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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since intermittent cardioplegic reperfusion during an ischemic period may reduce the ischemic stress of the heart at least by lowering myocardial temperature, we compared the post-ischemic recovery of the dog heart following cardioplegia and subsequent continuous ischemia of 1 X 300 minutes at 22 +/- 1 degree C (model 1) and following cardioplegia and subsequent 3 X 100 minutes of ischemia at 17 +/- 1 degree C with intermittent 4-minute cardioplegic reperfusion every 100 minutes (model 2). The parameters of post-ischemic recovery were the cardiac O2 consumption per beat at work (MVO2-E0): HR), the stability of cardiac rhythm, the left ventricular content of high-energy phosphates, and ultrastructure. Solution HTK with a magnesium concentration of 9 mM/L, in clinical use up to the beginning of 1984, resulted in a significantly better post-ischemic recovery in model 1, despite about 40% lesser ischemic stress in model 2. A reduction of Mg concentration from 9 to 4 mM/l, as in the HTK solution clinically tested since February 1984, did facilitate the post-ischemic recovery in model 1 as indicated by the stability of cardiac rhythm but led to a significant improvement of all parameters of recovery in model 2. Moreover, recovery in model 2 after reduced Mg was also clearly better than in model 1 corresponding to the lesser ischemic stress. The parameters myocardial O2 consumption (MVO2) and potassium loss during HTK perfusion containing 9 and 4 mM/l, respectively, gave indications of specific membrane labilizing effects of Mg in the cardioplegic solution HTK.
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PMID:Different effects of cardioplegic solution HTK during single or intermittent administration. 608 14

The effects of severe regional myocardial ischemia in vivo and total ischemia in vitro on energy production by anaerobic glycolysis in dogs are described. The critical feature of ischemic injury in terms of the adenine nucleotide pool is the fact that the demand of severely or totally ischemic tissue for HEP exceeds the capacity of the damaged myocytes to produce it. The consequent depletion of ATP to very low levels and the destruction of the adenine nucleotide pool are associated with, or may be casually related to, the loss of cellular viability.
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PMID:High energy phosphates, anaerobic glycolysis and irreversibility in ischemia. 686 79

In summary, myocardial ischemia is associated with the progressive depletion of HEP and the adenine nucleotide pool. Anaerobic glycolysis is essential for energy production in the severely ischemic myocyte and accounts for 80% of the HEP utilized by severely or totally ischemic myocardium. However, the rate of anaerobic glycolysis is too slow to prevent the progressive depletion of ATP. Anaerobic glycolysis stops entirely prior to the complete utilization of glycogen. Without remaining HEP stores or HEP production from anaerobic glycolysis, HEP utilization no longer can occur. This point occurs in vivo after about 40 minutes of severe ischemia and coincides with the onset of cell death. Modest depletion of ATP due to brief periods of transient ischemia may not cause cell death, but is associated with partial depletion of the adenine nucleotide pool. The slow repletion of this pool may be responsible for prolonged depression of contractile function.
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PMID:Energy metabolism in the reversible and irreversible phases of severe myocardial ischemia. 694 1

The aims of this study were (1) to investigate the effect of R 75231, a nucleoside transport inhibitor, on renin-angiotensin release after renal ischemia-reperfusion and (2) to establish a possible protective effect of this drug on renal function. We used a canine model for auto- transplantation of kidneys that had been subjected to 30 min of warm ischemia and subsequently to 24h of cold storage in HTK preservation solution, with immediate contralateral nephrectomy. R 75231 was injected intravenously into six dogs in two equal portions of 0.05 mg/kg both 30 min and 10 min before reanastomosis was established. Another six dogs were used as a control group. At 2 weeks post-transplantation, five out of six dogs in the R 75231 group and one out of six in the control group were still alive. Starting on day 4, serum creatinine was lower in the R 75231 group than in the control group (p < 0.005). In contrast to the control group, an inversion of the median preischemia adenosine/inosine ratio was observed in the R 75231 group after reperfusion (0.4 preischemia vs 4.0 after 60 min of reperfusion). Reperfusion of the graft resulted in an immediate increase in renin, angiotensin I, and angiotensin II venous blood levels in the control group. In the R 75231 group, renin, angiotension I, and angiotensin II levels were significantly lower. We conclude that administration of R 75231 before reperfusion has a protective effect on post-transplant function of kidneys that have been subjected to prolonged warm ischemia. This effect may, at least in part, be ascribed to inhibition of the breakdown and disposal of endogenous adenosine which, in turn, inhibits the excessive stimulation of the renin-angiotensin system in the early phase of reperfusion.
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PMID:Protection of canine renal grafts by renin-angiotensin inhibition through nucleoside transport blockade. 762 81

