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)

Physiologic effects of 1 hour of ischemia and 1 hour of reperfusion on equine jejunum and protective effects of systemic administration of dimethyl sulfoxide (DMSO, 1 g/kg of body weight) were investigated in 18 ponies, using neurally intact segments of jejunum perfused at constant flow with heparinized blood. Ponies were allotted to 4 groups: group 1, saline solution administered (control, n = 3); group 2, DMSO administered (DMSO, n = 3); group 3, ischemia induced and saline solution administered (ischemia, n = 6); and group 4, ischemia induced and DMSO administered (ischemia-DMSO, n = 6). Intestinal vascular resistance (R, mm of Hg/ml/min/100 g), oxygen consumption (VO2, ml/min/100 g), frequency and amplitude of rhythmic changes in intraluminal pressure, intestinal compliance (C, ml/mm of Hg), and arteriovenous potassium concentration difference (delta AV [K+], mEq/L) were determined and compared with stable preischemic values within groups. There were no significant changes in any variable in ponies of groups 1 or 2. In ponies of group 3, significant (P less than or equal to 0.05) changes included: an initial increase in R during reperfusion, followed by a decrease to values below preischemic values by 15 minutes of reperfusion; decreased VO2 during the entire reperfusion period; increased amplitude of rhythmic contractions during initial reperfusion; decreased frequency of rhythmic contractions during ischemia; and increased delta AV [K+] during initial reperfusion. Changes in ponies of group 4 were identical to changes in ponies of group 3, with the exception that DMSO administration prevented the decrease in R during reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of ischemia and dimethyl sulfoxide on equine jejunal vascular resistance, oxygen consumption, intraluminal pressure, and potassium loss. 293 25

When dehydration, infection, and mechanical trauma are prevented, procedures (such as cooling and/or oral antithromboxane) designed to diminish ischemia in experimental zone-of-stasis burns have been associated with no or only minor improvement in wound healing. To test the hypothesis that ongoing skin damage occurring postburn (PB) may in part be due to release of oxygen-derived free radicals during the 16-hour through 4-day PB period of reperfusion in such burns, beginning immediately and for a period of 5 days PB, equal numbers of guinea pigs received: allopurinol 150 mg/kg PO q 6 h vs. placebo, dimethylsulfoxide (DMSO) 75% applied topically q 12 h vs. placebo, or yeast-derived superoxide dismutase coupled with polyethylene glycol (PEG-SOD, Pharmacia) 10,000 U (Fridovich) given IV q 8 h producing a concentration of 16 U/cc of plasma 8 hr after injection vs. placebo. Gross and histologic examination of wounds by a 'blinded' investigator at 1 week and 3 weeks PB revealed no difference between treatment and control groups when rates of re-epithelialization and frequencies of hair-follicle retention were compared. Using the dosages, routes, and model described, treatment of a zone-of-stasis burn with PO allopurinol (a xanthine oxidase inhibitor), topical DMSO (a scavenger of the hydroxyl radical), or IV PEG-SOD (a scavenger of the superoxide radical) during the first 5 days PB was associated with no increase in the rate of re-epithelialization or frequency of hair follicle retention at 1 and 3 weeks PB when compared with controls.
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PMID:Oxygen-derived free radical inhibition in the healing of experimental zone-of-stasis burns. 302 94

The action of dimethyl sulfoxide (DMSO) was investigated employing an experimental model of intestinal perfusion in vivo of isolated loops of dog ileum before, during, and following 1-h ischemia. DMSO was administered either into the intestinal lumen or by a continuous injection via a branch of the artery supplying the experimental loop. In the intact intestine, intraluminal DMSO significantly decreased the net movement of water, electrolytes, and glucose without affecting either the active transport of phenylalanine and beta-methylglucoside or morphology. This inhibition was irreversible since, following DMSO removal, there was only partial recovery of water absorption, while the other parameters remained significantly low. Inhibition by DMSO was delayed when the substance was injected intraarterially (i.a.). Regardless of its route of administration, DMSO did not reduce the extent of ischemic injury in comparison with non-treated "Controls": during ischemia, all functional parameters were practically non-existent. Following the re-establishment of circulation, a net loss of water and electrolytes ensued, and active transport did not improve. In both instances, the structural alterations were those associated with ischemia of the experimental model employed: short, broad, club-shaped villi which had completely lost their epithelium, but fairly intact crypts. It can be concluded from the data presented that in the dog DMSO inhibits absorption in the intact ileum and exerts no protection against ischemic lesion.
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PMID:Effect of dimethyl sulfoxide on the function and structure of the intact and ischemic canine ileum. 362 74

