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

Reperfusion of the globally ischemic myocardium with mannitol has been shown to preserve myocardial function. However, it remains unclear whether the mechanism of mannitol protection relates to its hyperosmolar or free radical scavenging properties. Three groups of isolated, perfused rabbit hearts underwent 45 min of normothermic ischemia without cardioplegia in an experimental paradigm analogous to the clinical situation of coronary artery thrombosis with subsequent reperfusion. Six hearts were reperfused with an isosmolar solution, eight hearts were reperfused with a mannitol-containing solution (20 mOsm/liter), and five hearts were reperfused with a solution containing additional sodium chloride (10 meq/liter, 20 mOsm/liter) to control for the hyperosmotic effects of mannitol. Left ventricular developed pressure, its derivative dP/dt, and diastolic compliance were all significantly improved in the mannitol-reperfused hearts when compared with the hypertonic saline and control groups (p less than .05). There were no intergroup differences in myocardial edema formation, oxygen consumption, or lactate production. These data indicate that mannitol reperfusion offers significant myocardial protection independent of hyperosmolar properties. Free radical scavenging activity appears to be the most credible explanation for these observations, although confirmation of this mechanism awaits further biochemical and cellular investigation.
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PMID:Preservation of myocardial function with mannitol reperfusate. 392 90

Rabbit kidneys were stored for 24 or 48 hr at 0 degree C after single-passage vascular flush with 30 ml of cold hypertonic citrate solution or 0.9% isotonic sodium chloride solution. They were then subjected to in vitro biochemical assay for evidence of free-radical damage immediately after storage or after they had been orthotopically autotransplanted and reperfused with blood in vivo for 60 min. Kidney homogenates were incubated at 37 degrees C and assayed for fluorescent conjugated Schiff bases as indicators of lipid peroxidation, as well as for superoxide dismutase activity and reduced and oxidized glutathione. In kidneys flushed with hypertonic citrate, no evidence of peroxidation could be detected immediately after storage for 24 or 48 hr. However, after in vivo reperfusion significantly more peroxidation (P less than 0.01) was evident. Storage in isotonic saline solution produced still higher levels of peroxidation damage whether reperfused or not (P less than 0.001). Schiff base formation was inversely proportional to the reduced and oxidized glutathione levels measured. No changes in superoxide dismutase levels could be detected. It is concluded that lipid peroxidation is important during cold ischemia but most damage occurs during the 60-min of reperfusion in vivo immediately after transplantation.
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PMID:Evidence of free-radical-induced damage in rabbit kidneys after simple hypothermic preservation and autotransplantation. 394 13

Fructose-1,6-diphosphate (FDP) improves survival in experimental shock. To determine if FDP would protect against single organ damage, rats pretreated with an intravenous infusion of 5% FDP were subjected to 30 minutes of bilateral renal artery occlusion. Controls received an equal volume of a dextrose and sodium chloride solution. Renal function and histology were examined in all groups 24 hours after the insult. Following ischemia, FDP-treated rats had inulin clearances (FDP 897 +/- 129 vs control 349 +/- 59 microliter/min/100 gm BW; P less than 0.01) and solute excretion rates (FDP 6,386 +/- 1,346 vs control 2,602 +/- 396 mOsm/kg/min/100 gm BW; P less than 0.05) greater than control and not different (P-NS) from sham-operated rats. Renal histology was better preserved in the FDP-pretreated group. Thus, pretreatment with FDP provides histologic and functional protection from an ischemic renal insult.
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PMID:Protection from ischemic renal injury by fructose-1,6-diphosphate infusion in the rat. 405 95

Dimethylsulfoxide (DMSO) has been advocated as a central nervous system (CNS) protectant against ischemia and trauma. The present study was performed to evaluate acute cardiovascular effects of DMSO which might complicate the clinical treatment of CNS compromised patients. Intravenously administered DMSO in doses which reportedly provide CNS protection, 2 g/kg, were infused in 6 dogs; hemodynamic variables were measured and compared to infusion of equal volumes of 0.9% sodium chloride. Immediately after infusion, DMSO caused increases in cardiac index, heart rate, pulmonary capillary wedge pressures (WP), and pulmonary arterial (systolic, mean, and diastolic) pressures which were significantly greater than changes induced by saline. DMSO decreased systematic diastolic pressure and systemic vascular resistance at the end of infusion. Most DMSO induced changes returned toward pre-infusion values 10 min after the end of infusion. These results suggest transient DMSO effects different from equal volumes of saline, possibly due to hyperosmotic expansion of plasma volume. A decrease in systemic vascular resistances was also observed. Although neither CNS production, intracranial pressure or blood flow were studied, these data suggest that DMSO used for CNS protection would not have adverse acute hemodynamic consequences. This may be particularly relevant in traumatized, hypovolemic patients.
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PMID:Acute cardiovascular effects of dimethylsulfoxide. 731 58

