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)

In recent years the hypothesis that the number of villus cells regulates crypt cell proliferation in the epithelium of the small intestine has been brought forward by a number of investigators. To test this hypothesis, the villus cell population was reduced by clamping the superior mesenteric artery and vein in rats for 1 hr and the effects on the intestinal epithelium were studied during the first 24 hr. It was shown that temporary interruption of the blood flow to the small intestine led to a marked decrease in the number of functional villus cells within 2 hr; preferentially, cells from the upper part of the villus were lost and the number of crypt cells was not affected. This reduction in the number of villus cells led to an increase in the percentage of labeled crypt cells after pulse labeling with [3H]thymidine, and an expansion of the proliferative cell compartment in the crypt. After a peak of proliferative activity at 16 hr, the investigated crypt cell kinetic parameters approached control values after 24 hr, as did the number of villus cells. The enzyme activities of nonspecific esterase and neutral alpha-glucosidase showed marked decreases in isolated crypt and villus cell compartments as crypt cell proliferation increased. These data support the view that the feedback control of crypt cell proliferation by the functional villus cells, and confirm earlier data on the influence of changing cell kinetics on crypt cell maturation. Additional data which were obtained after creating temporary ischemia in part of the small intestine support the hypothesis of a feedback control of crypt cell proliferation by the functional villus cells, and confirm earlier data on the influence of changing cell kinetics on crypt cell maturation. Additional data which were obtained after creating temporary ischemia in part of the small intestine support the view that the feedback control of proliferation by the villus cells is a local control mechanism.
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PMID:The effect of ischemic villus cell damage on crypt cell proliferation in the small intestine: evidence for a feedback control mechanism. 96 70

We determined the relationship between cardiac angiotensin-converting enzyme (ACE) inhibition and anti-ischemic efficacy of several structurally different ACE inhibitors or their prodrug esters perfused through the isolated rat heart. Seven ACE inhibitors inhibited cardiac ACE to varying degrees due to differences in uptake during perfusion through nonischemic rat hearts. Zofenopril-sulfhydryl and fosinoprilic acid were the most effective of the free inhibitors. Among the prodrugs, zofenopril and S-benzoylcaptopril, hydrolyzed rapidly by cardiac esterase, were more effective than their component ACE-inhibitors, whereas fosinopril, ramipril and enalapril were poorly active. For studies in ischemic rat hearts, vehicle or drug treatment was initiated 10 min before a 25-min period of global ischemia and during a 30-min reperfusion period. Of five unesterified ACE inhibitors studied for anti-ischemic activity, only captopril and zofenopril-sulfhydryl were found to improve postischemic contractile function and reduce cell death in the isolated rat hearts. Fosinoprilic acid, ramiprilat and enalaprilat were not cardioprotective at high perfusion concentrations, despite the fact that nearly complete inhibition of cardiac ACE was achieved with all of the compounds studied. The S-benzoyl prodrugs of zofenopril-sulfhydryl and captopril were at least as potent as their component ACE inhibitors in reducing ischemic-reperfusion damage in the same model. Neither zofenopril nor captopril, however, had any effect on coronary flow before or after ischemia. Thus, it appears that the cardioprotective effects of zofenopril and captopril are independent of cardiac ACE inhibition or, at least, that ACE inhibition alone is not sufficient. Both captopril and zofenopril are sulfhydryl-containing compounds whereas the inactive compounds are not; and, thus, this group appears to be important in mediating their cardioprotective actions.
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PMID:Effects of different angiotensin-converting enzyme (ACE) inhibitors on ischemic isolated rat hearts: relationship between cardiac ACE inhibition and cardioprotection. 164 29

A stimulated autotransplantation of the rectus femoris muscle in the rabbit was performed by clamping of the blood vessels for 2 h and cutting and suturing of the nerve. Four months after this operation, isometric contractions of the reinnervated muscle were recorded. Comparing controls and postoperation cases, the recovered strength measured about 65%. Due to operation stress, the epinephrine content in plasma was about 420 pg/ml; in plasma of the ischemic muscle it was enhanced to more than 600 pg/ml. During or immediately after ischemia, conjugated epinephrine is assumed to be converted to the free hormone. In systemic blood additionally about 200 pg/ml epinephrine were identified as glucuronides. The activity of adenylate cyclase increased, while the acetylcholine esterase decreased to one-half after nerve cutting.
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PMID:Free epinephrine in the ischemic blood of muscle transplants in the rabbit. 183 55

