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)

In the present study, we quantified the biochemical [thiobarbituric acid (TBA) reactants, superoxide dismutase (SOD) and vitamin E] and histologic changes in the small intestinal tissue after ischemia and/or reperfusion. Sixty-seven Wistar rats were divided into 7 groups; N group: control, A-I group: 30 min. ischemia, A-II group: 120 min. ischemia, B-I group: Declamp after 30 min. ischemia, B-II group: 30 min. reperfusion after 30 min. ischemia, B-III group: 30 min. reperfusion after 120 min. ischemia, E group: vitamin E administration 30 min. reperfusion after 30 min. ischemia. The levels of TBA reactants were significantly different between A-II and B-II, B-II and E (all p less than 0.01). For SOD, there were significant differences between N and B-I (p less than 0.01), N and E (p less than 0.05). For vitamin E, there were significant differences between A-I and B-I, A-I and B-I, B-II and E (all p less than 0.01). Histologic changes showed that the grade of tissue injury was more severe in B-I and B-II than in A-I, and was less in E than in B-II. It is suggested that vitamin E protected cells from injury due to oxygen free radicals.
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PMID:[Experimental studies on the effects of alpha-tocopherol in small intestinal ischemia and reperfusion injury]. 163 Apr 35

Evidence suggests that physical activity is related to lower coronary risk factors in middle-aged subjects, but to date data are lacking for older persons. A total of 32 healthy male subjects in their seventh decade (64 +/- 3 years) were divided into 2 groups based on maximal exercise tests (Bruce protocol). Group I consisted of 14 individuals who showed "excellent" work capacity (exercise duration of greater than or equal to 10 min, 11 +/- 1 min), and Group II 18 individuals with "fair" work capacity (7.5 +/- 1 min). None of them showed ECG evidence of ischemia in these tests. As compared with Group II, Group I showed lower casual and 24 hour ambulatory blood pressure (136 +/- 21 vs 114 +/- 11 mmHg for the average daily systolic pressure respectively), higher apo A-I levels (116 +/- 36 vs 139 +/- 20 mg/dl) and lower apo B/A-I ratios. There was no significant difference in triglycerides, total and HDL cholesterol or apo-B levels between these two groups. Body mass index and smoking habits were similar in Groups I and II. These results suggest that even in older persons, excellent physical fitness is related to lower cardiovascular risk factors.
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PMID:[Relationship between exercise endurance capacity and cardiovascular risk factors in seventh decade subjects]. 204 60

Immediately after hepatic reperfusion in human orthotopic liver transplantation, high amounts of arginase are released from the graft, thereby influencing nitric oxide metabolism. This metabolic alteration may be one component of the ischemia-reperfusion syndrome in OLT with its hemodynamic disturbances (e.g., systemic hypotension, pulmonary hypertension). The aim of this study was to compare hemodynamic and metabolic changes following OLT in the pigs with those obtained under arginase infusions in catheterized, anesthetized pigs. Following liver revascularization in the pigs, plasma arginase concentrations increased from 48 +/- 19 IU/L to 2613 +/- 944 IU/L, resulting in a drop in plasma levels of L-arginine (-87%) and in a drop in nitrite (-82%) and nitrate (-53%) concentrations. Of the measured organ-specific hemodynamic alterations, the mean pulmonary arterial pressure increased from 17 +/- 2 mmHg to 30 +/- 5 mmHg, whereas the flow/pressure index of the portal vein decreased about 60%. A primed continuous infusion of arginase (25,000 IU) increased plasma arginase levels to a maximum of 3,690 +/- 962 IU and evoked a decrease of L-arginine, but did not alter plasma nitrite or nitrate levels. The administration of arginase in healthy pigs did not influence cardiac output, mean arterial pressure, heart rate, or total peripheral resistance, but led to an increase of mean pulmonary arterial pressure from 19 +/- 3 to 48 +/- 5 mmHg and to a reduction of arterial hepatic blood flow from 229 +/- 65 ml/min to 154 +/- 41 ml/min. From this we conclude that high levels of liver arginase cause hemodynamic alterations in the lung and the liver. We hypothesize that the pulmonary hypertension and the reduced hepatic blood flow found during the immediate reperfusion period after OLT are possibly related to the increased arginase release due to the hepatic damage of the graft.
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PMID:Arginase release following liver reperfusion. Evidence of hemodynamic action of arginase infusions. 777 69

