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)

The evolution of experimental myocardial infarction in the Rat with or without revascularization has been studied histochemically and histoenzymatically in 56 animals sacrified after 1, 6, 12, 24, 48 hrs and 7 days. Following permanent ischemis (14 animals), there appeared an extended transversal infarction marked by the complete disappearance of all phosphorylase activity (P-ase) after the first hour. During the first 6 hrs, changes appeared in succinodeshydrogenase (SHD) and cytochrome oxydase (Cyt-Ox). Glucose-6-phosphodeshydrogenase (G6PDH) presisted until lysis of the necrotic focus. It was possible to define a perinecrotic marginal area in which Pase activity is absent and SDH is granular "G3 in nature, characterized by continuous remodeling in the first 48 hrs. Following temporary ischemia (42 animals) the evolution was marked by rapid tissue reactions and early regression of the marginal zones. After 48 hrs and 7 days of survival, the planimetric evaluation of the infarcted area shows a definite reduction in the size of the infarctus in 50% of cases following removal of the ligature after 6 hrs, and in 66% of cases following removal of the ligature after 1 hr. It would appear probable that the revitalization of certain myocardial areas may extend from the marginal zones as is suggested by the reappearance in these zones several hrs after revascularization of P-ase and SDH activity. On the other hand, it is also true that the early restoration of blood flow does not always prevent the occurrence of an extended infarction. Certain recent observations have shown microcirculatory changes which are secondary to anoxia and should be studied further.
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PMID:[Histochemical and histoenzymatic study of experimental myocardial infarction in the rat by temporary and permanent ligation of the left coronary artery (author's transl)]. 16 14

Fowler-Stephens orchiopexy is the most common method of treating high-positioned undescended testes. Its success rate has been reported to be as high as 50-70% based on palpation or in a few circumstances on biopsy. Although it is convenient to evaluate testicular function by palpation and/or biopsy, this method is very subjective and is not scientific enough. To determine testicular function more precisely and objectively, we performed the Fowler-Stephens orchiopexy on Sprague-Dawley rats and observed the morphological and biochemical changes, including assays of LDH, SDH and the testosterone level. In our morphological study, with the use of Fowler-Stephens orchiopexy, only 17% (3/18) of the rat tests could be salvaged. The others revealed either necrosis or fibrosis. Testicular LDH, checked at the 4th postoperative week, revealed 0.62 +/- 0.04 U/mg which was statistically different (p less than 0.05) from that of the control group and the hemicastrated group (0.77 +/- 0.05 U/mg and 0.76 +/- 0.07 U/mg, respectively). The SDH obtained from the testes also revealed significant differences between the study group and the control and hemicastrated groups. Values obtained were 2.67 +/- 0.15 mU/mg, 3.77 +/- 0.4 mU/mg and 3.77 +/- 0.33 mU/mg, respectively (p less than 0.05). Using electrophoresis, 3 out of 18 rats had typical X bands, which is the classical picture of a normal mature testis. In contrast, the others showed faint X bands at the 2nd postoperative week, which subsequently faded thereafter. During testicular ischemia, the Leydig cells are more resistant than the Sertoli cells and the germinal cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Testicular morphological and biochemical changes after Fowler-Stephens orchiopexy in rats]. 198 47

Normothermic, 3 min lasting perfusion of isolated rat heart with Krebs-Ringer-Henseleit solution in which Ca was replaced by EDTA, followed by successive perfusion of Ca2+ containing medium resulted in structural and metabolic derangement of myocardial cells; this could be demonstrated electronmicroscopically and histochemically. Unlike in ischemia, Ca paradox left the enzymes LDH, SDH, beta-HBDH as well as alpha-glucan phosphorylase and ATP-ases better preserved in the subendocardial layer of the left ventricle. Ultrastructural analysis of this phenomenon showed good correlations with the histochemical findings. A large portion of cardiomyocytes in the subendocardial layer showed only slight changes. On the other hand, myocytes in the subepicardial layer were severely injured and all characteristics of the calcium paradox were present including hypercontraction bands with fusion of myofilaments, extrusion and accumulation of oedematous mitochondria containing electron dense material intracristally, sarcolemmal ruptures, separation of intercalated discs etc. The better preservation of the subendocardial region in experiments with calcium paradox could be explained by inadequate perfusion of this layer with Ca2+ free medium due to transmural anatomical inhomogeneity of the capillary supply, resulting in a better protection of these myocytes from Ca paradox. The heterogeneity in transmural distribution of injuries is a multifactorial phenomenon. In addition to factors such as intramural pressure gradient, transmural pressure, enddiastolic intraventricular pressure etc., the most important factors in both types of injuries should be regarded the amount of vascular supply, blood flow and perfusate volume.
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PMID:Differences in transmural distribution of cardiomyocyte injury Ca paradox versus postischemic reperfusion phenomenon. 249 17