To determine whether treatment with hyperbaric oxygen (HBO) or dimethyl sulfoxide (DMSO) could mitigate the fatal effects of cerebral ischemia, we anesthetized 68 gerbils with ketamine, ligated the right carotid artery (CA), and placed a snare occluder around the left CA. After 48 hours, 30 gerbils that were neurologically normal or had suffered only mild deficits were subjected to left CA occlusion without anesthesia for periods of 2 to 60 minutes. The onset of circling, posturing, falling, and lethargy began immediately; seizures and coma ensued 4 to 5 minutes later and persisted until release of the left CA occluder. All gerbils recovered after 2-minute staged bilateral CA occlusions. The mortality rate was 33% after both 5- and 10-minute occlusions and 100% after 20- and 60-minute bilateral occlusions. Twelve gerbils were placed in an HBO chamber (100% oxygen at 1.5 atmospheres) for 15 minutes during 20-minute bilateral occlusion; only 2 died (16% mortality rate). Thus, HBO therapy conferred significant protection against death from untreated ischemia (P less than 0.001). Histological examination showed that the extent of patchy bilateral ischemic neuronal damage was much less in surviving gerbils that received HBO therapy than in those that died after 20-minute occlusions. Fourteen gerbils were treated with DMSO, 2.5 g/kg intraperitoneally, during 5- or 10-minute bilateral CA occlusion; 12 died (86% mortality rate). Thus, DMSO provided no protection against fatal cerebral infarction; in fact, the results in the 10-minute reperfusion group suggest that DMSO may have a deleterious effect.
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PMID:Effect of hyperbaric oxygen therapy or dimethyl sulfoxide on cerebral ischemia in unanesthetized gerbils. 371 99

This study evaluates the effects of ethanol (blood levels of 200 mg/dl for one hour) and dimethyl sulfoxide (DMSO) on cerebral lesion volumes after pressure-induced focal ischemia during normotension and induced hypotension in the canine. This experimental design simulates the situation where an individual imbibes two to four alcoholic drinks over a one-hour period, then drives a motor vehicle, and suffers a head injury either without significant blood loss or where the cerebral perfusion pressure is reduced to the lower limits of autoregulation (mean arterial pressure of 50 mm Hg). Ethanol was shown to increase brain lesion volumes in both the normotensive (4.5 +/- 0.7 cm3) and hypotensive (14.9 +/- 2.2 cm3) groups when compared to controls (0.8 +/- 0.3 and 2.9 +/- 0.4 cm3, respectively). DMSO markedly attenuated this response in the normotensive and hypotensive ethanol groups. It is thought that the intermediate metabolites of ethanol provide a large source of hydroxyl-free radicals in the presence of neuronal tissue damage and that these free radicals are effectively scavenged by DMSO.
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PMID:An experimental study of craniocerebral trauma during ethanol intoxication. 375 24

