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)

Changes in tissue oxygenation of forearm muscles were measured by near infrared (NIR) spectrophotometry in 10 healthy adults during tourniquet ischemia and venous outflow restriction. Muscle O2 stores were depleted rapidly by forearm ischemia manifest by a progressive decrease in tissue oxyhemoglobin and oxymyoglobin over 4-5 min. Muscle ischemia significantly decreased the oxidation level of cytochrome aa3, to below resting base line after only 1.5 min, and the enzyme became fully reduced after 6.5 min. After 8 min of ischemia, tourniquet release was accompanied by a transient increase in muscle blood volume due to influx of oxyhemoglobin. The cytochrome aa3 oxidation level increased above resting base line within 1 min after tourniquet release. Transcutaneous PO2 measurements recorded simultaneously from the same forearm correlated poorly with the kinetics of O2 availability and cytochrome oxidation in the underlying muscle tissue; this was not unexpected because overlying skin did not contribute significantly to NIR muscle signals. Venous outflow restriction without inflow obstruction increased muscle deoxyhemoglobin and tissue blood volume but did not change muscle O2 stores or cytochrome aa3 oxidation level. The ability of the NIR technique to detect dynamic trends in tissue oxygenation reveals that muscle O2 is rapidly consumed during tourniquet ischemia and rapidly restored by hyperemic responses after brief ischemia.
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PMID:Near infrared monitoring of human skeletal muscle oxygenation during forearm ischemia. 340 28

The influence of malate and cytochrome c on fatty acid oxidation under control and ischemic conditions was investigated. In the medium without malate, cytochrome did not make fatty acid oxidation decreased during ischemia return to normal. Oxidation in the media containing malate and cytochrome did not differ from control only when it was measured after preliminary oxidation of endogenous substrates. The ratio of palmitoyl-CoA and palmitoyl carnitine to the respiration rates at state 3 was unchanged at 60 min ischemia. Apparently, no changes in carnitine acyltransferase playing a role in oxidation of palmitoyl-CoA took place. Thus, the decrease of fatty acid oxidation at early periods of ischemia is largely caused by a reduction in the content of cytochrome c and intermediates of Krebs cycle in the mitochondria.
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PMID:[Reasons for disorders of fatty acid oxidation in isolated heart mitochondria during ischemia]. 398 34

Spinal cord ischemia was produced by an occlusion of the thoracic descending aorta on experimental cats for the periods of 3, 5, 10, and 15 minutes. The reduction/oxidation (redox) ratio of cytochrome a,a3 was measured in vivo by reflectance spectrophotometry, simultaneously with the measurement of the following: blood pressure in the aorta distal to the occlusion; relative blood volume in the cord; oxygen tension in cord tissue; and cord potential in response to dorsal root stimulation. During aortic occlusion, the maximum increase in the redox ratio was reached somewhat more slowly than the maximum decrease in blood pressure, blood volume, and oxygen tension. Interneuron potentials began to decrease as the redox level increased, and completely disappeared soon after the redox ratio increased, and completely disappeared soon after the redox ratio increased maximally. During ischemia, therefore, oxygen consumption in the mitochondria was slightly lower than the decrease in oxygen tension; impairment of ADP phosphorylation, and accordingly that of ion pump, occurs simultaneously with the increase in the redox ratio. Recovery of the redox ratio after completion of aortic occlusion was also slightly slower than the recovery of blood pressure, blood volume, and oxygen tension. Complete recovery of interneuron potentials was much more delayed than that of the redox ratio; after 15-minute ischemia, uncoupling of ADP phosphorylation was noted. It can be concluded that the spinal cord function and metabolism are severely impaired after 15-minute occlusion.
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PMID:Oxidative metabolism during and following ischemia of cat spinal cord. 611 53