Dynamics of changes in the myocardium of rabbits subjected to food hypercholesterolemia lasting from 6 to 16 weeks was investigated. An intensification of coronary atheromatosis was proportional to the duration of the high-cholesterol diet. There were observed focal and growing in time damages of cardiomyocytes. They were sharply outlined in atherosclerotically changed coronary arteries. The following morphological and histochemical changes have been observed: increased acidophilia and fuchsinophilia in the single and grouped muscle fibres, foci of infiltrations by mononuclear cells, contraction bands, and outlines of myocardial fibres, separation of myofibrils, granular disintegration of cardiomyocytes, healed infarcts, depletion and excessive accumulation of glycogen in muscle fibres, presence of neutral fats, cholesterol and its esters in atheromatous plaques of coronary arteries, presence of neutral fats in some cardiomyocytes: focal acid phosphates, loss of activity of Mg- and Ca-dependent ATPases and SDH: oedema of mitochondria with disorganization of cristae, disorganisation of fibres and lysis of myofilaments, margination of chromatin in cardiomyocyte nuclei, increased number of lysosomes, intensified symptoms of egzocytosis, widening of channels of sarcoplasmatic reticulum, oedema of endothelium of capillary vessels and increased number of the collagenous fibres in the interstitial space. The results of histological, histochemical and microscopic-electron investigations correlated with each other. It may be considered that the observed damages of cardiomyocytes precede myocardial infarction and result from progressive and increasing ischemia, hypoxia and accumulation of fat substances and cholesterol and its esters in intima of coronary arterioles as well as in cardiomyocytes.
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PMID:[Dynamics of lesions to the myocardium in experimental hyper- cholesterolemia]. 281 56

The initiating factor in ARDS is a matter of controversy. Some investigators relate ARDS development to diffuse pulmonary microemboli after stress ranging from sepsis to non-thoracic and thoracic trauma. Others indicate hyperoxic exposure as the causative agent. This investigation looked for a common factor in ischemia and hyperoxic exposure in lung which could cause the genesis of ARDS. Studies of oxidative phosphorylation, succinate dehydrogenase activity and ATP level were performed on ischemic and 100% O2 exposed lung. Results in both showed decreased respiration rate below the basal rate, decreased SDH activity, followed by marked decrease in ATP levels in pulmonary tissue. Decrease in respiration (ATP production) capacity and ATP levels in ischemic lung were such that normal cell functions could not be sustained if returned to normal circulation. Hyperbaric O2 therapy would subsequently decrease energy metabolism in regions of normal circulation and in previously ischemic regions.
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PMID:A common denominator in the etiology of adult respiratory distress syndrome. 743 54

The study was performed on rats divided into 9 groups. Groups 1-3 served as controls. In groups 4 and 5 rat livers were subjected to 90-min ischemia followed by 12- or 24-hour reperfusion. In groups 6 and 7 rats were injected with intraperitoneal chlorfenvinphos (2 mg/kg b.w.) and sacrificed after 12 or 24 hours. In groups 8 and 9 rat livers were subjected to 90-min ischemia, 12- or 24-hour reperfusion and then rats were injected with chlorfenvinphos (2 mg/kg b.w.). Liver sections were evaluated morphologically, histochemically (SDH, LDH, G6Pase, glycogen, Mg2+ ATPase and AcP). The microsomal fraction of the liver was evaluated for cytochrome P450 content and NADPH-cytochrome P-450 reductase activity. It has been found that liver ischemia and reperfusion result in extensive necrosis, enzymatic disturbances, particularly in acinar zone 3. Ischemia as well as reperfusion decrease the cytochrome P450 content of hepatocytic microsomes and the activity of NADPH-cytochrome P-450 reductase. Intraperitoneal injection of chlorfenvinphos during ischemia and reperfusion dramatically intensifies damage to the liver, although chlorfenvinphos alone produces only mild nonspecific effects on the morphological and enzymatic structure of the liver.
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PMID:Effect of chlorfenvinphos on rat liver subjected to ischemia and reperfusion. 947 88

During complete ischemia we assessed myocardial utilization of the small amount of oxygen available. We also determined whether blood cardioplegia has any advantage over crystalloid cardioplegia in this setting. Patients with preserved left ventricular myocardial function and without anterolateral wall infarct or aneurysm were included to the study. Intermittent cold blood and crystalloid cardioplegia were used in 10 patients (group BC) and 9 patients (group CC), respectively. From myocardial biopsies, obtained before and after ischemia, complete electron transport system (ETS) enzyme activities (NDH, SDH, NCCR, SCCR, and COX) and lactate content were analyzed. Biochemical and hemodynamic analyses also were done. Myocardial and blood temperatures were monitored. Ischemic time was longer in group CC (p < 0.05). There were no important differences in biochemical and hemodynamic variables between the two groups. In addition, there was no difference in NDH and SDH activities as well as COX/SCCR and COX/RS-NCCR ratios between the two groups before and after ischemia. After Ischemia, RS-NCCR in group CC and SCCR and COX activities in both groups were lower than the control. For all enzymes, activity change ratios were not different between groups. Myocardial lactate content was increased in both groups after ischemia. However, the increase in group BC was less (p < 0.01). Based on our findings, we believe that the superiority of blood cardioplegia over crystalloid cardioplegia does not depend on oxygen content, but on other factors such as buffering and free oxygen radical scavenger effects among others. However, with the warm and continuous blood cardioplegia technique, oxygen content might be more important.
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PMID:Effect of partial oxygen supply on mitochondrial electron transport system during complete cardiac ischemia. 1102 67

