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)

The purpose of the present study was to determine whether Na(+)-H+ and Na(+)-Ca2+ exchanges modulate postischemic recovery of excitation-contraction coupling. Experiments were performed in 43 isolated isovolumic dog hearts perfused with blood (pH 7.40, 141 mmol/L Na+, 34 degrees C, paced at 2 Hz). A 3 x 3-mm region at the left ventricular (LV) apex was loaded with aequorin for monitoring [Ca2+]i simultaneously with LV pressure. No-flow ischemia for 2 to 3 minutes was followed by 20 minutes of aerobic reperfusion with (1) unmodified control blood (141 mmol/L Na+, pH 7.40), (2) acidemic blood (141 mmol/L Na+, pH 6.60, at 0 to 3 minutes of reperfusion), (3) hypernatremic blood (149 or 157 mmol/L Na+, pH 7.40, at 0 to 20 minutes of reperfusion), or (4) hyperosmotic blood (141 mmol/L Na+ + 30 mmol/L mannitol, pH 7.40, at 0 to 20 minutes of reperfusion). Reperfusion with unmodified control blood was immediately followed by an increase in [Ca2+]i and LV systolic and diastolic pressure that persisted for 2 to 3 minutes before returning to or below baseline. Ventricular arrhythmia occurred during this period (> 80%). This transient increase of [Ca2+]i was attenuated by acidemic or hypernatremic perfusate. With acidemic or hypernatremic reperfusion, recovery of LV developed pressure at 20 minutes was more complete than with unmodified control reperfusion: acidemic blood (n = 7), 93 +/- 3% (P < .01); hypernatremic blood (149 mmol/L Na+, n = 7), 89 +/- 2% (P < .02); hypernatremic blood (157 mmol/L Na+, n = 4), 91 +/- 2% (P < .01); and unmodified control blood (n = 17), 80 +/- 2%. With hyperosmotic reperfusion, recovery of LV developed pressure at 20 minutes was not improved (82 +/- 3%). From these results we conclude that (1) an increase in intracellular Ca2+ occurs transiently after no-flow ischemia and may cause arrhythmia and decreased Ca2+ responsiveness of the contractile elements, (2) acidemic and hypernatremic reperfusion ameliorates postischemic dysfunction by preventing the increase in intracellular Ca2+, suggesting that (3) Na(+)-H+ and Na(+)-Ca2+ exchange may play important modulatory roles during reperfusion.
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PMID:Acidemia and hypernatremia enhance postischemic recovery of excitation-contraction coupling. 818 86

Pharmacologic manipulation of free flaps to enhance tolerance to ischemia has become a subject of great interest in the research literature. In an effort to improve survival, perfusion washout of experimental free flaps was performed following an episode of primary ischemia. The perfusates utilized were lactated Ringer's solution (LR), University of Wisconsin solution (UW), a high-molecular-weight medium used in organ preservation, and urokinase, a thrombolytic agent. Seventy-five rats were used in this study and divided into groups of 5 each. A 3 x 6-cm abdominal free flap based on the superficial inferior epigastric vessels was raised in each rat. The free flaps were subjected to either 12 or 18 hr of primary ischemia. Following the period of ischemia, perfusion washout was performed with either LR, UW solution, or urokinase at increasing concentrations alone or in combination with UW solution. Urokinase was first evaluated as a perfusate alone at increasing concentrations. In the 12-hr ischemia group, free-flap survival was shown to increase from 0 percent in the LR-perfused flaps to 20 percent, 60 percent, and 80 percent in flaps perfused with 12,500, 25,000, and 100,000 U of urokinase, respectively (p < 0.05). A similar increase in survival was demonstrated in the 18-hr ischemia group, where 0 percent, 20 percent, and 40 percent of flaps survived following perfusion with 12,500, 25,000, and 100,000 U of urokinase, respectively (p < 0.05). Urokinase was then perfused along with UW solution to evaluate the combined effect on flap survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The additive beneficial effect of UW solution and urokinase on experimental microvascular free-flap survival. 851 98

