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)

Hepatic ischemia hinders the proliferative response of hepatocytes, necessary to restore the liver/body ratio after liver resection/transplantation. Folinic acid administered during the ischemic period following 70% hepatectomy plus 15 min of normothermic liver ischemia has restored the regenerative response to the levels of normoperfused livers. This unexpected finding has guided us to design the present study in order to find out whether the folinic acid is an hepatotrophic substance or not. Sprague-Dawley rats submitted to partial (40 or 70%) hepatectomies were used. Saline (2 cc) or folinic acid (2.5 mg/kg) have been administered i.v. Forty-eight hours after hepatectomy the hepatocyte's DNA content has been assessed by means of a cytophotometric technique, and the percentage of regenerating hepatocytes (PRH) has been calculated. Folinic acid administration has significantly increased the PRH in both resting (5.1 vs 1.2) and regenerating livers (70% hepatectomy) (22.2 vs 41) when compared with nontreated groups. Folinic acid administration after liver ischemia plus hepatectomy has shown similar results, corroborating our previous study. Although its mechanisms of augmentation of liver regeneration remain unclear and further studies are required, folinic acid seems to be a promising therapeutic tool in liver surgery.
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PMID:Hepatotrophic effect of folinic acid in rats. 865 37

We determined whether U-89232, a derivative of the ATP-sensitive potassium (KATP) channel opener cromakalim, is cardioselective and whether its action on the myocardium is still sensitive to glibenclamide. Experiments were performed in open-chest pigs subjected to a 60-min occlusion of the left anterior descending coronary artery (LADCA) and to 2 h of reperfusion. Four groups of animals were studied (n = 6 each). Animals received either U-89232, 3 mg/kg i.v. over a 15-min period (U), or glibenclamide, a selective KATP channel blocker, 1 mg/kg i.v. over a 15-min period (GLI) before the LADCA occlusion. In the GLI + U group, first glibenclamide (1 mg/kg/15 min) and then U-89232 (3 mg/kg/15 min) were infused before the 60 min of ischemia. Saline-treated animals served as controls (CON). Hemodynamic parameters were continuously monitored. Regional contractile wall function was quantified with ultrasonic crystals aligned to measure wall thickening. At the end of the protocol, infarct size (IS, as percentage of risk region) was determined by incubating the myocardium with p-nitrobluetetrazolium. With comparable myocardium at risk, infusion of U-89232 before 60 min of LADCA occlusion significantly reduced infarct size (IS, 18.5 +/- 3.7%; p < 0.001 vs. 63.2 +/- 3.3% for the controls), whereas glibenclamide had no effect on infarct size (IS, 69.5 +/- 4.4%). The administration of glibenclamide before U-89232 infusion blocked the infarct size-reducing effect of U-89232 [IS, 61.2 +/- 9.1 (NS) vs. controls and p < 0.001 vs. U]. Infusion of U-89232 had no effect on hemodynamic parameters or on regional wall function. At least in a pig model, U-89232 appears to be a cardioselective KATP channel opener, because in the absence of hemodynamic alterations, it exhibits a profound cardioprotective effect, which is fully reversible by blocking KATP channels.
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PMID:In swine myocardium, the infarct size reduction induced by U-89232 is glibenclamide sensitive: evidence that U-89232 is a cardioselective opener of ATP-sensitive potassium channels. 900 73