Oxygen free radicals have recently been found to mediate cell injury after ischemia in the kidney. We sought to determine whether oxygen free radicals mediate damage in mercuric chloride (HgCl2)-induced acute renal failure, a toxic model of acute renal failure. Neither superoxide dismutase nor allopurinol, which scavenges or inhibits production of superoxide radical, respectively, provided protection against renal dysfunction after HgCl2. Similarly, the hydroxyl radical scavengers tryptophan, N-acetyl-tryptophan, and ascorbic acid were unable to protect against HgCl2. However, dimethylthiourea and dimethyl sulfoxide, both hydroxyl radical scavengers, were beneficial. Dimethylthiourea completely prevented the rise in plasma creatinine concentration after HgCL2. In control rats plasma creatinine concentration rose from 0.4 mg/dl to 3.2 +/- 0.8, 5.1 +/- 1.0, and 6.1 +/- 1.6 mg/dl at 24, 48, and 72 hours after HgCl2. Dimethylthiourea-treated rats had plasma creatinine concentration less than 0.5 mg/dl at all times. Furthermore, a mixture of HgCl2 and equimolar amounts of dimethylthiourea was less toxic than HgCl2 alone. Dimethyl sulfoxide attenuated the HgCl2-induced rise in creatinine concentration: 1.3 +/- 0.2, 3.2 +/- 0.3, and 3.1 +/- 0.2 mg/dl at 24, 48, and 72 hours after HgCl2. Measurement of kidney malondialdehyde content after HgCl2 provided no evidence for oxygen free radical-mediated lipid peroxidation. We conclude that there is no convincing role for oxygen free radicals in the pathogenesis of HgCl2-induced acute renal failure. The ability of dimethylthiourea and dimethyl sulfoxide to protect against HgCl2-induced renal dysfunction may be related to their ability to form complexes with Hg2+.
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PMID:Free radical scavengers in mercuric chloride-induced acute renal failure in the rat. 392 Mar 37

Subsequent to traumatic injury of the spinal cord, a series of pathophysiological events occurs in the injured tissue that leads to tissue destruction and paraplegia. These include hemorrhagic necrosis, ischemia, edema, inflammation, neuronophagia, loss of Ca2+ from the extracellular space, and loss of K+ from the intracellular space. In addition, there is trauma-initiated lipid peroxidation and hydrolysis in cellular membranes. Both lipid peroxidation and hydrolysis can damage cells directly; hydrolysis also results in the formation of the biologically active prostaglandins and leukotrienes (eicosanoids). The time course of membrane lipid alterations seen in studies of antioxidant interventions suggests that posttraumatic ischemia, edema, inflammation, and ionic fluxes are the result of extensive membrane peroxidative reactions and lipolysis that produce vasoactive and chemotactic eicosanoids. A diverse group of compounds has been shown to be effective in ameliorating spinal cord injury in experimental animals. These include the synthetic glucocorticoid methylprednisolone sodium succinate (MPSS); the antioxidants vitamin E, selenium, and dimethyl sulfoxide (DMSO); the opiate antagonist naloxone; and thyrotropin-releasing hormone (TRH). With the exception of TRH, all of these agents have demonstrable antioxidant and/or anti-lipid-hydrolysis properties. Thus the effectiveness of these substances may lie in their ability to quench membrane peroxidative reactions or to inhibit the release of fatty acids from membrane phospholipids, or both. Whatever the mode of action, early administration appears to be a requirement for maximum effectiveness.
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PMID:Spinal cord injury and protection. 392 95

The radical anions of molecular oxygen reduction, superoxide (O2), hydrogen peroxide (H2O2), and hydroxyl radical (OH), have been implicated in a number of disease processes, including ischemic bowel injury. This report evaluates the effect of superoxide dismutase (SOD), catalase (CAT), dimethyl sulfoxide (DMSO), selenium treatment, and selenium deficiency on bowel integrity and survival in experimental intestinal ischemia in rats. Ischemic bowel injury was produced in 204 male Sprague-Dawley rats (wt 90 to 100 g) by a one-minute occlusion of the superior mesenteric artery (SMA) with a microaneurysm clip. Experiment I treatment animals (n = 20) received 2.5 mg/kg SOD dissolved in Ringer's lactate, and control animals (n = 71) received Ringer's lactate alone. Experiment II treatment animals (n = 16) received 1 cc of 100% DMSO gavage, and control animals (n = 11) received no treatment. Experiment III treatment animals (n = 17) received 25 mg/kg CAT dissolved in phosphate buffered saline, and control animals (n = 11) received nothing. Experiment IV treatment animals (n = 14) received 300 micrograms of sodium selenate by gavage dissolved in deionized water, and control animals (n = 15) receiving nothing. Experiment V treatment animals (n = 20) were raised from 35 to 50 g size on a selenium deficient diet, and control animals were raised (n = 20) on a normal rat chow diet, until they weighed 100 g when ischemia was induced. At seven days, survival, incidence of bowel perforation or necrosis, and length of survival were compared in each experiment between control and treatment groups using chi 2 analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Superoxide: a critical oxygen-free radical in ischemic bowel injury. 609 60