A previously validated small mammal trauma model, hind-limb ischemia secondary to infrarenal aortic ligation in the rat, was utilized to further investigate the effects of traumatic injury on the hepatic cytochromes P-450. In vitro drug metabolism studies with hexobarbital and zoxazolamine as substrates confirmed the post-traumatic depression of the cytochrome P-450-catalyzed oxidation of these drugs which was suggested by previous in vivo pharmacokinetic studies. Enzyme kinetic studies revealed diminished Vmax values with no change in Km, a finding which would seem to concur with the previously demonstrated decrease in hepatic cytochrome P-450 content after model trauma. Moreover, a battery of in vitro microsomal monooxygenase assays demonstrated that model trauma exerted a differential effect on various hepatic cytochrome P-450 isoenzymes. This phenomenon was confirmed by anion-exchange HPLC of solubilized hepatic microsomal hemoproteins. One of the most interesting aspects of this selective effect on cytochrome P-450 subtypes was the relative induction of cytochrome P-448 content and activity, in contrast to the variable decrease seen with cytochrome P-450 activities. The potential in vivo sequelae of this differential influence were suggested by changes observed in the urinary metabolic profile of antipyrine after model trauma.
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PMID:Effects of model traumatic injury on hepatic drug metabolism in the rat. III. Differential responses of cytochrome P-450 subpopulations. 614 9

To assess the residual effects of transient cerebral ischemia on mitochondrial oxidative metabolic function, changes in the reduction/oxidation state of cytochrome a,a3 and relative local blood volume were measured in situ from the exposed cerebral surface of rat brain before and after 10 minutes of carotid artery ligation. During the ischemic interval, cytochrome a,a3 became reduced and electrocortical activity was abolished. During the first 20 minutes of reperfusion cytochrome a,a3 was hyperoxidized beyond baseline with eventual recovery to the original steady state. Electrocortical activity returned more slowly. Increased energy demand induced by electrical stimulation of the cortex produced transient oxidation of cytochrome a,a3. The amplitude of this oxidative response was decreased during the first 30 minutes of reperfusion. During the first 2 hours of reperfusion the time required for re-reduction of the oxidative response was lengthened despite the recovery of baseline mitochondrial redox state. These data demonstrate residual metabolic dysfunction after transient ischemia not apparent under "resting" conditions but evident when the system is required to perform additional "work." We speculate this metabolic dysfunction could be due to relative substrate limitation.
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PMID:Disparate recovery of resting and stimulated oxidative metabolism following transient ischemia. 627 54

Cerebral blood volume, hemoglobin saturation and the cytochrome a, a3 redox state were monitored simultaneously by using three wavelengths of light in the near infrared portion of the spectrum for transillumination of the intact skull of rats. The changes in these parameters following incomplete cerebral ischemia were assessed in Wistar and Long-Evans rats submitted to carotid ligation. Another group of Wistar rats was submitted to vertebral + carotid occlusion. The experiments, performed under N2O/O2 anesthesia, showed that in all three groups carotid occlusion induced a decrease in blood volume, Hb saturation and a reduction of cyt. a, a3. However, the cytochrome redox state tended to normalize during ischemia as a consequence of higher O2 extraction from blood. The primary finding of this study was the marked hyperoxidation of cyt. a, a3 which occurred after reestablishing of the carotid blood supply, in spite of a secondary post-ischemic hypoperfusion of the brain. Although uncoupling of oxidative phosphorylation cannot be excluded the dissociation between blood supply and metabolism could well be due to ischemia-induced hypermetabolism of the central nervous tissue. In view of the marked oxidation of cyt. a, a3 during the reperfusion period as compared with the small extent of its reduction during the ischemic episode, the data also support the hypothesis that under steady state conditions in vivo, cytochrome oxidase is mainly reduced.
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PMID:Incomplete cerebral ischemia in the rat: vascular and metabolic changes as measured by infrared transillumination in vivo. 631 78

Differential cytochrome spectra and their fourth degree derivatives were recorded at 77 degrees K temperature. During myocardial ischemia (2-h autolysis), only cytochrome c content was found to be decreased in isolated mitochondria. According to these data mitochondrial state 3 respiration with succinate decreased only in a medium without cytochrome c. Before ADP addition mitochondrial respiration increased but in a medium with cytochrome c. This was followed by an increase in the respiration rate minimized by bromthymole blue, an inhibitor of dicarboxylate transport. It is inferred that these alterations seen in ischemia are linked with increased permeability of mitochondrial membranes: external for cytochrome c, and internal for inorganic ions and low-molecular compounds.
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PMID:[Changes in the quantitative composition of cytochromes and the functional activity of heart mitochondria during ischemia]. 631 61

