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

PD--the electric potential difference across the gastric mucosa--is a variable used to describe the gastric mucosal integrity and function. A new, reliable, and easily applied method for gastric PD measurements corrected for the disturbing liquid junction potentials between gastric juice and the PD measuring probe is presented. PD is measured with the gastric lumen negative, and a numeric reduction in PD is used as an expression of an injured mucosal condition. A reduced gastric PD is found along with a reduced gastric mucosal blood flow after intravenous indomethacin in anesthetized dogs. Increasing the FFA/albumin ratios in mini-pigs causes vasoconstriction and PD reduction. Short hypoxia and selective gastric ischemia cause a reversible PD reduction and no morphologic changes in anesthetized dogs, but ischemia for 1 h causes more permanent changes in PD, pH, and morphology. This damage can be reduced by allopurinol pretreatment, possibly due to the inhibition of oxygen-derived free radical formation. Gastric PD and pH were measured in volunteers and duodenal ulcer patients during Stroop's color word conflict test, in which mental stress causes sympathetic activation. A PD reduction and a pH increase were found along with stress induction, thereby indicating an influence of mental stress on stomach mucosal function. It is concluded that gastric PD measurement may be useful in ulcer pathogenetic research, and a sufficient gastric mucosal blood flow is stressed as being important for the mucosal defense.
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PMID:Gastric potential difference measurements. The gastric mucosal integrity and function studied with a new method for measurement of the electric potential difference across the stomach wall. 192 6

Iron-dependent oxy radicals have been implicated in reperfusion injury. Although the iron chelator desferoxamine (DFO) is beneficial, its hemodynamic effects and short vascular retention limit its use in vivo. We tested whether DFO conjugated to a high-molecular-weight starch might ameliorate in vivo hepatic microvascular injury without adverse side effects following 120 min of ischemia. Prior to reperfusion, conjugated DFO (100 mg/kg), vehicle (Veh), or saline (I/R) was administered. After 90 min of reperfusion, blood was collected for serum transaminase determination (ALT; U/liter), and fluorescein-albumin was injected to label perfused microvessels, which were quantified in frozen sections by a point-count technique. Tissue edema was estimated by wet to dry weight ratios (W/D). Reperfusion results in hepatocyte injury (rise in ALT and W/D) and a 30% loss of perfused microvessels. Intravenous administration of conjugated DFO produces no significant change in systemic hemodynamics, whereas both ALT and tissue edema were decreased by approximately 50%. Moreover, perfused microvessels were restored virtually to nonischemic control levels. Enhanced perfusion and attenuated cell injury with DFO suggest that microvascular failure and resultant cell death are mediated, at least in part, by iron-dependent mechanisms in reperfusion.
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PMID:Conjugated desferoxamine attenuates hepatic microvascular injury following ischemia/reperfusion. 193 29

Basic parameters of central and intracardiac hemodynamics were studied in 49 urological patients 24 of which with urolithiasis entered group I, 13 with hypertension-group II and 12 with varicocele-group III. The patients' age averaged 46.4, 41.6 and 28.6 years, respectively. The data were provided by routine clinical and laboratory examinations, ECG, one-passage radionuclide cardiography with 132I-albumin using a radiocirculographer of Hungarian manufacture and radiocardioanalyzer RKAZ-01 made in this country. Neither marked ischemic disturbances of the myocardium nor valvular defects were revealed. Ambiguous group-specific shifts presented in central and intracardiac hemodynamics. Total peripheral vascular resistance exhibited a moderate increase while left ventricular circulation time grew 1.5-2-fold. The greater resistance can be attributed to activation of renin-angiotensin system in prolonged ischemia of renal parenchyma due to nephrolithiasis. Group II patients demonstrated parallel elevation of arterial pressure, peripheral resistance, left ventricular performance and output suggesting myocardial functional stress. In group III there was a rise in blood volume, left ventricular performance and output, cardiac index, stroke volume. This myocardial overloading may result from changes in intravascular volumetric relations characteristic of hypervolemia. These hemodynamic changes reflect adaptation in urological patients and should be accounted for in treatment and operative interventions.
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PMID:[The radionuclide assessment of the central hemodynamic indices in patients with urolithiasis, arterial hypertension and varicocele]. 194 10