Investigations of changes in activity of renin and blood pressure after reperfusion of the kidney transplant using HTK solution were carried out by means of an autologous, heterotopic model of kidney transplantation applied to dogs. Duration of cold ischemia was 48 h. According to variations in the composition of the HTK perfusion solution three test groups were set up. During the first 20 min after recirculation in each test group the renal venous and arterial renin activities were measured. Parallel to renin activity, the arterial blood pressure was recorded. During the first few minutes following recirculation of the kidney transplant the renin levels in the venous blood of the kidney were higher in test group 1 (HTK solution, perfusion height 120 cm) than in either of the other two, showing a median maximal increase of 195 ng/ml.h. In test group 2 the maximal venous renin concentration fell to 145 ng/ml.h, while graphs take a more uniform course. Test group 3 (HTK/tryptophan) differed from the others in having further improved renin values. After the 7.5 min of observation normal venous renin concentrations were measured following earlier values for maximal increase between 23.1 ng/ml.h and 120 ng/ml.h (median 61.5 ng/ml.h). The best reperfusion of the kidney was observed in the tryptophan group, albeit without any recognizable positive effects on the other renal functions. Initially low renin values do not necessarily correlate with a smooth postoperative renal function and vice versa. Initial renin values cannot provide a secure basis for predicting instant as well as long-term postoperative functions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Change in renin activity and blood pressure in the dog autologous kidney transplant model with modified HTK solution]. 776 Jun 55

This study was undertaken in order to obtain information on the mode of reaction of the contractile apparatus after different forms of cardiac arrest, global ischemia and reperfusion, as well as on possible correlations between the contraction state of myofibrils and biochemical parameters. During the survival time, before the level of 3 mumol/gww creatine phosphate (CP) is reached, the contraction state shows only minor changes. During the revival time in which ATP tissue concentrations decay to 4 mumol/gww, the contribution of ATP, lactate, anorganic phosphate (Pa) and acidosis to the degree of relaxation depends on the method of cardiac arrest. At defined biochemical values, the degree of relaxation is comparable after aortic cross clamping (ACC) and St. Thomas perfusion, but significantly different compared to HTK perfusion. Thus, during the revival time, the relaxation of sarcomeres depends predominantly on the composition of the solutions used for cardiac arrest. The re-entry of contraction below 3 mumol/gww ATP is correlated with the ATP concentration, independent of the form of cardiac arrest. Reperfusion after HTK or St. Thomas cardioplegia and reversible ischemia leads to the focal formation of contraction bands, which do not occur during ischemia. This contraction state is significantly more pronounced after reperfusion of St. Thomas arrested hearts. Thus, the contraction state of myofibrils is influenced not only by alterations in metabolite concentrations, but also by the composition of cardioplegic solutions and by the characteristic conditions (sufficient energy, oxygen and Calcium) during reperfusion.
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PMID:The contraction state of myofibrils during global ischemia and after reperfusion following different forms of cardiac arrest. Correlation with metabolic parameters in the canine heart. 799 68

We have evaluated the influence of tumour temperature on the kinetics and extent of tumour cell death following induction of ischemia. Induction of ischemia in SCCVII tumours implanted subcutaneously in the back of syngeneic C3H mice results in a rapid cooling of the tumour from a resting value of 35.2 degrees C, towards ambient temperature. In the SCCVII tumour no significant cell kill is detected in the first hour of ischemia. At longer times cell kill was detected and a survival level of 2 x 10(-2) was attained after 6 h of ischemia. However, if the tumours were maintained at a temperature of 37 degrees C following induction of ischemia a more rapid and dramatic reduction in cell survival is observed with a survival level of approximately 10(-5) being attained after 4 h of ischemia. Qualitatively similar results are obtained using the Lewis lung tumour implanted in C57BL mice. Similar rapid cooling following occlusion of the blood supply is observed in the C3H/TIF tumour implanted in the foot. For the C3H/TIF induction of ischemia for up to 6 h resulted in no significant growth delay provided the tumours were kept at room temperature. However, if the tumours were maintained at a temperature of 37 degrees C during the ischemic insult significant growth delay was observed for all clamping times exceeding 1 h. These results show the importance of tumour temperature on the kinetics and extent of tumour cell kill during ischemia. This finding has particular relevance for studies in which agents known to reduce tumour blood flow are used in animals bearing superficially located tumours.
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PMID:The influence of tumour temperature on ischemia-induced cell death: potential implications for the evaluation of vascular mediated therapies. 815 81