Vasoconstriction, as a result of mechanical manipulation of blood vessels during microsurgery, may produce a decrease in blood supply and endanger flap viability. A study was undertaken to determine the effects of the topical vasodilator calcitonin gene-related peptide on the microcirculation of flaps after mechanically induced ischemia. A neurovascular island flap based on the superficial epigastric vessels was raised in 42 rats. Blood cell flux in the flap was recorded continuously with a laser Doppler flux meter. The feeding artery was pinched to induce vasospasm, and different concentrations of calcitonin gene-related peptide (10(-7), 10(-8), 10(-9), 10(-10) mol) or a control of sodium chloride 0.9% was applied topically to relieve the ischemia. Results showed that calcitonin gene-related peptide at a concentration of 10(-7) mol significantly shortened the time to reach 50% of the original blood cell flux values (270 +/- 123 seconds) and significantly increased the number of flaps in which the blood cell flux values were restored to prestress levels within 30 minutes. The data support the conclusion that, in this model, topical calcitonin gene-related peptide at the concentration of 10(-7) mol was effective in promoting recovery of the microcirculation after mechanically induced ischemia, without the adverse effects associated with other commonly used vasodilators.
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PMID:Calcitonin gene-related peptide increases microcirculation after mechanically induced ischemia in an experimental island flap. 748 41

Forty-five ASA physical status I volunteers, divided in three groups of 15 each, received intravenous regional anesthesia (IVRA) of the upper limb with 40 mL meperidine 0.25%, lidocaine 0.5%, or 0.9% sodium chloride (isolated ischemia) by random allocation. Using a double-blind method, the onset and recovery of sensory block was tested at six sites of the forearm and hand. The onset of complete motor block was also assessed. The symptoms after deflation of the tourniquet were recorded. The onset of block, as determined by pin-prick touch, and cold was significantly faster in the meperidine group (P < 0.001) than in the saline group, but also slower (P < 0.001) than in the lidocaine group. After the tourniquet was deflated, recovery occurred in reverse order. A complete motor block was noted in all volunteers from the meperidine and lidocaine groups, but in only 11 cases from the 0.9% sodium chloride group (P < 0.01). In the meperidine group, motor block developed concomitantly or prior to sensory block. There was a significant increase in the incidence of dizziness, nausea, and pain at the injection site in the meperidine group in comparison with the lidocaine group. We conclude that meperidine has local anesthetic action on the peripheral nerve in vivo, but that its single use for IVRA should be a second choice for patients allergic to local anesthetics.
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PMID:Intravenous regional anesthesia with meperidine. 953 32

Acinar necrosis in patients with acute pancreatitis can be due to enzymatic injury, ischemia, or both. We hypothesized that novel therapy aimed at an improvement of pancreatic microcirculation early in the course of pancreatitis may reduce the lethality and acinar damage. Forty-six dextran-resistant rats received controlled intraductal infusion of glycodeoxycholic acid (10 mmol/L), followed by intravenous cerulein (5 micrograms/kg/h) for 6 hours. Beginning 30 minutes after the induction of pancreatitis, all animals were resuscitated with Ringer's lactate (RL) (8 mL/kg/h intravenously for 9 hours). In addition, they were given intra-aortic bolus infusions (2 mL/kg at 30, 60, 90, and 150 minutes) of either RL, sodium chloride (NaCl) (7.5%) and dextran 60,000 (10%) (HHS-60), NaCl (7.5%) and dextran 500,000 (10%) (HHS-500), or NaCl (0.9%) and dextran 500,000 (10%) (DEX-500). Despite high-volume fluid resuscitation in the groups that received RL and HHS-60, 70% of the animals in each of these groups died within 24 hours. In contrast, the mortality rates in the groups of animals that received HHS-500 and DEX-500 were dramatically reduced to 0% and 10%, respectively (p = 0.005, p = 0.02). Histopathologic scores for acinar necrosis were significantly lower in the group of animals that received DEX-500 (p < 0.009) compared with those that received RL and HHS-60. Finally, total amounts of trypsinogen activation peptides in ascites were significantly lower in the animals that received HHS-500 (p < 0.004) and DEX-500 (p < 0.02) compared with those that received RL and HHS-60. Rapid bolus infusion of hyperoncotic ultrahigh molecular weight dextran solution with or without hypertonic saline but not RL or hypertonic-hyperoncotic saline-dextran significantly reduced pathologic trypsinogen activation, prevented acinar necrosis, and improved survival in acute experimental pancreatitis. We speculate that a sustained improvement of pancreatic microcirculation by ultrahigh molecular weight dextran is the mechanism of action.
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PMID:Hyperoncotic ultrahigh molecular weight dextran solutions reduce trypsinogen activation, prevent acinar necrosis, and lower mortality in rodent pancreatitis. 767 89