Ischemia/reperfusion of organs and cells induces apoptosis through a complicated series of changes in mitochondria, mainly the generation of oxygen free radicals, permeability transitions, calcium translocations, and release of apoptogenic factors such as cytochrome c and Bcl-2 family members. The liberation of these factors occurs very early after reoxygenation and it has been assumed that it takes place without any structural alteration of the mitochondrial membranes. The aim of this study was to detect ultrastructural changes of mitochondria in the initial stages of reperfusion at the time when Bcl-2 and succinic dehydrogenase, located in the outer and inner membranes, respectively, were released. Ischemia/reperfusion was produced in adult rats by clamping one renal artery for 60 min and reoxygenating for 60, 120, 180, and 240 min. A model of chemical hypoxia with intra-arterial 50 mM sodium azide served as comparison, allowing free blood flow for 30, 60, 120 and 180 min. Light and electron microscopy, immunostaining for Bcl-2, and enzyme histochemistry for succinic dehydrogenase were performed. Our results showed mitochondrial swelling, rupture of inner and outer membranes, and leakage of mitochondrial matrix into the cytoplasm in ischemia after 120 min of reperfusion. Bcl-2 immunoreactivity and focal lowering of SDH reactivity were also noted and became more pronounced at the same time that the mitochondrial ultrastructure demonstrated more evident changes including rupture of the inner and outer membranes. Our studies seem to indicate that in early ischemia-reperfusion and in chemical hypoxia-induced apoptosis, the earliest ultrastructural changes take place in mitochondria and that swelling and rupture of mitochondrial membranes occur in parallel with the loss of Bcl-2 and SDH activity.
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PMID:Morphologic, biochemical and molecular mitochondrial changes during reperfusion phase following brief renal ischemia. 1119 33

Energetic function impairment is one of the main reasons of liver ischemia-reperfusion injury. The aim of the study was to estimate the influence of temporary rat liver ischemia on energetic functions of the organ in the early and late reperfusion period and to answer the question whether the reduction of destructive factors release in sinusoids in the early phase of reperfusion can prevent liver energetic function impairment. To perform the experiment 55 Wistar rats divided into 5 experimental groups were used. 60 min. partial ischemia of the liver was applied, with 30 min, 72 h and 5 days reperfusion period. Suppression of KC was performed by intravenous administration of GdCl3. In the group of animals subjected to liver ischemia a considerable decrease of reaction to SDH and LDH activity was observed in the reperfusion period. In animals with KC suppression the loss of reaction to SDH intensity in zones I of acini was insignificant and the decrease of reaction to LDH was more orderly and proceeded in a more regular manner. The value of AKBR fell significantly after 30 min. of reperfusion in both groups of animals subjected to ischemia, while the serum level of AspAT and LDH increased rapidly. Temporary ischemia of the rat liver induces a decrease of the organ energetic functions in the early and the reperfusion period. The elimination of Kupffer cell activity in the early reperfusion phase does not prevent liver energetic functions impairment, but reduces the time in which they return to initial values in remote observation.
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PMID:Influence of temporary ischemia on energetic functions of rat liver in early and late reperfusion period. 1138 14

Arterial ketone index (AKBR) which is the ratio of acetoacetic acid to 3-hydroxybutyric acid in the arterial blood, is believed to reflect the mitochondrial reduction potential of hepatocytes and general energy state of the liver. In the presented paper we challenged this hypothesis by analysing the correlation between AKBR and the results of typical liver blood tests (AspAT, AlAT, LDH, CRP) and biotransforming potential of the liver (cytochromes P450, b5 and their corresponding NADPH and NADH reductases) in the model of ischemia-reperfusion injury of rat liver. The results were compared with histochemical analysis of distribution and activity of SDH, LDH and G-6-Pase, the key marker enzymes of the liver. We have shown that, except in the case of acute phase protein (CRP), a decrease in AKBR correlated well with the increase of the level of indicator enzymes in serum. Histochemical analysis also confirmed that AKBR correlates with the degree of damage to hepatocytes during early stage of reperfusion after 60 min of liver ischemia. In the Spearman test, AKBR was significantly correlated with the changes in cytochrome P450 content and its NADPH reductase activity which indicates a high sensitivity of this test. We conclude that the decrease of AKBR value reflects the impairment of basic energy pathways and detoxicative capability of the liver.
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PMID:Arterial ketone index in assessing liver function and its detoxicative capability after ischemia-reperfusion injury. 1199 3


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