We detected the delayed accumulation of 45Ca in the lateral part of the striatum 3 days after distal middle cerebral artery (MCA) occlusion in stroke-prone spontaneously hypertensive rats (SHRSP). However, the mechanism of delayed neuronal damage in the striatum, which is not supplied by the occluded MCA, remains unknown. The aim of this study was to evaluate whether the delayed damage involves alterations in the extracellular release of neurotransmitter monoamines and amino acids. Chronological changes in the distribution of neuronal damage were determined by 45Ca autoradiography. The microdialysis probes were inserted into either the medial or lateral part of the striatum. The dialysate content of monoamines, their metabolites and amino acids was determined by analytical techniques. 45Ca accumulation was detected only in the cortex and corpus callosum by 24 hours postischemia and extended to the pyramidal tract, thalamus and lateral portion of the striatum by 3 days. A 3-fold increase in glutamate content, and a 2-fold increase in dopamine content were observed only in the lateral part of the striatum following ischemia. The results suggest that excessive release of glutamate and dopamine is related to delayed neuronal damage that occurs in the lateral part of the striatum in this ischemic model.
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PMID:Delayed neuronal damage following focal ischemic injury in stroke-prone spontaneously hypertensive rats. 887 Jul 96

Glibenclamide has been shown to prevent ischemia-induced shortening of action-potential duration (APD) and to prolong effective refractory period (ERP). Glibenclamide also has been shown to prolong APD under normal conditions. The aim of this study was to test the hypothesis that glibenclamide would prolong APD and ERP in the nonischemic heart by blocking adenosine triphosphate-sensitive K+ (K(ATP)) channels in myocardium, thus reducing defibrillation energy requirements. Hearts from 15 adult male New Zealand White rabbits, weight 3.1 +/- 0.1 kg, were perfused with a Krebs-Henseleit solution containing either no drugs (five hearts) or glibenclamide (10 hearts) at six concentrations ranging from 30 nM to 10 microM. Two 140-mm2 Pt-Ir mesh patch electrodes were sutured onto the ventricles. A 3.5/2.5-ms biphasic pulse (impedance, 95 +/- 16 omega) with randomly selected voltages of 20, 30, 50, 70, 90, or 110, defibrillated the heart after 10 s of fibrillation. The APD, ERP, fibrillation threshold (FT), and defibrillation threshold (DFT) were determined from monophasic action potentials, computer-controlled pacing, 50-Hz sinusoidal pacing, and multiple defibrillation shocks, respectively. Defibrillation thresholds were determined from a total of 180 fibrillation and defibrillation sequences, conducted in each preparation, and the results were fitted to a sigmoid dose-response curve by logistic regression analysis. Five repeated observations of APD, ERP, FT, and DFT showed no change over a 5-h period, whereas for DFT, there was a significant increase between first and next four determinations. With glibenclamide (100 and 300 nM, and 1 and 10 microM), a dose-dependent difference (p < 0.05) compared with controls was observed. There was an increase in APD, ERP, and FT and a decrease in DFT at 50% success (V50). The maximal effect for each parameter occurred at 300 nM. Glibenclamide dose-dependently reduced DFT and increased FT in an isolated nonischemic rabbit heart preparation. A probable mechanism is through APD and ERP prolongation by blocking ATP-sensitive K+ channels, suggesting that these channels may be important in modifying the APD and ERP during electrical defibrillation. This might be of particular interest in reducing electrical-defibrillation thresholds, thereby minimizing heart damage.
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PMID:Reducing electrical defibrillation thresholds with glibenclamide in an isolated rabbit heart preparation. 938 39