We studied the electrophysiologic and antifibrillatory properties of MS-551 (1,3-dimethyl-6-((2-[N-hydroxy-ethyl)-3-(4-nitrophenyl) propylamino] ethylamino) 2,4(1H,3H) pyrimidinedione hydrochloride) in a conscious canine model of sudden cardiac death. Three to 5 days after surgically induced myocardial infarction (MI: 2-h occlusion of the left anterior descending coronary artery, LAD), animals were subjected to programmed electrical stimulation (PES) to identify those at risk for sudden cardiac death. MS-551 was administered (2.0, 3.0, or 4 x 2.0 mg/kg intravenously, i.v.). Vehicle-treated animals received 0.9% sodium chloride solution for injection. MS-551 (multiple-dose regimen) increased ventricular effective refractory period (VERP) from 112 +/- 4 to 137 +/- 4 ms (p < 0.05) as compared with vehicle treatment, which did not alter VERP (125 +/- 6 to 121 +/- 5 ms). MS-551 prolonged QTc interval from a predrug value of 293 +/- 8 to 333 +/- 18 ms postdrug. The size of surgically induced MI did not differ among groups: 2.0 mg/kg, 23 +/- 4%; 3.0 mg/kg, 28 +/- 2%; 4 x 2.0 mg/kg, 25 +/- 3%; and vehicle, 28 +/- 3% of the left ventricle. Single bolus administration of MS-551 (2.0 or 3.0 mg/kg i.v.) did not confer significant protection against sudden cardiac death. However, repeated administration of MS-551 protected against sudden cardiac death in 8 of 10 dogs as compared with 2 of 12 in the vehicle-treated group (p < 0.05). The data indicate that a multiple-dose regimen of MS-551 provides protection against ischemia-induced ventricular fibrillation (VF) in the postinfarcted heart. The mechanism by which MS-551 achieves its antifibrillatory effect most likely depends on its ability to prolong VERP of myocardium without altering ventricular conduction velocity.
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PMID:MS-551 protects against ventricular fibrillation in a chronic canine model of sudden cardiac death. 775 58

The objective of this study was to test the hypothesis that ischemia reperfusion damage in kidney transplantation is associated with lipid peroxidation and that inhibition of lipid peroxidation by antioxidants improves the function of the transplanted kidney. Lipid peroxidation was assessed by measuring the plasma malonaldehyde content (as thiobarbituric acid reaction product) with high-performance liquid chromatography. Kidney function was assessed by plasma creatinine and creatinine clearance. Thirty patients of an ongoing series were randomly selected into two groups, with 14 controls and 16 patients in the antioxidant therapy group. Therapy consisted of two ampoules of Omnibionta (which contains vitamins C, E, A and B complex) diluted in 500 ml physiological sodium chloride, which was infused intravenously prior to reperfusion onset. No significant differences existed for the age of the patients in the control (43.00 +/- 9.86 years) and the therapy group (41.56 +/- 14.14 years) nor in the kidney preservation time, which was 24.12 +/- 8.73 and 18.43 +/- 9.97 hours in the control and therapy group, respectively. The controls showed a transient increase of plasma lipid peroxides as measured by malonaldehyde with a peak one hour after onset of reperfusion. Compared to the baseline value of 0.74 +/- 0.26 (mean +/- SD) the one hour malonaldehyde value increased to 1.46 +/- 0.22 nmol/ml (P < 0.001). In the therapy group the plasma malonaldehyde level did not increase, but slightly decreased by about 20% compared to the baseline value. The difference of plasma malonaldehyde between the two groups one hour after reperfusion onset was highly significant (P > 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A multivitamin infusion prevents lipid peroxidation and improves transplantation performance. 847 29

The electrophysiologic and antifibrillatory properties of 5-hydroxydecanoate, a KATP channel antagonist, were studied in a conscious canine model of sudden cardiac death. After a surgically induced myocardial infarction, animals were subjected to programmed electrical stimulation to identify those at risk for sudden cardiac death. 5-Hydroxydecanoate was administered as a bolus (10 mg/kg i.v.) followed by an infusion, 10 mg/kg/h (group 1, n = 12) or 30 mg/kg bolus followed by an infusion, 30 mg/kg/h (group 2, n = 8) i.v., while vehicle treated animals received a 0.9% sodium chloride solution (group 3, n = 11). The administration of 5-hydroxydecanoate did not alter the ventricular effective refractory period or the QTc interval. Anterior wall myocardial infarcts, expressed as a percentage of the left ventricle, did not differ among groups. Infusions of 5-hydroxydecanoate did not confer significant protection from sudden cardiac death (death within 60 min of posterolateral ischemia) due to ventricular fibrillation: group 1, 50%; group 2, 38%; and group 3, 18%. The data demonstrate that a continuous infusion of 5-hydroxydecanoate (10 and 30 mg/kg/h, i.v.) does not provide protection from ischemia-induced ventricular fibrillation in the postinfarcted conscious canine.
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PMID:5-hydroxydecanoate fails to attenuate ventricular fibrillation in a conscious canine model of sudden cardiac death. 881 21


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