The effects of arginine (L-arg), promoter of nitric oxide (NO) production and NO synthesis inhibitors, NG-monomethyl-L-arginine (L-NMMA) and N omega-nitro-L-arginine (L-NNA), on arteriolar responses and capillary perfusion after 30 min ischemia were studied in the cheek pouch preparation under pentobarbital anesthesia and intravenous drug infusion. Capillary density, venular leukocyte sticking, and vessel diameters were investigated by fluorescence microscopy. Damage due to photoactivation of intravascular dyes was investigated by injecting fluorescent dextran 150,000 MW prior to and after ischemia reperfusion. No difference was found indicating that effects were independent from exposure time to photoactivated dyes. Capillary perfusion reduction was always present after reperfusion in untreated, L-NMMA-treated, and L-NNA-treated animals, with increased venular leukocytes adhesion. Arteriolar vasomotion was induced by L-NMMA treatment. Capillary perfusion recovered in L-arg-treated hamsters, where capillary blood flow velocity was lower than in L-NMMA group and the number of adhering leukocytes was lower than in untreated controls, L-NMMA, and L-NNA groups. It is concluded that L-arg determines perfusion with increased blood flow heterogeneity while inhibition of NO preserves capillary perfusion causing appearance of vasomotion in the arterial network.
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PMID:Capillary reperfusion after L-arginine, L-NMMA, and L-NNA treatment in cheek pouch microvasculature. 853 97

Basic amino acid, L-arginine has been known to have several biological actions including nitric oxide production. The real effects caused by L-arginine administration to heart has not been fairly understood in the setting of ischemia-reperfusion process. The effects of L-arginine on recovery of myocardial contractile function and oxidative metabolism were studied in a model of reversible global normothermic ischemic injury using an isolated, buffer-perfused rabbit heart preparation. 1 mM L-arginine or vehicle was infused into hearts for 2 minutes at the onset of 35 minutes of ischemia in L-arg. group or in control group, respectively. Oxygen consumption (MVO2), lactate release into coronary vessels, and cardiac function including developed pressure, +dp/dt, -dp/dt and diastolic pressure-volume relationship (PVR) were measured and high energy phosphates were also evaluated by 31P-NMR spectroscopy. Endothelial function was also evaluated by acetylcholine (Ach) infusion with monitoring of constant perfusion pressure. L-arginine caused a significant increase in the PVR and profund decline in systolic function when compared to control group. MVO2 was significantly impaired to cause a decrease of high energy phosphates (phosphocreatine and ATP). Lactate release into coronary vessels on reperfusion was significantly higher in L-arg group than that in control group, suggesting a promotion of anaerobic glycolysis. Deterioration of endothelial function and smooth muscle function of artery were evidenced by Ach infusion test. Although the mechanisms of injury are speculatory, possible mechanisms of this injury are stimulation of nitric oxide production by L-arginine and cation change, especially calcium accumulation. We concluded that L-arginine was able to cause aggravation of ischemia-reperfusion injury with reduced contractile function and mitochondrial function and increased anaerobic glycolysis after ischemia-reperfusion in an isolated model of reversible ischemic injury.
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PMID:[Basic amino acid, L-arginine aggravates ischemia-reperfusion injury]. 871 63

The effects of NO donor--L-arginine (L-arg) and ischemic preconditioning (IP) on the hemodynamics and myocardial infarct size were examined in the anesthetized rabbit subjected to myocardial ischemia-repefusion to define whether exogenous L-arg could exert a beneficial effect in this pathological model, and whether the L-arg-NO pathway was involved in the cardioprotection provided by IP. The results obtained were as follows: (1) During the course of ischemia (30 min)-reperfusion (180 min), blood pressure, heart rate and myocardial oxygen consumption decreased progressively, and the myocardial infarct size occupied 33.9 +/- 2.4% of the whole left ventricle. (2) The myocardial infarct size could be reduced to 20.1 +/- 2.2% (P < 0.01) by pretreatment with L-arg (300 mg/kg). This myocardial protective effect of L-arg was abolished by NO synthesis inhibitor--Nitro-L-arginine (L-NNA), thereby indicating the involvement of L-arg-NO pathway. (3) IP significantly reduced the infarct size to 21.9 +/- 2.1% (P < 0.01), indicating the prominent cardioprotective effect of such an intervention. Since L-NNA showed no effect on the cardioprotection afforded by IP, it was implied that the L-arg-NO pathway was not involved in the cardioprotective mechanism of IP. (4) Exogenous L-arg might markedly augment cardioprotection provided by IP. The above results strongly suggested that the cardioprotective effect of L-arg on ischemia-reperfused myocardium was mediated by L-arg-NO pathway, which, however, was not involved in the cardioprotection provided by IP.
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PMID:[Ischemic preconditioning and exogenous L-arginine reduce infarct size in rabbit heart]. 938 55