Neurons in the hippocampus and striatum are vulnerable to the ischemic insult. In the present study we focused on the vulnerability of acetylcholine (ACh)-containing neurons in the striatum. To determine the change of ACh content in the striatum, we employed a simple sensitive brain microdialysis method with high performance liquid chromatography electrochemical detection. Morphological change of cholinergic neurons was studied by ACh-esterase staining during ischemic insult. After bilateral carotid artery occlusion, local cerebral flow decreased less than 5 ml/min/100 g in the striatum. Ach content in dialysate for 20 min after the occlusion was elevated to 135% of the control. ACh content decreased to 15% of the control 2hs after the ischemia. Density of Cholinergic fibers and cell bodies was reduced 10 min after the ischemia and further decreased 20 min after the occlusion. Our study suggests that the transient elevation of ACh content was probably due to diffusion of ACh from destruction cholinergic terminals after the ischemic insult. The increase of ACh immediately after arterial occlusion may affect severity of ischemic damage in the brain by its excitatory effect.
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PMID:[Dynamics of extracellular acetylcholine of the gerbil striatum during cerebral ischemia monitored by intracerebral microdialysis]. 191 Sep 31

During early postischemic reperfusion, the vulnerable brain regions (e.g., hippocampal CA1) show a relatively high deoxyglucose accumulation. To investigate if this accumulation is a marker for the later-occurring regional cell death and to determine its cellular localization, we studied the glucose metabolism in the CA1 region post ischemia after removal of its pre- or postsynaptic components. A 20-min period of cerebral ischemia was used for selective removal of the main postsynaptic component in CA1 pyramidal cells, and a bilateral intraventricular injection of kainic acid for removal of the majority of presynaptic axon terminals in this region (and postsynaptic terminals and cell bodies in CA3). The glucose metabolism was studied in these two lesion types and in sham-operated animals before and after a period of ischemia. There was a 60% reduction of metabolism after ischemia in the nonvulnerable regions, whereas CA1 and sometimes CA3 showed a columnar pattern of high and low metabolism. CA1 and CA3 devoid of the postsynaptic component showed increased postischemic metabolism. The latter was due to the presence of macrophages, as demonstrated by an enzyme histochemical stain for nonspecific esterase. CA1 with no presynaptic component showed a postischemic depression of the glucose metabolism similar to the rest of the brain. It is suggested that the level of the postischemic glucose metabolism in the ischemia-vulnerable regions is determined by the presence of both synaptic components. The presence of macrophages in a region gives rise to apparently normal values of glucose metabolism.
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PMID:Postischemic glucose metabolism is modified in the hippocampal CA1 region depleted of excitatory input or pyramidal cells. 230 41

Using experimental cerebral ischemia induced in rats with 4-vessel occlusion, the effects of 2-hour ischemia (ligation group) and 30-minute ischemia followed by 72-hour reperfusion (reperfusion group) on cholinergic system (ChS) was investigated with acetylcholine receptor (AChR), choline acetyltransferase (CAT) and acetylcholine esterase (AChE) as indicators of ChS in seven sections of the brain. The activity of CAT was reduced just after ischemia and tended to decrease further after reperfusion. CAT is known as the specific enzyme of cholinergic neuron (ChN), so the reduction of activity of CAT probably means that the ischemic change of ChN was irreversible after 30-minute occlusion. The activity of AChE was also reduced just after ischemia but tended to recover after reperfusion. AChE is not specific in ChN, so the activity of this enzyme may also reflect activity of postsynaptic neuron. The recovery tendency of AChE, therefore, may have the meaning that the ischemic change of the postsynaptic neuron was reversible. The number of AChR was found to have the tendency to increase after ischemia in more sections of reperfusion group compared with ligation group, which is supposed to show that compensatory reactive increase of the receptor may be retained after reperfusion.
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PMID:[The effects of ischemia and postischemic reperfusion on the brain cholinergic system of the rat]. 273 67

Changes in the maximal rate of some cerebral enzymatic activities related to 400ene transduction and neurotransmission (lactate dehydrogenase; citrate synthase and malate dehydrogenase; total NADH-cytochrome c reductase and cytochrome oxidase; glutamate dehydrogenase; acetylcholine esterase) were assayed both in the crude or purified mitochondrial fraction and in the crude synaptosomal fraction from rat whole brain or cerebral cortex. The evaluations were performed in rats before and after a postdecapitative normothermic ischemia of 5, 10, 20 and 40 min duration. Modification observed in some of these activities wer discussed for comparison with other experimental results from different researchers. At present no definite conclusions can be drawn, but certainly the observed modifications in activity of enzymes are not passive but expression of deranged metabolism of ischemic neurons.
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PMID:Brain enzymes and ischemia. 626 30

