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

A prostaglandin I2 (PGI2) analogue and superoxide dismutase (SOD) were administered to dogs with pulmonary denervation, and their effects on warm ischemic damage to the lung were studied. Twenty-seven adult mongrel dogs were divided into a control group (6 dogs), a PGI2 group (7 dogs), an SOD group (6 dogs), and a heparin group (8 dogs). The left pulmonary hilum was dissected, with PGI2 (1 microgram/kg) being administered to the PGI2 group and heparin (100 U/kg) to the heparin group. Then the left lung was placed in a warm ischemic state for 1 hour. The SOD group also received 20 mg/kg of SOD intravenously 1 minute before reperfusion. Before warm ischemia, immediately after reperfusion, and 1 hour and 2 hours afterward, the blood gases, left pulmonary vascular resistance, and other data were measured under right pulmonary artery clamping. Arterial oxygen tension showed significantly better values in the SOD and PGI2 groups than in the control and heparin groups. The left pulmonary vascular resistance increased with time in the control group but did not increase in the PGI2 group. Pulmonary microangiography showed that dilatation of the pulmonary arterioles was prominent in the PGI2 group. The quantity of pulmonary extravascular fluid was significantly less in the PGI2 and SOD groups than in the control and heparin groups. Histological examination showed marked collapse of capillaries, intraalveolar hemorrhage, and edema in the control and heparin groups, whereas these changes were only slight in the PGI2 and SOD groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prostaglandin I2 and superoxide dismutase on reperfusion injury of warm ischemic lung. 141 87

Nitric oxide (NO) and prostacyclin (PGI2) were determined in effluents of Langendorff-perfused rabbit hearts subjected to 2 h of global low-flow ischemia and subsequent reperfusion. PGI2 release [6-oxo-prostaglandin (PG) F1 alpha] was significantly enhanced during early reperfusion and remained elevated. NO formation was reduced during ischemia but did increase substantially during reperfusion. Indomethacin (3 microM) significantly suppressed ischemia-related 6-oxo-PGF1 alpha and NO release. This was accompanied by severely diminished myocardial recovery. NG-nitro-L-arginine (L-NNA) (100 microM) suppressed NO generation without major effects on 6-oxo-PGF1 alpha generation and cardiac dysfunction but with a remarkable increase in coronary perfusion pressure. These effects of L-NNA were antagonized by L-arginine, whereas the effects of indomethacin were not. There was a substantial loss of creatine kinase specific activity from reperfused ischemic hearts, which was further aggravated by indomethacin but not by L-NNA. These data demonstrate a cardioprotective and endothelium-protective role of PGI2 in myocardial ischemia, which also involves preservation of NO generation. Endogenous NO appears to be important for local regulation of coronary flow.
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PMID:Prostacyclin rather than endogenous nitric oxide is a tissue protective factor in myocardial ischemia. 144 94

The balance between prostacyclin and thromboxane has been suggested to be of great importance for the maintenance of patency in veins. In order to investigate prostacyclin and thromboxane release, segments from the human saphenous veins were investigated in 53 patients. Twenty-seven patients (10 males, 17 females) underwent surgery for varicose veins. Twenty-six patients (14 nondiabetics, 12 diabetics) underwent surgery for lower limb ischemia (rest pain or gangrene) with use of the saphenous vein as arterial conduit. Vein segments were gently excised and perfused ex vivo for five 15 minute periods, with a balanced salt solution and determination of the stable degradation products 6-keto-PGF1 alpha and TxB2. Saphenous veins from patients with varicose veins had an initial prostacyclin release of 61 +/- 13 pg/mm2/15 min declining to 4 +/- 1 pg/mm2/15 min after 60 min (p < 0.001) and increasing after addition to arachidonic acid to 37 +/- 7 pg/mm2/15 min (p < 0.001). Segments from nondiabetic patients with lower limb ischemia did not differ from those of varicectomy patients, but diabetic segments had a significantly lower prostacyclin release than both these groups, 34 +/- 11 pg/mm2/15 min, 1 +/- 1 pg/mm2/15 min, and 7 +/- 5 pg/mm2/15 min, respectively (p < 0.05). The addition of arachidonic acid failed to increase the prostacyclin release in diabetics. Three patients from each group were studied regarding thromboxane release and there was almost no detectable thromboxane in any group. These findings suggest that diabetics have a lowered prostacyclin release from the saphenous vein and that the deficiency is at the cyclo-oxygenase level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostacyclin release from the human saphenous vein in diabetics in lower than in nondiabetics. 145 86