Ischemia and reperfusion causes severe mitochondrial damage, including swelling and deposits of hydroxyapatite crystals in the mitochondrial matrix. These crystals are indicative of a massive influx of Ca2+ into the mitochondrial matrix occurring during reoxygenation. We have observed that mitochondria isolated from rat hearts after 90 minutes of anoxia followed by reoxygenation, show a specific inhibition in the electron transport chain between NADH dehydrogenase and ubiquinone in addition to becoming uncoupled (unable to generate ATP). This inhibition is associated with an increased H2O2 formation at the NADH dehydrogenase level in the presence of NADH dependent substrates. Control rat mitochondria exposed for 15 minutes to high Ca2+ (200 nmol/mg protein) also become uncoupled and electron transport inhibited between NADH dehydrogenase and ubiquinone, a lesion similar to that observed in post-ischemic mitochondria. This Ca(2+)-dependent effect is time dependent and may be partially prevented by albumin, suggesting that it may be due to phospholipase A2 activation, releasing fatty acids, leading to both inhibition of electron transport and uncoupling. Addition of arachidonic or linoleic acids to control rat heart mitochondria, inhibits electron transport between Complex I and III. These results are consistent with the following hypothesis: during ischemia, the intracellular energy content drops severely, affecting the cytoplasic concentration of ions such as Na+ and Ca2+. Upon reoxygenation, the mitochondrion is the only organelle capable of eliminating the excess cytoplasmic Ca2+ through an electrogenic process requiring oxygen (the low ATP concentration makes other ATP-dependent Ca2+ transport systems non-operational).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitochondrial generation of oxygen radicals during reoxygenation of ischemic tissues. 206 Aug 40

Since advanced glycosylation end products have been suggested to mediate hyperglycemia-induced microvascular atherogenesis and because aminoguanidine (AG) prevents their generation, we examined whether AG could prevent or ameliorate the physiologic and biochemical indices of streptozotocin (STZ)-induced experimental diabetic neuropathy. Four groups of adult Sprague-Dawley rats were studied: group I received STZ plus AG (25 mg.kg-1.day-1), group II received STZ plus AG (50 mg.kg-1.day-1), group III received STZ alone, and group IV was a control. We monitored conduction and action potential amplitudes serially in sciatic-tibial and caudal nerves, nerve blood flow, oxygen free radical activity (conjugated dienes and hydroperoxides), and the product of the permeability coefficient and surface area to 125I-labeled albumin. STZ-induced diabetes (group III) caused a 57% reduction in nerve blood flow and in abnormal nerve conduction and amplitudes and a 60% increase in conjugated dienes. Nerve blood flow was normalized by 8 weeks with AG (groups I and II) and conduction was significantly improved, in a dose-dependent manner, by 16 and 24 weeks in sciatic-tibial and caudal nerves, respectively. The permeability coefficient was not impaired, suggesting a normal blood-nerve barrier function for albumin, and the oxygen free-radical indices were not ameliorated by AG. We suggest that AG reverses nerve ischemia and more gradually improves their electrophysiology by an action on nerve microvessels. AG may have potential in the treatment of diabetic neuropathy.
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PMID:Aminoguanidine effects on nerve blood flow, vascular permeability, electrophysiology, and oxygen free radicals. 206 89