The aim of the study was to determine whether the induction of HSP70 by Zn2+ is able to protect the small bowel of rats against ischemia. Twenty-four male Wistar rats (weight 200-300 g) were divided into four groups: (1) saline treatment for 24 h (n = 4); (2) Zn2+ treatment for 24 h (n = 4); (3) Saline pretreatment for 24 h and ischemia (n = 8); (4) Zn2+ pretreatment for 24 h and ischemia (n = 8). Pretreatment with Zn2+ was carried out by intraperitoneal administration of 50 mg/kg zinc bis (DL-hydrogen aspartate) = 10 mg/kg Zn2+. Ischemia in a defined segment of the small bowel was produced by ligation of the mesenteric vein and artery and ligation of both ends of the segment. Tissue samples were collected before and 2, 4 and 6 h after ligation and investigated by histology, immunohistochemistry and Western blotting. Twenty-four h after i.p. Zn2+ injection, the small bowel expressed increased HSP70 tissue levels. Histology with subsequent grading of ischemic tissue injury showed significantly decreased tissue necrosis after Zn2+ pretreatment and HSP70 induction compared with saline pretreated controls. In conclusion, this study proves that Zn2+ is inducing HSP70 in the small bowel in vivo and hereby able to protect the small bowel against ischemia.
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PMID:Induction of heat shock protein 70 (HSP70) by zinc bis (DL-hydrogen aspartate) reduces ischemic small-bowel tissue damage in rats. 904 56

Selegiline (L-deprenyl) has shown neuroprotective effects in a variety of degenerative processes. The present experiments were designed to test whether post-ischemia administered selegiline would alleviate delayed neuronal death of the gerbil hippocampal pyramidal cells following transient global ischemia. Common carotid arteries were occluded for 5 min. Saline or selegiline, 0.25 mg/kg s.c., was administered 2 h after the ischemia followed by a daily injection for either 3 or 7 days. After decapitation, the delayed death of the hippocampal CA1 pyramidal cells was assessed using Nissl-stained sections. In situ hybridization was used to reveal the expression of hsp70 mRNA 1, 3 or 7 days after the ischemia. Animals treated with selegiline for 7 days showed significantly lower damage score (scale 0-3: 0, normal; 1, < 10% of the neurons damaged; 2, 10-50% damaged; 3, > 50% damaged) compared to the saline-treated animals 1.73 +/- 0.18 and 2.41 +/- 0.16 (mean +/- S.E.M., P = 0.0133), respectively. A similar trend was found in animals after the 3-day treatment: 1.68 +/- 0.32 vs. 2.06 +/- 0.25 (P > 0.5). The expression of hsp70 mRNA in the CA1 pyramidal cell layer was strong still 3 days after the ischemic insult but vanished by 7 days. Densitometric measurements using 14C-plastic standards showed that the intensity of the CA1a hsp70 signal on the 3rd day correlated negatively to the cell-damage score (r = -0.72, P < 0.001), suggesting that hsp70 does not serve as a quantitative marker for CA1 neuronal injury in this model. Instead, the hsp70 expression was associated with improved neuronal survival lasting often longer in selegiline-treated animals (P > 0.5). The results show that a low dose of selegiline can alleviate the delayed hippocampal neuronal death in gerbils when administered 2 h after an ischemic insult.
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PMID:Selegiline treatment after transient global ischemia in gerbils enhances the survival of CA1 pyramidal cells in the hippocampus. 920 Jul 55

OG-VI is a solution composed of 30 mM inosine, 30 mM sodium 5'-guanylate, 30 mM cytidine, 22.5 mM uridine, and 7.5 mM thymidine, expecting to use for total parenteral nutrition. We examined the effect of OG-VI on myocardial contractile dysfunction during reperfusion after ischemia (myocardial stunning) in dogs. Pentobarbital-anesthetized dogs were subjected to 20-min left anterior descending coronary artery ligation followed by 30-min reperfusion. Saline, OG-VI or its constituents [inosine and sodium 5'-guanylate mixture (IG), and cytidine, uridine, and thymidine mixture (CUT)], or 5-amino-4-imidazole carboxamide riboside (AICAr) was infused at 0.1 mL.kg-1.min-1, starting 30 min before the ischemia. The contractile function was determined by ultrasonometry and assessed as % segment shortening (%SS). %SS was markedly decreased by ischemia, and returned toward pre-ischemic level after reperfusion, although the recovery was incomplete. The %SS was almost completely recovered by OG-VI and IG, and to a lesser extent by AICAr; CUT was ineffective. In the presence of 1 mg.kg-1 of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, a selective adenosine A1 receptor antagonist), cardioprotective effect of OG-VI on stunned myocardium was still observed. In conclusion, infusion of OG-VI improved myocardial contractile dysfunction in stunned myocardium. This effect was more potent than its constituents and AICAr. Adenosine A1 receptors are not involved in the mechanism.
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PMID:Limitation of stunning in dog myocardium by nucleoside and nucleotide mixture, OG-VI. 922 40