We evaluated the correlation between hypoplasia of the circle of Willis detected by MR angiography and ischemia of the white matter in patients with Binswanger-type cerebrovascular disease. We defined P1 hypoplasia as the condition in which the posterior cerebral artery at P1 protein was narrower than the posterior communicating artery, and A1 hypoplasia as that in which the ratio of the one anterior cerebral artery to the other at A1 portion was 1:2 or less. Of 68 patients with this disease. 33 (48.5%) had P1 hypoplasia and 23 (30.9%) had A1 hypoplasia. These incidences were significantly higher than those of patients with lacunar infarction (138 cases), where P1 and A1 hypoplasia were 29.0% and 18.1% respectively. P1 hypoplasia tended to be found more frequently in patients with lacunar infarction having advanced periventricular hyperintensity than in those having mild one. The large intracranial vessels, as seen by MR angiography, were less stenotic, and the serum concentration of apolipoprotein A-I was higher and B/A-I was lower in hypoplasia cases suffering from Binswanger-type cerebrovascular disease than in non-hypoplasia cases. In summary, hypoplasia of the circle of Willis was considered to precipitate the onset or progression of this disease without any relationship to arteriosclerosis.
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PMID:[The significance of hypoplasia of the circle of Willis in patients with Binswanger-type cerebrovascular disease]. 961 70

The effects of hypercholesterolemia on ischemic renal failure were evaluated in rats subjected to 60 min of left renal artery clamping and contralateral nephrectomy. One group of rats (HC) was kept on a cholesterol-supplemented diet for 3 weeks before renal injury and compared to a group fed a regular diet (ND). Two days after renal ischemia, inulin clearance (C(in), ml/min per 100 g BW) was lower in HC-rats (0.033 +/- 0.011) than in ND-rats (0.227 +/- 0.037; P < 0.01). indicating that hypercholesterolemia potentiated renal ischemic injury. Twenty-one days after renal ischemia the C(in) of HC-rats did not differ from ND-rats, suggesting that hypercholesterolemia did not limit late recovery. Since nitric oxide production is impaired in HC, L-arginine (50 mg/kg BW i.v.) was administered immediately after ischemia. Two days after ischemia, L-arg did not protect ND-rats from ischemia, while the C(in) and renal blood flow were higher in L-arg-treated HC rats than in untreated HC rats (C(in) = 0.125 +/- 0.013 rats vs. 0.033 +/- 0.011; P < 0.001) (RBF = 3.96 +/- 0.64 vs. 2.40 +/- 0.20 ml/min per 100 g BW; P < 0.05), indicating that L-arg protects HC rats from renal ischemia. The administration of D-arginine to ND rats induced a significant decrease of the C(in) and a significant increase of FE H2O, FE Na and FE K compared to the L-arginine and not treated groups. Cultures of inner medullary collecting duct cells from ND rats were resistant to 24-h hypoxia. In contrast, IMCD cell cultures from HC rats showed higher LDH release after 24-h hypoxia than normoxic cells (69.2 +/- 3.4 vs. 30.9 +/- 3.6%, P < 0.001); 1 mM L-arg added to the medium attenuated LDH release (44.3 +/- 2.4%, P < 0.01). These data demonstrate that HC predisposes renal tubular cells to hypoxic injury and L-arg protects cells of HC.
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PMID:Protective effect of L-arginine on hypercholesterolemia-enhanced renal ischemic injury. 1021 61

