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

Cortical reflectance, mean arterial blood pressuees, electroencephalograms, and cortical blood flow were continuously recorded together with fluorescence of reduced pyridine nucleotides (PN) at various carbon dioxide tensions before, during, and following middle cerebral artery occlusion in 10 squirrel monkeys receiving halothane or babiturate anesthesia. Measurements were continued through a nitrogen breathing cycle and to death produced by anoxia. The anesthetic agent produced no detectable differences in PN fluorescence in cerebral tissue during ischemia and anoxia. The known cerebral protective action of barbiturates is apparently unrelated to the intracellular redox state.
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PMID:Intracellular redox states under halothane and barbiturate anesthesia in normal, ischemic, and anoxic monkey brain. 3 37

Whole excis ed rat hearts were treated with 5, 10, or 15% (v/v) dimethyl sulfoxide/glycerol and then some were frozen in liquid nitrogen while the balance remained unfrozen. Freezing and thawing rates were approximately 30degreesC/min. Ventricular tissue was examined for histological damage, glycogen depletion, and enzyme sites, using histological, histochemical, and electron microscopy techniques. Early signs of cellular degeneration and ischemia were observed in all unfrozen groups; depletion of glycogen reserves, fuchsinophilic staining, vacuolization and granulation of the sarcoplasm were noted. Results from frozen groups were similar, but ultrastructural damage was more severe and extensive. Alkaline phosphatase and succinic dehydrogenase sites were abundant in unfrozen specimens and absent or markedly reduced in frozen specimens which also exhibited widespread nonspecific staining throughout intercellular spaces.
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PMID:Cryoprotectant-treated myocardium evaluation. 6 Nov 4

Using a time-sharing fluorometer-reflectometer, pyridine nucleotide (NADH) and flavoprotein (Fp) fluorescence, as well as reflected light at the excitation wavelength, were measured and correlated with the electrical activity of an awake cerebral cortex. Exposure of the rat to a nitrogen atmosphere (anoxia) led to an increase in signals representing the reduction of pyridine nucleotides and flavins, with very similar kinetics. Inducement of partial ischemia by bilateral carotid artery ligation led to an increase in NADH, accompanied by a very small effect on the electrical activity (ECoG). In most animals, 2-3h after ligation, the ECoG became flat or depressed. Exposure of this ischemic cerebral cortex to KC1 solution caused depression of the electrical activity without metabolic response probably due to the limitation of oxygen supply. The metabolic state of an awake cerebral cortex was identified by exposing the brain to various levels of oxygen, epileptoform activity, spreading depression, hyperbaric pressure of oxygen and an uncoupler. From our results we conclude that the awake cerebral cortex is close to the resting state, state 4, rather than to the active state, state 3.
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PMID:Brain energy metabolism of the conscious rat exposed to various physiological and pathological situations. 18 22

The effect of experimentally induced uniocular trauma was investigated in the adult albino rabbit by means of iris fluorescein angiography. Paracentesis, blunt trauma, occlusion of all four vortex veins or of the two long posterior ciliary arteries, or local instillation of nitrogen mustard, were performed in a number of animals, some of which received systemic aspirin preoperatively. Iris angiograms of the injured and the contralateral eye were performed immediately after the traumatic insult. The injured eye always showed an increased permeability to fluorescein. Except for paracentesis, the ipsilateral response often included ischemia of the iris. The contralateral eye always showed an increase in fluorescein permeability into the aqueous. In some cases, sector ischemia of the contralateral iris was seen. Aspirin inhibited some ipsilateral responses but had no effect on the consensual reactions. It is concluded that ipsilateral trauma almost invariably causes a contralateral reaction in the rabbit eye, which is more severe if the injury creates ischemia of the iris. Since these reactions are inefficiently blocked by aspirin, they are not prostaglandin-mediated. The interocular pathway involved may be neural or vascular in nature.
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PMID:Anterior segment reactions after experimental trauma to rabbit eyes. 31 Nov 67

