would not appear under conditions of ischemia. In contrast, after 15-25 min of ischemia at 25 degrees C the appearance of the sinus nodal cells was strikingly different from that of the non-ischemic sinuatrial cells. More than 10% of the nodal cells showed typical ischemic alterations, e.g., mitochondrial swelling, clumping of nuclear chromatin, loss of glycogen particles, and cell swelling in varying degrees. Because they look very pale, these nodal cells have been described as pale cells in the literature. Intercalated clear cells appear mainly in non-ischemic nodal tissue. Pale cells are ischemically damaged sinus nodal cells.
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PMID:Intercalated clear cells or pale cells in the sinus node of canine hearts? An ultrastructural study. 1096 34

Liver steatosis is frequently encountered at organ harvest and, although functionally inapparent in the donor, may seriously affect the functional recovery of the graft after ischemic preservation. The present study was aimed to investigate the diagnostic value of alpha-glutathione S-transferase (GST) in non-ischemic and ischemic livers with or without compensated steatosis. A histologically documented mild to moderate steatosis was induced in livers of male Wistar rats by fasting for 2 days and subsequent feeding of a fat-free diet enriched in carbohydrates. Fatty livers (FL) were retrieved and perfused in vitro for 45 min either immediately or after ischemic preservation at 4 degrees C in HTK solution. Effluate was collected during isolated perfusion and later analysed for liver specific enzymes, including GST. Normal livers (NL) were excised from healthy rats and underwent the same protocol. Non-ischemic livers showed similar enzyme release (FL versus NL) for ALT or GLDH but significant differences in GST. After ischemic preservation of NL, enzyme release increased mildly with respect to the non-ischemic reference values for ALT, remained unchanged for GLDH and rose substantially for GST. In FL, there was a more than 10-fold increase in all parameters, being most pronounced for GLDH as a marker of mitochondrial damage. It is concluded that GST may discriminate between healthy and suboptimal steatotic livers prior to ischemia and that the release of GST upon postischemic reperfusion of normal livers proves to be the most sensitive indicator for hepatocellular injury. However, GST turned out to be less useful for the detection of postischemic reperfusion injury in steatotic grafts.
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PMID:Value of alpha glutathione S-transferase for in vitro evaluation of preservation injury in normal and steatotic livers. 1111 71

Complete resumption of cardiac function after cardioplegic arrest presupposes a well-preserved myocardial ultrastructure during and after ischemia. Therefore, we determined ischemia-induced ultrastructural alterations in the myocardium during and after reversible cardioplegic ischemia using stereological methods. Cardiac arrest was induced with St. Thomas' Hospital- or Custodiol (HTK) solution. Reperfusion with Tyrode's solution followed after reversible cardioplegic ischemia in situ. Samples were taken 1) from beating hearts, 2) from cardioplegically arrested hearts immediately after the end of coronary perfusion, 3) from ischemic hearts incubated in the cardioplegic solution at 25 degrees C, and 4) from reperfused beating hearts after ischemia in situ at 22 degrees C. Cellular swelling was determined as the barrier thickness of capillary endothelium and as the sum of cardiomyocyte volume fractions of free sarcoplasm and mitochondria. In St. Thomas'-arrested hearts, intraischemic volume increase was significantly more pronounced in endothelial cells than in cardiomyocytes. Reperfusion at the intraischemic practical limit of resuscitability (ATP levels of 4 micromol/gww) significantly reduced intraischemic swelling of cardiomyocytes, but not of capillary endothelial cells. Mitochondrial damage was more pronounced in capillary endothelial cells during ischemia and after reperfusion. Thus, after reversible cardioplegic arrest, structural recovery of cardiomyocytes is better than that of capillary endothelial cells. An incomplete structural protection of capillary endothelial cells may predominantly contribute to postischemic dysfunction in the reperfused heart.
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PMID:Different preservation of myocardial capillary endothelial cells and cardiomyocytes during and after cardioplegic ischemia (25 degrees C) of canine hearts. 1204 37