One-hour ischemia followed by rat liver reoxygenation brings about the accumulation of endogenous products of lipid peroxidation (LPO) and deterioration of the monooxygenase system (the drop of cytochrome P-450 content, amidopyrine N-demethylase and NADP X H cytochrome reductase activity). Application of the antioxidant ionol inhibited LPO and protected the monooxygenase system from reoxygenation but not from ischemic injuries. Phenobarbital alone and combined with ionol did not protect the monooxygenase system from ischemic and reoxygenation injuries but provided the retention of high absolute indicators of the system. Ionol and its combination with phenobarbital also increased the survival of rats with ischemized liver.
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PMID:[Protective action of antioxidants and microsomal monooxygenase inducers in ischemic and reoxygenation damage to the liver]. 683 Oct 14

The purpose of this investigation was to compare the effects of hypoxia, asphyxia, and ischemia on brain cortical oxidative metabolism. This study was carried out using 14 New Zealand White rabbits. The effects of episodic stress were measured simultaneously on brain functional metabolism by monitoring cortical oxygen tension (brain pO2), cortical cerebral blood flow (cCBF), cortical blood volume, and mitochondrial oxidative metabolism. During hypoxia (when the fraction of inspired O2 (FiO2) was reduced to 10%) and asphyxia (induced by turning the respirator off), there was a decrease of brain pO2 but an increase of cCBF and blood volume. Similarly, there was a reduction of cortical oxidative metabolism. In post-asphyxic conditions, an overshoot of brain pO2 and post-asphyxic oxidation of cytochrome (Cyt.) aa3 were usually shown. Under ischemic conditions (induced by sudden severe hypotension plus bilateral common carotid occlusion), cCBF and blood volume were decreased. There was also a decrease of brain pO2 and a reduction of Cyt. aa3 following ischemia. These techniques are applicable in intraoperative monitoring of patients.
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PMID:Cortical oxidative metabolism under conditions of ischemia, hypoxia, and asphyxia in the rabbit. 686 84

The effects of dietary supplementation with eicosapentaenoic acid (EPA) on ventricular arrhythmias during myocardial infarction were examined in a canine model. EPA was incorporated into cellular membranes after ingestion of EPA-ester (100 mg/kg body weight/day) for 8 weeks. The ratio of EPA to arachidonic acid (AA) in platelet cell membranes and myocardial microsomes was significantly increased (7% to 37% in platelet cell membranes; p < 0.01, 3% to 12% in non-infarcted cardiac microsomes; p < 0.01, and from 2% to 8% in infarcted cardiac microsomes; p < 0.01). Dietary supplementation with EPA significantly reduced the incidence and severity of arrhythmias during coronary artery occlusion. Immediately after coronary artery occlusion, all of the animals in the control group that were given a toxic dose of digitalis developed ventricular tachycardia (VT) or ventricular fibrillation (Vf), whereas none of the animals in the EPA-supplement group developed VT or Vf within 15 min after administration of digitalis. Regardless of the presence of an infarcted area, the specific activity of the Ca(2+)-pump enzyme ((Ca(2+)-Mg2+)-ATPase) within the myocardial microsomal fraction of the EPA-supplemented group was significantly higher than in that of the control group (Vmax: 140.5 +/- 19.1 vs 94.8 +/- 28.9 nmol/mg/min in non-infarcted cardiac microsomes, p < 0.01, 130.9 +/- 18.4 vs 90.2 +/- 26.4 nmol/mg/min in infarcted cardiac microsomes, p < 0.01, EPA vs control group, respectively). The specific activities of the Na(+)-pump enzyme ((Na(+)-K+)-ATPase) and NADPH-dependent cytochrome C reductase in infarcted and non-infarcted cardiac microsomes did not differ between these groups. These results indicate that EPA supplementation increases the (Ca(2+)-Mg2+)-ATPase activity within myocardial membranes that is involved in Ca2+ metabolism in myocardial cells by increasing the ratio of EPA to AA within cellular membranes. These cellular alterations are likely to reduce the severity of ventricular arrhythmias by inhibiting the rapid accumulation of intracellular Ca2+ following ischemia.
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PMID:Antiarrhythmic effects of eicosapentaenoic acid during myocardial infarction--enhanced cardiac microsomal (Ca(2+)-Mg2+)-ATPase activity. 769 37


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