Recovery of contractile function and of fatty acid oxidation may be delayed in viable postischemic myocardium. To determine whether a metabolic reserve is preserved after reperfusion of reversibly injured myocardium, we studied the effect of epinephrine on myocardial fatty acid oxidation in isolated rat hearts perfused retrogradely with erythrocyte enriched buffer containing albumin 0.4 mM, palmitate 0.4 mM, and glucose 11 mM. Hearts were subjected to 60 min of low-flow ischemia (5% of control flow) followed by 60 min of reperfusion. Five minutes following the onset of reperfusion, developed left ventricular pressure (DLVP) and oxidation of palmitate were reduced to 53% (p less than 0.01) and 46% (p less than 0.01), respectively, of values measured in nonischemic control hearts. Subsequently, DLVP and oxidation of palmitate gradually recovered to 78% (NS) and 91% (NS) by 60 min of reperfusion. Epinephrine 5.10(-1) M elicited an immediate stimulation of both contractile function and palmitate oxidation. Early after reperfusion stimulated DLVP and palmitate oxidation were still lower compared to values measured in control hearts exposed to the same concentration of epinephrine. Later than 15 min after the onset of reperfusion the response of DLVP and of palmitate oxidation to epinephrine no longer differed between control and reperfused hearts. These results indicate that viable postischemic myocardium exhibits a remarkable oxidative metabolic reserve. The observation provides further evidence for the view that impairment of myocardial energy production is not responsible for contractile dysfunction early after reperfusion.
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PMID:Epinephrine-stimulated contractile and metabolic reserve in postischemic rat myocardium. 207 95

The sequence of acute ischemia, reperfusion, and elevated tissue pressure, with subsequent neuromuscular damage, results in the clinical entity known as the compartment syndrome. We have developed a canine hindlimb model that successfully replicates these clinical features. Surgical devascularization of both hindlimbs at the popliteal level isolates perfusion to a single vascular pedicle. Total ischemia is produced in the left limb for 8 h, while the right limb serves as a surgical control. Ischemia is confirmed by measurement of transfascial oxygen tension (TF-PO2) as well as lactate and blood gases in the venous effluent. Pressure in the anterior compartment of the hindlimb is monitored by the slit catheter technique. After reperfusion, muscle damage is assessed by histology, creatine phosphokinase (CPK), and uptake of technetium-99m pyrophosphate (Tc-PyP), expressed as a ratio of the experimental (L) limb to the control (R) limb (L/R ratio). Muscle necrosis was greatest in untreated controls; the L/R ratio was 8.9 +/- 5.0. Significant diminution of muscle necrosis was achieved by fasciotomy prior to reperfusion (2.6 +/- 0.8), mannitol (1.8 +/- 0.6), albumin-conjugated superoxide dismutase (SOD) 2.8 +/- 0.8), native SOD (2.3 +/- 1.0), fasciotomy combined with SOD (1.9 +/- 0.7), and continuous heparin (1.6 +/- 0.4) (p less than .01 vs controls). When fasciotomy was delayed until 2 h after reperfusion, there was no significant decrease in the L/R ratio (5.4 +/- 1.5; p = .15). Early fasciotomy following prolonged severe limb ischemia remains the treatment of choice, although these results suggest an emerging role for nonsurgical therapies as well. A summary of work done with this model as well as a review of other techniques is presented, along with a discussion of the pathophysiology of the compartment syndrome.
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PMID:Replication of the compartment syndrome in a canine model: experimental evaluation of treatment. 212 42

Kainic acid (KA) is a potent neuroexcitatory drug widely used in the experimental study of seizure activity. Subcutaneous injection of KA into rats (10 mg/kg in saline 10 mg/ml; pH 7.0) induced longlasting status epilepticus followed by damage of CNS tissue in the entorhinal/pyriform cortex and in the hippocampus. The studies covered by this report demonstrated the formation of cytotoxic brain edema characterized by massive swelling of perineuronal and perivascular astroglia with microcirculation disturbance after KA injection, resulting in parenchymal necrosis of the affected region; furthermore perivenous hemorrhages and necroses corresponding to herniation lesions of the brain appear. Tracer studies with Na-fluorescein, Evans blue, albumin, and horseradish peroxidase revealed only a mild increase in the permeability of cerebral vessels, topographically unrelated to areas of brain edema. Treatment of brain edema with dexamethasone did not influence the incidence and severity of edematous brain damage. Treatment with mannitol, however, completely prevented the lesion in 54% of animals injected with KA. The present results indicate that brain edema plays an important role in the pathogenesis of epileptic brain damage following systemic KA intoxication. It is suggested that in this model brain edema develops due to massive ionic imbalance caused by KA induced persistent neuronal excitation. In addition the model demonstrates the possible pathogenetic role of selective astrocytic swelling in the production of local hippocampal ischemia followed by herniation and its sequels. Such pathology originating from astrocytes probably may occur also in closed brain injury.
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PMID:Some mechanisms of brain edema studied in a kainic acid model. 213 Jun 48