The effects of complete ischemia and of in vivo pharmacological treatment with trimetazidine were studied on some enzymatic activities related to energy transduction: lactate dehydrogenase for anaerobic glycolysis; citrate synthase and malate dehydrogenase for the Krebs' cycle; total NADH-cytochrome c reductase and cytochrome oxidase for the electron transport chain; glutamate dehydrogenase for amino acid metabolism and acetylcholine esterase for acetylcholine metabolism. These enzymatic activities were evaluated in brains of 10-day-old rats, at three different subcellular levels: homogenate in toto, purified mitochondrial fraction, crude, synaptosomal fraction. Complete normothermic post-decapitative ischemia of 30 min duration increased the activity of cytochrome oxidase in the homogenate in toto and increased the activities of citrate synthase and malate dehydrogenase in the purified mitochondrial fraction, the activities of the enzymes evaluated in the crude synaptosomal fraction being unaffected. The i.p. treatment with trimetazidine (at the dose level of 50 mg . kg-1) was without any significant effect on the tested enzymatic activities.
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PMID:Effects of ischemia and pharmacological treatment on subcellular fractions from neonatal rat brain. 628 22

The maximal rate of some cerebral enzymatic activities related to energy transduction (hexokinase; phosphofructokinase; lactate dehydrogenase; citrate synthase; malate dehydrogenase; total NADH-cytochrome c reductase; cytochrome oxidase), amino acid metabolism (glutamate decarboxylase; glutamate dehydrogenase) and cholinergic metabolism (acetylcholine esterase) were tested in the cerebral cortex and in sub-cortical area of rats. The evaluations were performed both in the homogenate in toto and in the crude mitochondrial fraction, before and after a postdecapitative normothermic ischemia of 5, 10, 20, and 40 min duration. The results are discussed also with respect to the pharmacological pretreatment with two biological substances which may modulate amino acid (L-alanine) and phospholipid metabolism (CDP-choline). The analysis of the present data suggests the occurrence in brain tissue of a variety of interrelated factors implicated in the ischemia-induced changes of the maximal rate of the enzymatic activities related to the energy transduction. These include: (a) rearrangement of the enzymatic activities because of the changed metabolic and chemico-physical condition; (b) decrease in the activity of enzymes related to the electron transfer chain and glycolysis; (c) changes in enzymes related to mitochondrial membranes. The effects of in vivo administration of alanine or CDP-choline, even if significant, are not consistent throughout the time period studied.
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PMID:Changes induced by ischemia on some cerebral enzymatic activities related to energy transduction and amino acid metabolism. 685 30

To examine the role of neutrophils, their presence and the degree of infiltration, as important determinants of ischemia and reperfusion injury of the liver, male Sprague-Dawley rats were subjected to 60 and 90 min of total-liver ischemia. The presence of neutrophils, assessed by the measurement of liver tissue myeloperoxidase (MPO), and the degree of neutrophil liver infiltration, determined by the naphthol AS-D chloroacetate esterase technique, correlated well with animal survival and response to FK506 and cyclosporine administration. Lipid peroxidation, measured by the malondialdehyde (MDA) test in liver tissue, was another factor closely linked with liver function and survival. Pretreatment with FK506 (0.3 mg/kg) and CsA (5 mg/kg) was given at 4 hr and 1 hr before ischemia and at the time of reperfusion. Control ischemic animals showed increased neutrophil liver infiltration, high MPO and MDA liver levels, and diminished overall survival. FK506 and CsA-treated animals had better survival and diminished neutrophil liver infiltration, as well as MPO and MDA levels. The mechanism by which FK506 and CsA protected the animals from severe liver ischemic injury is unknown. Our data indicated that the presence and the degree of infiltration of neutrophils were important components of liver ischemia/reperfusion injury in the rat. So it is possible that one of the fundamental effects of the FK506 and CsA might be through the inhibition of the presence and infiltration of neutrophils in liver tissue.
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PMID:Neutrophil infiltration as an important factor in liver ischemia and reperfusion injury. Modulating effects of FK506 and cyclosporine. 768 32


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