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

Effects of methylprednisolone were studied on isolated, blood-perfused cat hearts subjected to 1 hr of normothermic ischemic arrest. Untreated hearts sustained decreases in peak ventricular pressure pulse, dP/dt, and ventricular compliance. Ischemic hearts also became edematous, gained sodium, and lost potassium and creatine kinase enzyme activity. Steroid treatment did not significantly alter any of these ischemia-induced changes. Methylprednisolone treatment did increase resting coronary flow and also increased the hyperemic response after reperfusion. These results, in isolated hearts, provide no evidence that steroid treatment exerts a direct protective effect on the globally ischemic myocardium.
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PMID:Methylprednisolone sodium succinate treatment in global ischemia of the cat isolated heart. 9 82

Methylprednisolone was given at different intervals before warm ischemia of the heart (37 degrees C. for 60 minutes), and viability of these hearts was evaluated after transplantation into the abdomen of another dog. Animals were divided into four groups: Group 1 received no methylprednisolone: Groups II, III, and IV received 30 mg. of methylprednisolone per kilogram 10 minutes, 60 minutes, and 120 minutes before warm ischemia. In all parameters measured, the animals of Group IV performed better than the other groups. It is concluded that methylprednisolone, when given 2 hours before warm ischemia, exerts a protective effect on the ischemic myocardium.
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PMID:Myocardial protection with methylprednisolone. Evaluation of viability of hearts subjected to warm ischemia before transplantation. 37 Apr 61

Canine kidneys subjected to 90 min of warm ischemia (37 degrees C) were protected by the administration of methylprednisolone but not by furosemide or mannitol. There was no protective effect observed through the vasodilating or diuretic effect of furosemide in the ischemic canine kidney. Mannitol-induced diuresis before warm ischemia also did not prove to be beneficial for severely ischemic kidneys. Methylprednisolone (30 mg/kg) given 2 h prior to warm ischemia prevented irreversible kidney damage observed in the control and experimental groups. By day 8 the serum creatinine and creatinine clearance returned to normal levels.
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PMID:Study of the protective effect of methylprednisolone, furosemide, and mannitol on ischemically damaged kidneys. 38 34

Temporary occlusion of hepatic inflow would be ideal during extensive operations for liver trauma or tumors, since this always is handicapped by accompanying massive blood loss. Since the liver is relatively low in tolerance to ischemia an attempt has been made to protect the liver with steroids during experimental warm ischemia. Total hepatic ischemia was produced in rabbits by ligating the portal triad and gastrohepatic ligament for 30 minutes. A survival rate of only 10 per cent was obtained in controls, whereas if methylprednisolone was given before occlusion, 100 per cent of the rabbits survived. If methylprednisolone was given immediately after the occlusion, the survival rate was 54 per cent. Further experiments extending occlusion to one hour resulted in a 50 per cent survival rate as compared with zero per cent in the one hour controls. Methylprednisolone protects the liver during warm ischemia, especially if given before occlusion, and dramatically decreases the mortality rate from this maneuver in our model. The mechanism of protection is probably by stabilizing and protecting the integrity of the hepatic cell during the anoxic insult.
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PMID:Steroid protection of the liver during experimental eschemia. 111 28

Occlusion of the afferent liver circulation for variable periods of time would be advantageous to temporarily control bleeding from profound lacerations or during extensive resections. Because of its low tolerance to ischemia we attempted to protect the liver with steroids during inflow occlusion. Total hepatic ischemia was produced in rabbits by ligating the portal triad and gastrohepatic ligament for 30 minutes. A 10 per cent survival was obtained in untreated controls whereas pre-treatment with methylprednisolone improved survival to 100 per cent. Methylprednisolone injection after occlusion improved survival only to 57 per cent. There were profound pathohistologic and electron microscopic changes in untreated controls. In animals treated with methylprednisolone either before or after occlusion changes were minimal or absent. This treatment was used in four trauma patients in whom occlusion of the liver inflow was carried out for various periods of time. Even though no significant statement can be made from such small group, the early postoperative course was remarkably smooth and stable. Methylprednisoline protects the liver during warm ischemia, especially if given before occlusion, and decreases the mortality from this maneuver in experimental animals.
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PMID:Protective effect of steroids on liver ischemia. 118 54