Cerebral ischemia was induced in rabbits by selective injection of 4 beta-phorbol-12 beta-myristate-13 alpha-acetate (PMA) into the left carotid artery. PMA provoked intravascular platelet and neutrophil aggregation. After PMA injection, a significant decrease in platelet and neutrophil counts was observed. Platelet and neutrophil emboli caused ischemia of the brain and brain barrier damage with accumulation of sodium fluorescein in the cerebrospinal fluid. Regional tissue analysis showed an ipsilateral alteration of the cerebral energy state and increased lactate levels. Pretreatment with the prostacyclin infusion completely blocked the alterations in both platelet and leukocytes counts and decreased the cerebral energy failure. Nimodipine administration decreased the changes in platelet and neutrophil counts and prevented the development of both brain barrier and cerebral energy failure. Nicergoline had no statistically significant beneficial effect on PMA-induced cerebrovascular injury.
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PMID:Effects of nimodipine and nicergoline on cerebrovascular injuries induced by activation of platelets and leukocytes in vivo. 146 72

The ability of prostaglandins to protect the kidney against ischemic and toxic renal injury was evaluated by in vivo and in vitro models of renal ischemia. The prostaglandin E1 analogue, misoprostol, was found to provide significant protection against ischemia-induced renal dysfunction in rats subjected to 40 minutes of renal artery occlusion. Misoprostol-treated rats had glomerular filtration rates almost threefold greater than control animals, although renal blood flow and renal vascular resistance were not significantly different. Improved tubular function was reflected in a lower fractional excretion of sodium and a higher urine-to-plasma creatinine ratio. Misoprostol also provided similar protection in a model of toxic renal injury produced by mercuric chloride. In an in vitro model employing primary cultures of proximal tubule epithelial cells subjected to hypoxia and reoxygenation, misoprostol limited cell death. Posthypoxic cells had apical membrane disruption and loss of microvilli when examined by transmission electron microscopy. These changes were not seen in misoprostol-treated cells. The "cytoprotective" effect was also produced by prostaglandin E2 and prostacyclin. The ability of prostaglandin E to protect against toxic and ischemic renal injury did not appear to be due to an antioxidant effect because misoprostol did not limit lipid peroxidation in vivo and did not protect against oxidant injury by tert-butyl hydroperoxide in vitro. Although the exact mechanism of prostaglandin protection was not revealed, these studies demonstrate that prostaglandins protect renal tubule epithelial cells from hypoxic injury at the cellular level independent of hemodynamic factors or inflammatory responses. Such a "cytoprotective" effect of prostaglandins may be a generalized phenomenon since it has also been demonstrated in gastrointestinal epithelium.
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PMID:Prostaglandins protect kidneys against ischemic and toxic injury by a cellular effect. 147 66