We have previously reported that the combined administration of mannitol and perfluorochemical blood substitutes is evidently effective in protecting the brain from cerebral ischemia. This experimental study was designed to develop more effective method in suppressing brain infarction than the combined treatment of mannitol and PFC. Using the "Canine model of complete ischemic brain regulated with a perfusion method" in which it is possible to control the degree of blood flow to a cerebral hemisphere via a perfusion pump, the effect of eight agents including six kinds as the free radical scavenger on cerebral ischemia was investigated. Eight agents were mannitol, vitamin E (Vit. E), dimethyl sulfoxide (DMSO), vitamin C, glycerol, nizofenone (Y-9179), dexamethasone (Dexa.) and suloctidil (MY-103). After pretreatment with each agent, blood flow was reduced via the pump to 1/10 of the normal state and 1 hour later, return to the normal state was allowed. Subsequent changes in EEG were observed and the effects of the drugs evaluated. In the control group, no recovery of electrical activity was seen, but in six groups among eight treated groups, i.e., treated with mannitol, Vit. E, DMSO, MY-103, Y-9179 and Dexa, gradual emergence of slow waves was observed. And more favorable effects were found when the combined administration of mannitol, Vit. E and Dexa was made in the same experimental schedule as compared with the single administration of each of these drugs. Furthermore in the animals administered with PFC in combination with mannitol, Vit. E and Dexa, flattening of electrical activity could not be seen throughout the period of severe ischemia. Moreover, the power of electrical activity recovered nearly to the preischemic state immediately after recirculation. Although the possible mechanisms are not yet completely clarified, the present results are thought to indicate that this new combination therapy utilizing PFC with mannitol, Vit. E and Dexa may be useful in the treatment of cerebral ischemia.
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PMID:[Experimental study of cerebral protective effect on cerebral ischemia of various antioxidants and other agents. With special reference to the combined treatment of mannitol, vitamin E, dexamethasone and perfluorochemicals]. 632 77

Direct and empirical evidence indicates that intravenous administration of DMSO can arrest or reverse cerebral and extracerebral ischemia following experimental or clinical injury. When the delivery of oxygen and nutrients to the tissue is deficient or unavailable (as in ischemia), cell damage or death with all its attending pathological consequences becomes an end-point. In the brain, this equates to build-up of intracranial pressure, impairment of neural transmission to vital centers, and loss of function or death. We have reviewed a number of studies that show the usefulness of DMSO in preventing significant pathology from developing in various experimental injury models and in clinical subjects. We have proposed that the action of DMSO in biochemical, morphological, and functional subsystems is not specific but rather interactive. Figure 5 illustrates this point. Any one effect by DMSO on these subsystems that does not affect the others seems highly unlikely. How DMSO or similar drugs affect these systems, could provide important clues in clarifying the pathogenesis of ischemia and in reducing its severity. We conclude from the available evidence that ischemic injury is a dynamic process constantly promoting biochemical, vascular, and morphological changes and that DMSO is able to intervene at various levels of this pathochemical cascade. DMSO may do this by its ability to normalize tissue perfusion when this is lacking or impaired. We speculate that this effect by DMSO is predominantly on the PG-TX and platelet systems, since these appear to be the most important candidates implicated in vessel occlusion and spasm. It is further concluded from the available and theoretical evidence presented here, that clinical trials using DMSO in cerebral and extracerebral organ ischemia should be designed in order to evaluate the efficacy of this compound to other antithrombogenic therapies. It is reasonable to assume that DMSO may provide a primary approach to the treatment of cerebral, myocardial, renal, and platelet-induced ischemic disorders.
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PMID:Role of dimethyl sulfoxide in prostaglandin-thromboxane and platelet systems after cerebral ischemia. 634 94


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