We tested the hypothesis that impaired coronary autoregulation, decreased flow reserve, and diminished reactive hyperemic response in hypertrophied hearts with coronary arterial hypertension may be reversible after relief of pressure overload. In 4-week ascending aortic banded rats, in vivo peak systolic left ventricular pressure increased to 178 +/- 8 mm Hg (103 +/- 6 mm Hg in sham-operated control group). This increased pressure produced myocardial hypertrophy, and the left ventricular weight/body weight ratio was 46% above that of the control group. After the rats were killed, the coronary perfusion pressure-flow relations were obtained during resting conditions and maximal vasodilation after a 40-second period of ischemia in beating but nonworking isolated hearts perfused with Tyrode's solution with bovine red blood cells and albumin. In hearts from control rats, coronary autoregulation (i.e., a slight decrease in flow with reduction of pressure) was observed in the range of 50-100 mm Hg of perfusion pressure. A pronounced reactive hyperemic response was observed: a peak flow/resting flow ratio of 2.9 +/- 0.1 and a repayment ratio of 1.7 +/- 0.2 at 100 mm Hg of perfusion pressure. In hearts of banded rats the resting pressure-flow relation was rectilinear in the range of 25-175 mm Hg of perfusion pressure. Flow reserve and the time of reactive hyperemia to one half peak flow decreased at 50, 100, and 150 mm Hg of perfusion pressure compared with values in control rat hearts. Four weeks after debanding, peak systolic left ventricular pressure and cardiac hypertrophy had normalized. The impaired autoregulation, decreased flow reserve, and diminished reactive hyperemic response had completely reversed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Normalization of impaired coronary circulation in hypertrophied rat hearts. 214 25

Reactive oxygen species are a major cause of damage occurring in ischemic tissue after reperfusion. During reperfusion transitional metals such as iron are required for reactive oxygen species to mediate their major toxic effects. Xanthine oxidase is an important source of reactive oxygen species during ischemia-reperfusion injury, but not in all organs or species. Because cytochrome P-450 enzymes are an important pulmonary source of superoxide anion (O2-.) generation under basal conditions and during hyperoxia, and provide iron catalysts necessary for hydroxyl radical (.OH) formation and propagation of lipid peroxidation, we postulated that cytochrome P-450 might have a potential role in mediating ischemia-reperfusion injury. In this report, we explored the role of cytochrome P-450 enzymes in a rabbit model of reperfusion lung injury. The P-450 inhibitors 8-methoxypsoralen, piperonyl butoxide, and cimetidine markedly decreased lung edema from transvascular fluid flux. Cimetidine prevented the reperfusion-related increase in lung microvascular permeability, as measured by movement of 125I-albumin from the vascular space into lung water and alveolar fluid. P-450 inhibitors also prevented the increase in lung tissue levels of thiobarbituric acid reactive products in the model. P-450 inhibitors did not block enhanced O2-. generation by ischemic reperfused lungs, measured by in vivo reduction of succinylated ferricytochrome c in lung perfusate, but did prevent the increase in non-protein-bound low molecular weight chelates of iron after reperfusion. Thus, cytochrome P-450 enzymes are not likely a major source of enhanced O2-. generation, but serve as an important source of iron in mediating oxidant injury to the rabbit lung during reperfusion. These results suggest an important role of cytochrome P-450 in reperfusion injury to the lung and suggest potential new therapies for the disorder.
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PMID:Role of cytochrome P-450 in reperfusion injury of the rabbit lung. 217 18


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