The aim of this study was to investigate the angiogenic response to exogenously administered basic fibroblast growth factor (FGF-2) in normal and ischemic skin, using the hairless mouse ear microcirculatory model. The hairless mouse ear is a well-established model for in vivo studies of skin microcirculation. Using this model, angiogenesis- and angiogenesis-associated changes in the microcirculation can be directly and continuously viewed and quantified in a variety of different experimental settings. To create ischemia in the mouse ear, all but one of the three to four feeding vessels nourishing the ear were ligated 3 days prior to a local subdermal injection of FGF-2 (9.3 + 1-0.5 mm/mm2) or saline into the dorsum of the ears. Angiogenesis was quantified by direct observation, at high magnification, of the injection site where increases in total vessel length (TVL) were measured repeatedly over 18 days following injection. We found a significant (P < 0.01) increase in TVL in normal and ischemic ears injected with FGF-2. Saline injection also induced a significant increase in TVL in ischemic ears. However, the angiogenic response to FGF-2 in ischemic ears was significantly stronger than saline alone in ischemic ears or saline or FGF-2 in normal ears. This response could be used clinically to accelerate angiogenesis and thus increase perfusion in ischemic tissue.
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PMID:Ischemia increases the angiogenic potency of basic fibroblast growth factor (FGF-2). 939 66

The effects of hypothermia on production of nitric oxide (NO) in ischemic brain were investigated by using in vivo microdialysis. Male Wistar rats were randomly divided into three groups; saline-treated normothermic group (37 degreesC, n=6), 30 mg/kg N-nitro-l-arginine methyl ester(l-NAME)-treated normothermic group (n=6), and saline-treated hypothermic group (30 degreesC, n=6). Transient forebrain ischemia was produced by bilateral common carotid artery occlusion combined with hypotension (MABP=50 mmHg). Saline-treated normothermic animals resulted in a reduction of LCBF to 9% of baseline. Saline-treated hypothermic rats revealed the similar changes of LCBF. In contrast, l-NAME administration reduced the basal CBF to 85% of saline-treated group and to 8% after ischemia. NO products were decreased during ischemia and transiently increased after reperfusion in saline-treated groups. However, the increase of NO products after reperfusion was less significant in the hypothermia. l-NAME-treated group showed a constant reduction of NO production during ischemia and after reperfusion.
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PMID:Consecutive in vivo measurement of nitric oxide in transient forebrain ischemic rat under normothermia and hypothermia. 976 79

We asked whether crystalloid administration improves tissue oxygen extraction in endotoxicosis. Four groups of anesthetized pigs (n = 8/group) received either normal saline infusion or no saline and either endotoxin or no endotoxin. We measured whole body (WB) and gut oxygen delivery and consumption during hemorrhage to determine the critical oxygen extraction ratio (ERO2 crit). Just after onset of ischemia (critical oxygen delivery rate), gut was removed for determination of area fraction of interstitial edema and capillary hematocrit. Radiolabeled microspheres were used to determine erythrocyte transit time for the gut. Endotoxin decreased WB ERO2 crit (0.82 +/- 0.06 to 0.55 +/- 0.08, P < 0.05) and gut ERO2 crit (0.77 +/- 0.07 to 0.52 +/- 0.06, P < 0.05). Unexpectedly, saline administration also decreased WB ERO2 crit (0.82 +/- 0.06 to 0.62 +/- 0.08, P < 0.05) and gut ERO2 crit (0.77 +/- 0.07 to 0.67 +/- 0.06, P < 0.05) in nonendotoxin pigs. Saline administration increased the area fraction of interstitial space (P < 0.05) and resulted in arterial hemodilution (P < 0.05) but not capillary hemodilution (P > 0.05). Saline increased the relative dispersion of erythrocyte transit times from 0.33 +/- 0.08 to 0.72 +/- 0.53 (P < 0.05). Thus saline administration impairs tissue oxygen extraction possibly by increasing interstitial edema or increasing heterogeneity of microvascular erythrocyte transit times.
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PMID:Effect of crystalloid administration on oxygen extraction in endotoxemic pigs. 980 68