There is as yet no adequate animal mode for human myocardial ischemia. The commonly utilized technique of coronary arterial ligation in large animals may induce regional ischemia but introduces variables that make it difficult to compare studies in different laboratories. A model of global ischemia in an isolated perfused rat heart that offers a rapid, inexpensive means for producing graded, controlled, stable state and reproducible ischemia is described. The technique has been utilized with success to study the hemodynamic and metabolic effects of ischemia and to evaluate pharmacologic interventions designed to protect the ischemic myocardium. Propranolol has been shown to improve bioenergetics and reduce anaerobic glycolysis by a depression of the hemodynamic response of ischemic myocardium. Methylprednisolone appears to exert its primary effect by direct coronary vasodilation, increasing resting or control flow and providing an enhanced reserve when ischemia is imposed. Mannitol improves cardiac performance by reducing the increased myocardial cell water content induced by hypoxia or anoxia.
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PMID:Metabolic evaluation of agents designed to protect the ischemic myocardium and to reduce infarct size. 125 90

In a pilot-study (n = 66) and subsequent controlled experiment (n = 32) the ischemic tolerance of dog liver is examined by means of various clinical and laboratory parameters. During normothermia and without venous decompression the time of ischemic tolerance amounts to 60 minutes. Hypothermia and systemic administration of Aprotinin (Trasylol) and Methylprednisolone (Urbason) do not prolong the tolerance time of ischemia. This time is significantly extended by pre-operative administration of a thiourea-derivate (Propycil). Basing on this decisive improvement of the ischemic tolerance of dog liver, new advances in increasing the ischemic tolerance of human liver are offered.
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PMID:[Efficacy of various treatment methods to extend the ischemia tolerance time of the liver. Experimental studies in dogs]. 170 Aug 71

In acute nonsurvival studies, eight anesthetized lambs were subjected to cord compression at T13 by means of an epidural balloon distended to a pressure of 200 mm Hg for 40 minutes. Subsequent to withdrawal of the balloon, each animal received 30 mg/kg of methylprednisolone succinate in an intravenous bolus followed by a continuous infusion of 10 mg/kg/hr for the duration of the experiment. Spinal cord blood flow (SCBF) and spinal evoked potential (SEP) determinations were obtained sequentially prior to, during, and at 1/2, 1 1/2, and 2 1/2 hours following compression. In spite of the absence of ischemia following compression, SEPs failed to recover. Methylprednisolone had no apparent effect on blood flow or on the recovery of SEPs when compared with results in ten control animals that received saline alone.
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PMID:Methylprednisolone in spinal cord compression. 264 34

With methylprednisolone as a chemical inhibitor of leukocytes, extended preservation was conducted with an isolated rabbit lung model. The heart-lung blocks of 39 New Zealand white rabbits were flushed in situ with 100 ml of Euro-Collins' solution, harvested, inflated (70%), and preserved at 4 degrees C. Lungs immediately reperfused with whole blood (control lungs, group 1) were compared with lungs preserved without methylprednisolone for 5, 12, and 24 hours (groups 2 to 4) and those preserved with methylprednisolone for 12 and 24 hours (groups 5 and 6, respectively). Methylprednisolone (30 mg/kg) was administered before harvest and was used as an additive to the flush and in the blood reperfusate. Hypothermia and Euro-Collins' flush alone provided adequate preservation for up to 5 hours; however, lung edema was evident by 12 hours of cold ischemia and became severe by 24 hours. By all measured parameters, the lungs in group 5 (treated with methylprednisolone) demonstrated values equal to or better than control lungs. By 24 hours of preservation the beneficial effects of the steroid treatment were no longer evident. Histologic evaluation revealed mild to moderate injury after 5 hours of cold ischemia; progressive edema and hemorrhage were found after 12 and 24 hours of preservation. This injury was significantly ameliorated by methylprednisolone treatment at 12 hours but not at 24 hours. This study suggests that static preservation for up to 5 hours is possible with hypothermia and a Euro-Collins' flush and that extended preservation to 12 hours is possible with pharmacologic dosages of methylprednisolone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved static lung preservation with corticosteroids and hypothermia. 319 47

The correlation of changes in cortical neuron activity with water content and local cerebral blood flow was investigated in cats with brain edema produced by air exposure. The further effect of high-dose methylprednisolone on these factors was studied. Six hours after exposure of the brain surface to air, the water content of the white matter significantly increased. The local blood flow of the cortex and white matter significantly decreased with significant suppression of cortical neural activity (direct cortical response), indicating that ischemia was responsible for neural suppression. A single, large dose of methylprednisolone (30 mg/kg, i.v.) at the beginning of air exposure significantly reduced brain edema of the cortex and white matter 12 h after air exposure and improved the local blood flow of the cortex. Methylprednisolone also caused a remarkable improvement in cortical neural activity. This steroid effect on cortical neural function may play a role in the rapid neurologic improvement observed with their use in addition to the effect on brain edema.
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PMID:Effects of methylprednisolone on cortical neural activity, blood flow, and water content in air exposure-induced cerebral edema. 370 35


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