The purpose of this study was to determine whether depletion of circulating neutrophils, using an antineutrophil monoclonal antibody (RP3), would attenuate ischemia/reperfusion injury in rat skeletal muscle. A 3- and 5-hr period of ischemia was induced unilaterally into the hindlimbs of rats; the isolated limbs were then reperfused for 24 hr after ischemia. The gastrocnemius muscle was then removed, and blood was taken simultaneously. The hematologic parameters were measured, muscle neutrophil sequestration was assessed by myeloperoxidase (MPO) activity, free radical production was evaluated by the tissue lipid peroxides (LPO) levels, muscle viability was assessed by tissue levels of adenosine triphosphate (ATP) and creatine phosphate (PCr) levels, and muscle wet/dry weights were determined. Treatment with RP3 selectively and sufficiently depleted the circulating neutrophil population, markedly reduced MPO, and significantly attenuated LPO and the tissue water content after both 3- and 5-hr of ischemia. After 3 hr of ischemia, ATP and PCr levels were significantly increased by neutrophil depletion; however, after 5 hr of ischemia, the same effect was not demonstrated. These results suggest that neutrophil depletion after 3 hr of ischemia restrains free radical production and edema formation, and also attenuates skeletal muscle ischemia reperfusion injury; however, after 5 hr of ischemia, ischemic damage was so severe, that neutrophil depletion did not reduce ischemia reperfusion injury.
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PMID:Selective neutrophil depletion with monoclonal antibodies attenuates ischemia/reperfusion injury in skeletal muscle. 952 29

Deletions in the mitochondrial DNA (mtDNA) of Balb/c mouse cerebrums, resembling deletions found in elderly humans or in patients with certain disorders, were detected by PCR. Analysis was carried out on mice of various ages and on mice in which the bilateral common carotid arteries had been incompletely ligated to reconstruct cerebral ischemia. A 3,867 bp mtDNA deletion was present only in old or ischemic mouse groups. Among the non-ischemic groups, it was found in 0 of 12 weaning, 0 of 12 young, and four of eight old mice. Among the ischemic groups, it was found in 12 of 17 young and 11 of 11 old mice. Moreover, the percentage of total mtDNA containing deletions was 22% for the old non-ischemic group, 37% for the young ischemic group, and 69% for the old ischemic group. In addition, PCR analysis detected two other deletions of 3,726 bp and 4,236 bp in 4 of the 11 old ischemic cerebrums. The results indicate that mtDNA deletions are associated with aging, that ischemia increases the incidence of mtDNA deletions, and that mtDNA deletions resulting from ischemia are more likely to occur in old mice than in young mice.
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PMID:Mitochondrial DNA deletions are associated with ischemia and aging in Balb/c mouse brain. 1073 47

Dialysis access induced limb ischemia (DAILI) is a rare complication after the creation of an arteriovenous fistula in infancy but can cause irreversible ischemic limb damage in severe cases. The incidence of DAILI is higher in bridge graft fistulas than in native fistulas. DAILI patients may be managed by surgically reducing the volume flow in the fistula. However, in the pediatric age group, such a reduction of volume flow may result in thrombosis or an inadequate flow for effective dialysis. Several methods have been described to achieve the delicate balance between essential flow in the fistula and adequate limb perfusion pressure. We have developed a new method employing preoperative duplex ultrasonography to predict quantitatively the reduction in volume flow in the fistula that will allow effective dialysis while providing adequate limb perfusion. The preoperative assessment was reproduced on the operating table using intraoperative duplex. A 3-year-old girl thus treated has had resolution of her ischemic symptoms and maintains long-term patency of her dialysis access.
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PMID:Dialysis access induced limb ischemia corrected using quantitative duplex ultrasound. 1140 14