The effects of cholecystokinin (CCK) receptor agonists and antagonists on hypoxia/hypoglycemia (ischemia)-induced decrease in CA1 presynaptic fiber spikes elicited by the stimulation of Schaffer collaterals were investigated using rat hippocampal slices. Treatment with the CCKB receptor agonist CCK tetrapeptide (CCK4, 0.01-10 microM) exacerbated the ischemia-induced decrease in the CA1 presynaptic potential in a concentration-dependent manner. Whereas, treatment with the CCKB receptor antagonist [(3R(+)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4- benzodiazepin-3-yl)-N1-(3-methylphenyl)-urea] (L365260), and not with CCKA receptor antagonist [(3S(-)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4- benzodiazepin-3-yl)-1H-indole-2-carboxamide] (L364718), produced a concentration-dependent attenuation of the ischemia-induced decrease. The magnitude of recovery of the CA1 field potentials in L365260-treated groups at 10 and 100 nM was 34% and 45%, respectively. The neuroprotective effect of L365260 (0.01 and 0.1 microM) was completely blocked by co-treatment with CCK4 (0.1 microM), a concentration that did not affect the decreased presynaptic potential induced by ischemia. These results demonstrated that the stimulation of the CCKB receptor played a detrimental role in the development of ischemic damage, whereas the blockade of CCKB receptors played a neuroprotective role in ischemic damage, suggesting a facilitatory role of CCK receptor-operated function in ischemia-induced neuronal deficits.
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PMID:Neuroprotective effect of cholecystokininB receptor antagonist on ischemia-induced decrease in CA1 presynaptic fiber spikes in rat hippocampal slices. 817 34

The efficiency of a preservation medium, histidine-buffered lactobionate solution (HBLS), was determined by measuring post-ischemic recoveries of ATP and intracellular pH under Krebs-Henseleit buffer (KHB) perfusion. We used NMR spectroscopy to study the effect of 24-h cold ischemia, followed by 4 degrees C then 37 degrees C reperfusion on the isolated rat liver. Three media were compared: University of Wisconsin solution (UW-lactobionate); Bretschneider's solution (HTK); HBLS and HBLS supplemented with 2 mM Gly and 2 mM Cys (HBLSg2) or with 10 mM Gly and 2 mM Cys (HBLSg10). All values were compared to control values measured during pre-ischemic cold perfusion with KHB (ATP = 8.60 +/- 0.6 mumol/g of dry weigh and pH(in) = 7.41 +/- 0.05). The main result from 31P NMR data concerned ATP recovery during cold reperfusion, which was significantly higher in the HBLS group (112 +/- 10%) as compared to the UW and HTK groups (around 66%). The presence of glycine decreased ATP recovery (88 +/- 8% in HBLSg2, 79 +/- 15% in HBLSg10). Higher values of recovered pHin were observed in livers stored in histidine buffered solutions (around 7.30) as compared to UW (around 7.20); histidine was by 13C NMR proved to accumulate in the liver cells, thus ensuring a good buffering capacity. The thermal transition induced a decrease in both ATP level and pHin in all groups. This might be the result of a stimulation of the carbohydrate metabolism (as demonstrated by 13C NMR) especially when glycine was present in the storage solution.
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PMID:31P NMR studies of rat liver cold preservation with histidine-buffered lactobionate solution. 830 4

This study investigates how far mitochondrial swelling in the ischemic heart is influenced by factors pertaining to anaerobic energy turnover. Canine hearts were arrested by aortic cross clamping or cardioplegically with St. Thomas or HTK solution and incubated at 25 degrees C in the solution used for cardiac arrest. Samples of the left ventricle were taken at the end of cardiac arrest and during ischemia for structural evaluation and biochemical analysis. The extracellular pH in the interventricular septum was measured. Mitochondrial swelling was determined with the surface to volume ratio, a parameter independent of the reference space. Values obtained for different swelling were related to defined metabolite concentrations and pHe values to establish possible correlations between structural and biochemical parameters in the ischemic heart. At the onset of ischemia and during the breakdown of creatine phosphate (CP) to 3 mumol/g wet weight mitochondrial volume depends on the method of cardiac arrest and does not increase significantly in any of the three groups. The degree of mitochondrial swelling after depletion of CP correlates with the decline in ATP independent of the form of cardiac arrest. Characteristic values of the surface to volume ratio ascertained at different times of ischemia for all groups correspond to determined ATP concentrations. Acid pHe values seem to intensify mitochondrial swelling. With increased lactate concentrations mitochondria swell, but first initially the degree of swelling differs significantly in the forms of cardiac arrest investigated. Thus, the surface to volume ratio is a powerful and valid ultrastructural parameter, which makes correlations between mitochondrial structure and metabolism possible and furthermore indicates a strong correlation between mitochondrial swelling and ATP-concentration in the ischemic heart.
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PMID:Close correlations between mitochondrial swelling and ATP-content in the ischemic canine myocardium. A combined morphometric and biochemical study. 833 76


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