Celsior, a new preservation solution in thoracic organ transplantation was evaluated for efficacy in cold preservation of human hepatocytes and compared with University of Wisconsin solution (UW) and histidine-tryptophan-ketoglutarate solution (HTK, Custodiol). Human hepatocyte cultures were preserved at 4 degrees C in Celsior, UW and HTK for 2, 6, 12, 24 and 48 h with 6 h of reperfusion. Levels of lactate dehydrogenase (LDH; cell necrosis), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT; mitochondrial function), and adenosine 5'-triphosphate (ATP; loss of intracellular energy) were measured. Cell necrosis, mitochondrial dysfunction, and loss of ATP were significantly ( P<0.001, P<0.001, P<0.002, respectively) lower in Celsior than in HTK. The amount of cell necrosis and mitochondrial dysfunction in Celsior solution (CS) and UW was equal ( P=n.s.) up to 24 h and significantly lower in UW after 48 h ( P<0.001). Additionally, the intracellular level of ATP was significantly higher after ischemia ( P<0.001) and reperfusion from long-term ischemia (24, 48 h) ( P<0.002). We can conclude that Celsior was superior to HTK and equal to UW in the protection of human hepatocytes against cold preservation injury from ischemia and reperfusion. Furthermore, Celsior was effective in long-term preservation of human hepatocytes.
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PMID:Celsior solution compared with University of Wisconsin solution (UW) and histidine-tryptophan-ketoglutarate solution (HTK) in the protection of human hepatocytes against ischemia-reperfusion injury. 1269 41

Cold preservation results in cell death via iron-dependent formation of reactive oxygen species, leading to apoptosis during rewarming. We aimed to study cold-induced damage (i.e., injury as a consequence of hypothermia itself and not cold ischemia) in proximal tubular cells (PTC) in various preservation solutions presently applied and to clarify the role of mitochondria in this injury. Primary cultures of rat PTC were incubated at 4 degrees C for 24 h in culture medium, UW, Euro-Collins or HTK solution with and without the iron chelator desferal and rewarmed at 37 degrees C in culture medium. Cell damage, morphology, and apoptosis were studied and mitochondrial membrane potential was assessed by fluorescence microscopy. Cold incubation of PTC in culture medium followed by rewarming caused marked cell damage compared to warm incubation alone (LDH release 39+/-10% vs. 1.6+/-0.3%). Cold-induced damage was aggravated in all preservation solutions (LDH release 85+/-2% for UW; similar in Euro-Collins and HTK). After rewarming, cells showed features suggestive for apoptosis. Desferal prevented cell injury in all solutions (e.g., 8+/-2% for UW). Mitochondrial membrane potential was lost during rewarming and this loss could also be inhibited by desferal. Trifluoperazine, which is known to inhibit mitochondrial permeability transition (MPT), was able to prevent cold-induced injury (LDH 85+/-5% vs. 12+/-2%). We conclude that cold-induced injury occurs in PTC and is aggravated by UW, Euro-Collins, and HTK solution. Iron-dependent MPT is suggested to play a role in this damage. Strategies to prevent cold-induced injury should aim at reducing the availability of "free" iron.
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PMID:Hypothermia causes a marked injury to rat proximal tubular cells that is aggravated by all currently used preservation solutions. 1296 15

Occurrence of primary graft nonfunction of pancreatic islets demands research for new methods of organ preservation during cold ischemia conditions. Digestive enzymes released during preservation injure the islets for subsequent rewarming and islet isolation processes. The aim of our study was to assess the amylase level in preservation solution as a marker of exocrine tissue injury, allowing the prognosis of islet yield and viability. The experiments undertaken on rats used three commercially available preservation solutions: ViaSpan (UW); Custodiol (HTK); and Euro-Collins (EC). After 180 minutes of cold ischemia, the highest islet recovery was observed among pancreata stored in UW solution (508 +/- 139 vs HTK 344 +/- 103; P <.05 vs EC 322 +/- 113; P <.05). These islets also revealed the highest insulin stimulation index in glucose static tests (1.19 +/- 0.30 vs HTK, 0.87 +/- 0.43; P <.01, vs EC.25 +/-.06; P <.001). The highest amylase level in the preservation solution was associated with a decreased yield of islets during the isolation process and lowest insulin stimulation index (increasing 139 +/- 18% for EC, 108 +/- 12% for HTK; P <.05 vs 87 +/- 10% for UW; P <.05). Our data strongly suggest, that the dynamic of amylase release during pancreas preservation at 4 degrees C correlates with a reduced number and viability of isolated islets. These results suggest that measurement of amylase levels after pancreas preservation may have potential clinical application as a marker to evaluate pancreatic tissue injury.
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PMID:Amylase levels in preservation solutions as a marker of exocrine tissue injury and as a prognostic factor for pancreatic islet isolation. 1452 37