Differential survival times of various organ allografts in the rat across the same histocompatiblity barrier were studied by transplanting the kidney, heart, intestine, pancreas, and skin from (BN X Le)F1 hybrid donors to Lewis recipients. Some (one-third) of the kidney grafted rats survived for a prolonged period of time (32-72 days, plus one rat surviving over 9 months), whereas all other organs and skin were promptly rejected between 7 and 21 days. Possible factors responsible for the prolonged kidney survival are discussed; the reason for this was not clear but was not related to the period of operative ischemia or postoperative blood-urea-nitrogen, nor were animals tolerant to donor antigen as evidenced by the popliteal lymph node weight assay and signs of mild rejection on histology of grafted kidneys. A hypothesis of autoenhancing mechanism is presented.
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PMID:Differential survivals of F1 hybrid allografts in parental recipients. 77 4

The effects of atrial pacing on tissue metabolite levels known to be sensitive to ischemia were examined. Anesthetized dogs were thoracotomized and a pacing electrode was sutured to the right atrium. Pacing at rates of 200 or 250 beats/min (10 animals per group) was performed for 15 min after base-line hemodynamic data had been obtained. At the end of the pacing period, a transmural biopsy was taken, frozen in liquid nitrogen, and sectioned into subepicardial, midmyocardial, and subendocardial layers. ATP, phosphocreatine, lactate, and glycogen were extracted and analyzed. Significant (P less than 0.001) transmural gradients of each of these metabolites existed in the control group. Pacing had no significant (P greater than 0.2) effect on any metabolite from layer to layer at 200 or 250 beats/min. However, indices of heart work (i.e., contractility (dP/dt), stroke work, and stroke volume) demonstrated significant reductions (P less than 0.01) due to pacing, while circumflex artery blood flow increased more than twofold (P less than 0.001) at the highest rate. These data suggest that physiologic autoregulation occurred during pacing and protected the subendocardium from stress-induced ischemic insult.
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PMID:Transmural metabolic gradients in the normal dog left ventricle: effect of right atrial pacing. 88 64

Isolated blood-perfused rabbit interventricular septa were adapted for studies of global ischemia by enclosure in a constant-humidity nitrogen atmosphere. During ischemia, developed tension (DT) and maximal rate of relaxation (-dP/dt) declined monoexponentially, lambda = 0.39 min-1 at 37 degrees C and 72 beats/min with a Q10 of 1.4 for DT and a Q10 of 1.9 for -dP/dt. After a 60- to 90-s delay the maximal rate of tension development (+dP/dt) declined at the same rate as DT. Time-to-peak tension (TPT) shortened immediately with ischemia but action potential duration shortened after 60-90 s. Calcium at a concentration of 5 mM slowed the rate of decline of +dP/dt to lambda = 0.26 min-1. Upon reperfusion after 10 min of ischemia the rates of recovery of DT, +dP/dt, and -dP/dt were similar, lambda = 0.21-0.23 min-1, and were not temperature dependent. The magnitude of recovery was 10-17% less at 37 degrees C than 28 degrees C. Potassium at a concentration of 10 mM did not alter the rate of decline of mechanical function, but significantly (P less than 0.01) increased the magnitude of mechanical recovery. The results suggest depletion and/or repletion of single compartments as the rate-limiting steps in ischemia and reperfusion.
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PMID:Ischemia in isolated interventricular septa: mechanical events. 98 8

The role of arterial blood flow in hepatic metabolic functions was compared to that of portal flow in two groups of totally depancreatized dogs. Survival times and glucose and nitrogen excretion were significantly greater in dogs with ligation of the hepatic artery than in dogs with an Eck fistula. The dogs with ligated hepatic arteries also showed a significantly slower rise in plasma ketones. The course of diabetes was compared in three additional groups of partially depancreatized dogs consisting of a) dogs with ligated hepatic arteries, b) dogs with Eck fistulas, and c) controls. Hepatic arterial ischemia: 1) increased survival, without insulin treatment (a--650, b--167, c--124 days) 2) did not decrease tracer-determined rate of glucose production 3) led to a greater urinary excretion of glucose, ketone bodies and nitrogen than portal ischemia. Partially depancreatized dogs with either arterial or portal hepatic ischemia maintained a high rate of glucose disappearance on acute deprivation of endogenous insulin (clamping of vessels of their pancreatic remnant) due probably to decreased insulin degradation by the ischemic liver. The dogs died in coma after losing all fat depots. There was severe fatty change in the livers of dogs with hepatic artery ligation, slight in those with Eck fistulas and no fat in the livers of controls.
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PMID:Effects of arterial or portal ischemia on survival and metabolism of partially and totally depancreatized dogs. 105 92