We investigated the roles of A1, A2A, or A3 receptors and purine salvage in cardioprotection with exogenous adenosine, and tested whether A2A -mediated reductions in perfusion pressure modify post-ischemic recovery. Treatment with 10(-5) or 5 x 10(-5) M adenosine improved contractile recovery from 20 min ischemia 45 min reperfusion in isolated mouse hearts. Protection was attenuated by adenosine kinase inhibition (10(-5) M iodotubercidin) and receptor antagonism (5 x 10(-5) M 8-rho-sulfophenyltheophylline, 8-SPT). Enzyme efflux mirrored contractile recoveries. A 3 agonism with 10(-7) M 2-chloro- N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA) improved ischemic tolerance whereas A1 agonism with 5 x 10(-8) M N6-cyclopentyladenosine (CPA) and A2A agonism with 10(-9) M 2-[p-(2-carboxyethyl) phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS21680) or 2 x 10(-8) M methyl-4-(3-[9-[4S,5S,2R,3R)-5-(N-ethylcarbamoyl)-3,4-dihydroxyoxolan-2-yl]-6-aminopurin-2-yl)]prop-2-ynyl) cyclohexane-carboxylate (ATL-146e) were ineffective. Protection via A1 receptor overexpression was enhanced by adenosine, but unaltered by A1 or A2A agonists. Finally, post-ischemic dysfunction in hearts perfused at constant flow was dependent on coronary pressure, with A2A AR-mediated reductions in pressure reducing diastolic contracture, and elevated perfusion pressure worsening contracture. Data indicate that cardioprotection with exogenous adenosine in asanguinous hearts involves purine salvage and activation of A3 but not A1 or A2A receptors.
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PMID:Adenosine-mediated cardioprotection in ischemic-reperfused mouse heart. 1174 34

A previous study demonstrated that continuous enteric luminal perfusion of fetal bovine serum (FBS) protects the small intestine from total ischemia/reperfusion injury (IRI) and increases the intestinal mass. In this study, we further investigated the changes in plasma interleukin-8 (IL-8) level caused by total ischemia/reperfusion of the small intestine and the effect of FBS on plasma IL-8 levels. A 3-h total ischemia was induced in a 15-cm segment of terminal ileum and then reperfusion was instituted. Luminal perfusion of FBS was conducted via an osmotic minipump connected to the stomach through a fine polyethylene tube, starting 3 days prior to total ischemia. The rats were killed after 10 and 30 min and 1 and 3 h of total ischemia, and 1, 6, and 12 h or 1, 2, and 3 days after initiation of reperfusion. Plasma IL-8 was measured by enzyme-linked immunosorbent assay. The results were compared among the FBS-treated and untreated groups. The plasma IL-8 level was elevated from 1 h of total ischemia to 6 h after initiation of reperfusion ( P< 0.05) with a peak of 641.5 +/- 36.9 pg/ml in the untreated group and 471.6 +/- 42.2 pg/ml in the treated group. Luminal perfusion of FBS significantly suppressed plasma IL-8 levels after 1 h of total ischemia and 1 h after initiation of reperfusion ( P< 0.05). The results suggest that FBS might play a role in the treatment of total IRI of the small intestine.
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PMID:Suppression of elevated plasma interleukin-8 levels due to total ischemia and reperfusion of the small intestine by luminal perfusion with fetal bovine serum. 1195 73

We present an angiographic feature of anoxic encephalopathy in the acute phase. A 68-year-old woman suddenly presented with deep coma. Examinations of her blood and electrocardiography did not reveal the origin of consciousness disturbance, and computed tomographic (CT) scans demonstrated no significant findings. We immediately performed cerebral angiography because we suspected brain stem infarction. A 3-vessel study (bilateral carotid and left vertebral angiography) revealed remarkable delays in cerebral circulation time or arteriovenous circulation time, although it did not show occlusion of cerebral vessels. The follow-up brain magnetic resonance (MR) images revealed anoxic encephalopathy, which might be derived from transient cardiac arrest. The patient has been in a vegetative state for one year. Although many reports have described CT scans and MR images of anoxic encephalopathy in the acute or subacute phases, there have been no reports about the angiographic features. We found remarkable delays in cerebral circulation time in the acute phase of anoxic encephalopathy, which was considered to be caused by cytotoxic edema from severe hypoxia or ischemia.
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PMID:[Angiographic features of anoxic encephalopathy in the acute phase: a case report]. 1472 39


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