The main goal of transplantation is to restore good renal function and to improve the quality of life of thousands of dialysis patients, something which can only be achieved by providing them with well functioning grafts. Delayed renal allograft function is a serious problem. It is important to prevent this complication because it makes the diagnosis of acute rejection in the early postoperative period difficult, increases the necessity for diagnostic procedures, introduces dialysis treatments and prolongs hospital stay. The aetiology of delayed graft function (DGF) is multifactorial, and factors including donor management, technique used for organ procurement and preservation, age, anatomical variations in the graft, ischemia periods, use of cyclosporine A (CyA) or recipient immunological reactions have been implicated. Using different preservation solutions DGF rates vary from 30% to 60%. Recent clinical data have demonstrated better preservation and improved renal function posttransplant with HTK and University of Wisconsin (UW) solutions compared to EuroCollins solution. In a randomized multicenter study in collaboration with the Eurotransplant organ exchange organization, the efficacy of the HTK solution in renal transplantation was compared to EuroCollins and UW solutions in two parallel prospective randomized trials. The first preliminary results comparing HTK and EuroCollins solutions are reported here.
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PMID:A preliminary report of the HTK randomized multicenter study comparing kidney graft preservation with HTK and EuroCollins solutions. HTK Study Group. 1462 38

Ischemia-reperfusion syndrome significantly influences the function of a kidney transplanted from a non-heart-beating donor (NHBD). An animal model of NHBD was used to monitor the influence of the exogenous addition of selenium in the perfusion solution (HTK, Custodiol) on the generation of free oxygen radicals between 0 and 120 minutes after transplantation of the NHBD organ. During this interval, the malondialdehyde concentration, an indicator of free oxygen radicals in the venous blood of the transplanted kidney, significantly decreased. The augmentation of the anti-oxidant capacity of the preservation solution might represent a possible improvement in the function of kidneys transplanted from NHBDs.
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PMID:Can ischemia-reperfusion syndrome in transplanted kidneys procured from non-heart-beating donors be influenced by adding selenium into the reperfusion solution? An experimental study. 1469 94

Adenosine 5'-triphosphate (ATP) depletion is a major cause of cellular injury during ischemia and reperfusion in organ transplantation. Therefore, histidine-tryptophan-ketoglutarate solution (HTK; alpha-ketoglutarate) and University of Wisconsin solution (UW; adenosine) were supplied with energy substrates to achieve graft viability. Nevertheless, their efficacy for maintaining the ATP level, particularly in human liver endothelial cells, was uncertain. Furthermore, it is of interest whether a high ATP level is beneficial in human liver endothelial cell viability. We used human liver endothelial cells between the 3rd and 6th passages in a cell culture model. Human liver endothelial cells were exposed to hypothermic preservation (4 degrees C) in HTK and UW for 2, 6, 12, 24 and 48 h with subsequent reperfusion of 6 h. ATP and lactate dehydrogenase (LDH) were measured after each interval. In comparison to HTK, UW demonstrates a statistically significantly higher level of ATP after each interval of ischemia (p < 0.001) and reperfusion (p < 0.002). Additionally, UW-preserved human liver endothelial cells exceed the ATP level of the warm control during all intervals of ischemia. The loss of cell viability (LDH) was statistically significantly higher after ischemia (p < 0.01) and reperfusion (p < 0.01) in HTK than in UW except after the interval of 48 h. In conclusion, adenosine was more effective than alpha-ketoglutarate in maintaining a high ATP level in human liver endothelial cells after ischemia and reperfusion. Different pathways of energy substrate utilization were a contributing factor. The beneficial effect of the higher ATP level caused by adenosine to human liver endothelial cell viability was limited to 24 h of ischemia. Beyond this ischemia time we could not prove a favorable impact of adenosine on human liver endothelial cells.
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PMID:Value of energy substrates in HTK and UW to protect human liver endothelial cells against ischemia and reperfusion injury. 1473 Feb 20

Reperfusion injuries after organ transplantation affect graft function and influence long-term graft survival. As hypothermic storage, which minimizes the extent of unspecific tissue injury after ischemia and reperfusion, is significantly influenced by the composition of preservation solutions, strategies to optimize the different components may lead to longer graft survival. In the present study the effects of the preservation solution B2 on early renal function and histopathological changes were compared to histidine-tryptophan-ketoglutarate solution (HTK, Bretschneider) in a model of isolated blood-perfused porcine kidneys. B2-preserved kidneys displayed a lower renal resistance and significantly better creatinine clearance as compared to HTK. Mean differences were also found for filtration fraction and sodium fraction reabsorption. The functional data were also related to histopathological changes. Together, these data indicate that the recently developed preservation solution B2 offers new principles of preservation and is a useful preservation solution for experimental isolated perfused kidney models. B2 may also be an interesting model for optimizing preservation within other organ perfusion models.
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PMID:Protective effects of B2 preservation solution in comparison to a standard solution (histidine-tryptophan-ketoglutarate/Bretschneider) in a model of isolated autologous hemoperfused porcine kidney. 1498 62


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