Oxygen metabolites formed during reperfusion of ischemic kidneys prevent recovery of renal function after short periods of renal ischemia. The administration of ATP-MgCl2 is beneficial to the survival of animals after hemorrhagic shock, severe burns, septicemia-peritonitis, post-ischemic hepatic failure, bowel ischemia, and endotoxic shock. In this study, the effect of ATP-MgCl2 on lipid peroxidation and its curative effect were evaluated by measuring the decomposition products of lipid peroxidation, detected as thiobarbituric-acid reactive substances in homogenized kidney tissues in ischemic and reperfused rabbit kidneys. Ischemia was performed by clamping the right renal artery for 60 minutes followed by 30 minutes of reperfusion. Thirty-six rabbits were classified into 6 groups containing 6 rabbits in each. In the first group, no renal ischemia-reperfusion (I-R) was designed (Sham group), the right kidney was removed 90 minutes later. In the second group, I-R was established but nothing given. Saline 0.25 cc/kg was given into the right renal artery in group 3 two minutes before ischemia, and in group 4 two minutes before reperfusion. ATP-MgCl2 17.5 mumol/kg (0.25 cc/kg) was given two minutes before ischemia in group 5, and before reperfusion in group 6. The right kidneys of the rabbits were removed and thiobarbituric-acid reactive substances in the homogenates were measured. In addition, histopathological evaluation was performed. High lipid peroxidation products were recorded in groups 2-5, whereas in group 6, these levels were low similar to those obtained in Sham group (76.72 +/- 1.01 nmol/g tissue). On histopathological evaluation, a considerable cell damage resulting from I-R trauma especially in proximal tubules was observed. In groups which were under saline effect, no histopathological damage was found. Histophatological preservation was better in group 6 rather than in group 5. The results of this study indicate that ATP-MgCl2 is remarkably effective for preventing the lipid peroxidation if given before reperfusion but not before ischemia in experimental I-R injury in rabbit kidneys.
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PMID:The effect of ATP-MgCl2 on lipid peroxidation in ischemic and reperfused rabbit kidney. 1020 3

The effects of blood sugar level on transient focal brain ischemia were examined by consecutive diffusion-weighted EPI and (1)H echo planar spectroscopic imaging. A remote-controlled rat intraluminal suture middle cerebral artery occlusion (MCAO) model was prepared. Animals were divided into three experimental groups: control, 1 g/kg, and 2 g/kg glucose groups (n = 6 for each). Saline or glucose was infused intraperitoneally 30 min prior to MCAO. The glucose-loaded groups showed increased lactate accumulation and marked decreases in average diffusion coefficient in the ischemic region during 40-min MCAO. These changes were correlated with blood sugar levels at the onset of MCAO. After reperfusion, all rats in the control and 1 g/kg groups recovered from the ischemic changes, but three rats with marked hyperglycemia in the 2 g/kg group showed irreversible changes. The adverse effects of hyperglycemia on transient focal brain ischemia were clearly demonstrated by sequential 2D images. Magn Reson Med 42:895-902, 1999.
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PMID:Effects of blood sugar level on rat transient focal brain ischemia consecutively observed by diffusion-weighted EPI and (1)H echo planar spectroscopic imaging. 1054 48


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