Tetrodotoxin has been reported to cause prolonged systemic hypotension without resultant ischemic damage. We tested its ability to protect the kidney during 60 minutes of warm ischemia in uninephrectomized rats. Protection was observed when tetrodotoxin was given intravenously at two microgram./kg. and four microgram./kg. as assessed by serial plasma blood urea nitrogen and creatinine measurements over two weeks. Tetrodotoxin was protective when given immediately before or immediately after the ischemic period. The renal protection of tetrodotoxin was not due to its effects on renal nerves as renal denervation did not protect the kidney from the ischemic damage. The renal protective effects of four microgram. tetrodotoxin/kg. were similar to those of four mg. captopril/kg. but the combination of the two was paradoxically without effect. We tested whether tetrodotoxin and captopril chemically antagonized each other, but in the presence of tetrodotoxin, captopril was still a potent inhibitor of the conversion of angiotensin I to angiotensin II. These results indicate that tetrodotoxin could be useful in elucidating the sequence of events associated with ischemic-reperfusion renal injury and in identifying ways of preserving renal function during renal surgery.
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PMID:Tetrodotoxin protects against acute ischemic renal failure in the rat. 131 Jan 25

Hind limb ischemia and reperfusion have been shown to result in high plasma levels of leukotriene B4 (LTB4) and polymorphonuclear neutrophil (PMN) sequestration in the pulmonary microvasculature. This study tests whether LTB4 is derived from PMNs and its role in mediating ischemic plasma-induced diapedesis. Plasma derived from rabbit hind limbs after 3 hours of tourniquet ischemia and 10 minutes of reperfusion (n = 6) showed an increased LTB4 level of 560 pg/ml, higher than sham plasma values of 106 pg/ml (p less than 0.05). Introduction of ischemic plasma in abraded skin chambers placed on the dorsum of normal rabbits (n = 6) led after 3 hours to PMN diapedesis of 1175 PMN/mm3, associated with a further increase in LTB4 levels to 820 pg/ml (both p less than 0.05). In contrast, ischemic plasma derived from neutropenic animals (n = 4; nitrogen mustard, 2 mg/kg; PMNs less than 30/mm3) contained lower levels of LTB4, 160 pg/ml (p less than 0.05). When introduced in skin chambers in normal rabbits (n = 4), this plasma induced accumulations of only 163 PMN/mm3, accompanied by a smaller increase in LTB4 levels in the blister fluid after 3 hours, 397 pg/ml (both p less than 0.05). A correlation was found between LTB4 levels in ischemic plasma and PMN accumulations in blister fluid (r = 0.92; p less than 0.05). Intravenous pretreatment of rabbits (n = 4) used in the blister chamber bioassay with the LT receptor antagonist FPL-55712, 40 micrograms/kg/hr, attenuated diapedesis induced by ischemic and ischemic-neutropenic plasma, 103 and 35 PMN/mm3, respectively (both p less than 0.05). Pretreatment with superoxide dismutase, 1500 units/kg, and catalase, 5000 units/kg, both conjugated to polyethylene glycol (n = 4), prevented ischemic plasma-induced LTB4 synthesis, as well as ischemic plasma-induced diapedesis, 12 PMN/mm3 (p less than 0.05). Finally, pretreatment with allopurinol, 25 mg/kg, was similarly effective in preventing LTB4 synthesis and PMN migration. These data suggest that oxygen free radicals are essential for ischemia-induced PMN synthesis of LTB4 that in turn mediates their diapedesis.
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PMID:Oxygen free radicals are required for ischemia-induced leukotriene B4 synthesis and diapedesis. 131 74


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