It has previously been shown that endothelin (ET)-receptor antagonists protect the myocardium from ischemia and reperfusion (I/R) injury. The mechanism behind this effect is unclear. The aim of this study was to elucidate the possible interaction between ET(A)-receptor antagonism and nitric oxide (NO) during I/R. Anesthetized pigs were subjected to 45-min ligation of the left anterior descending coronary artery (LAD) followed by 4 h of reperfusion. Vehicle (n = 7), the ET(A)-receptor antagonist LU 135252 (LU; 0.1 mg/kg, n = 7), the combination of LU and the NO precursor L-arginine (15 mg/kg, n = 7; LU + L-arg), the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA; 0.2 mg/kg, n = 6), or the combination of LU and L-NMMA (LU + L-NMMA; n = 6) were injected into the LAD during the last 10 min of ischemia and the first 5 min of reperfusion. There were no significant differences in coronary flow, pulmonary capillary wedge pressure, mean arterial pressure, or heart rate between the groups before ischemia or at the end of reperfusion. The area at risk was similar in all five groups. The infarct size of the vehicle group was 79 +/- 6% of the area at risk. LU and LU + L-arginine (L-arg) reduced the infarct size to 39 +/- 6% and 35 +/- 8%, respectively (p < 0.001 vs. vehicle). L-NMMA completely prevented the infarct-limiting effect of LU. Thus the infarct size in the LU + L-NMMA group was 83 +/- 4% (p < 0.001 vs. LU alone); L-NMMA did not affect infarct size per se (79 +/- 4%). ET immunoreactivity increased threefold in the I/R myocardium of the vehicle group. The increase in ET immunoreactivity was significantly attenuated in the LU and LU + L-arg groups (p < 0.001), but not in the groups given L-NMMA or LU + L-NMMA. In conclusion, ET(A)-receptor blockade results in cardioprotection and attenuation of the increase in myocardial ET levels after I/R. Both effects were inhibited by NO synthase blockade, suggesting that they are dependent on maintained production of NO.
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PMID:Cardioprotection from ischemia and reperfusion injury by an endothelin A-receptor antagonist in relation to nitric oxide production. 1097

Hyperhomocysteinemia (HH) is an independent risk factor for atherosclerosis, including peripheral arterial occlusive disease (PAOD). Because angiogenesis and collateral vessel formation are important self-salvage mechanisms for ischemic PAOD, we examined whether HH modulates angiogenesis in vivo in a rat model of hindlimb ischemia. Rats were divided into 3 groups: the control group was given tap water, the HH group was given water containing L-methionine (1 g x kg(-1) x d(-1)), and the HH+L-arg group was given water containing methionine (1 g x kg(-1) x d(-1)) and l-arginine (2.25 vol%). At day 14 of the dietary modifications, the left femoral artery and vein were excised, and the extent of angiogenesis and collateral vessels in the ischemic limb were examined for 4 weeks. Plasma homocysteine levels significantly increased (P:<0.001), and plasma and tissue contents of nitrite+nitrate as well as tissue cGMP levels significantly decreased in the HH group compared with the control group (P:<0.01). Laser Doppler blood flowmetry (LDBF) revealed a significant decrease in the ischemic/normal limb LDBF ratio in the HH group at days 7, 14, 21, and 28 (P:<0.01 versus control). Angiography revealed a significant decrease in the angiographic score in the HH group at day 14 (P:<0.001 versus control). Immunohistochemistry of ischemic tissue sections showed a significant reduction in the capillary density in the HH group (P:<0. 001 versus control). Oral l-arginine supplementation in rats with HH (HH+L-arg) restored the decreased plasma and tissue nitrite+nitrate and cGMP contents (P:<0.05) as well as angiogenesis, as assessed by LDBF (P:<0.05 versus HH), angiographic score (P:<0.01 versus HH), and capillary density (P:<0.001 versus HH). In summary, HH impaired ischemia-induced angiogenesis and collateral vessel formation in a rat model of hindlimb ischemia in vivo. The mechanism of the HH-induced impairment of angiogenesis might be mediated in part by a reduced bioactivity of endogenous NO in the HH state.
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PMID:Hyperhomocysteinemia impairs angiogenesis in response to hindlimb ischemia. 1111 56


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