The hypothesis that dietary fish oil would protect dogs from ischemic acute renal failure was tested. Fish oil (eicosapentaenoic acid, 55 mg/kg per day, and docosahexaenoic acid, 40 mg/kg per day was given to eight instrumented, female, beagle dogs for 6 wk, while seven control dogs received vehicle. After 3 wk, unilateral nephrectomy was performed and a pneumatic cuff with flow probe was placed around the remaining renal artery of each dog. Three weeks thereafter, the cuff was inflated for 120 min. Renal function, RBF, and prostanoid excretion were measured 24 and 72 h after ischemia. In dogs receiving fish oil, blood pressure, GFR, RBF, renal vascular resistance (RVR), cholesterol, triglycerides, and prostanoid excretion were measured weekly for 6 wk. Further, cytosolic calcium was measured before and five times after fish oil. Blood pressure decreased, serum cholesterol and triglycerides decreased, and the cytosolic calcium within platelets decreased. The urinary excretion (expressed as picograms per milligram of creatinine) of the thromboxane (TX) metabolite TXB2 and the excretion of prostaglandin (PG)E2, as well as the excretion of the PGI2 metabolite 6-keto PGF1 alpha were decreased. GFR, RBF (Cl inulin and Cl para-aminohippuric acid), and RVR were not influenced by fish oil. Unilateral nephrectomy decreased GFR and RBF and increased RVR as expected, whereas it further decreased prostanoid excretion. Acute renal ischemia caused a significant, reversible decrease in GFR and urine volume in vehicle-treated animals, whereas no significant effect on renal function or urine volume was observed in animals pretreated with fish oil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration of ischemic acute renal failure by dietary fish oil administration in conscious dogs. 147 27

A PGI2 derivative, OP-41483, and a hyperosmotic agent, glycerol, were tested for possible beneficial effects on brain edema, metabolism and pathological changes in cerebral ischemia. Combination treatment with these agents was also tested. Cerebral ischemia was produced in spontaneously hypertensive rats, using bilateral common carotid artery ligation (BLCL). OP-41483 was administered four times, hourly (500 ng/kg x 4, i.p.). Ten percent glycerol was administered intravenously (6.6 ml/kg). And, for the combination treatment, OP-41483 was administered three times, hourly (500 ng/kg x 3, i.p.), and 10% glycerol was administered intravenously (6.6 ml/kg) in the same manner as the glycerol treated group. In ischemic controls, saline was administered intravenously (6.6 ml/kg). After 3 h of ischemia, brain water content and metabolites were determined and pathological observation was conducted using electron microscopy. OP-41483 treated animals maintained higher levels of ATP concentration and reduced accumulation of lactate, but showed no difference in brain water content compared to saline treated controls. Glycerol treated animals showed significance in terms of reduction of brain water content and accumulation of lactate. Glycerol abated the depletion of ATP concentration. OP-41483+glycerol treated animals showed the most significant effect on the reduction of brain water content and accumulation of lactate. The combination treatment also maintained higher levels of ATP concentration. Additionally, swelling of astrocytic foot processes and mitochondria with destroyed crista were not observed pathologically in the combination treated animals. These results show that OP-41483, glycerol and combination treatment are beneficial in the treatment of cerebral ischemia. They also indicate that the combination treatment significantly enhances the protective effects compared to individual treatment.
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PMID:Effect of a prostacyclin derivative (OP-41483) and a hyperosmotic agent (glycerol) on brain edema and metabolism in cerebral ischemia. 147 49

After 6 hours of cold ischemia the quality of lung preservation was assessed in a canine heart-lung transplant model comparing three clinically used methods for lung preservation: donor core cooling by means of extracorporeal circulation (group I); pulmonary artery flush perfusion with either Euro-Collins solution after prostacyclin application (group II); or University of Wisconsin solution after donor pretreatment with prostacyclin (group III). In all cases St. Thomas Hospital solution was used for myocardial protection. Heterotopic heart and orthotopic left lung allotransplantation was performed in three groups of six mongrel dogs each according to the method of lung preservation. After transplantation cardiorespiratory function was assessed at FiO2 of 0.4 for a maximum of 12 hours. After surgery, significantly improved oxygenation of the donor lung was observed in groups II and III, compared to group I (p less than 0.01). Between groups II and III, no significant differences were found in the oxygenation during the first 5 hours, but in the later postoperative course pO2 values decreased in group II although they remained stable on a higher level during the entire postoperative course in group III (p less than 0.05). University of Wisconsin solution for lung preservation in combination with prostacyclin donor pretreatment provides superior postoperative oxygenation of the transplanted lung compared to currently used clinical standards represented by donor core cooling and Euro-Collins flush perfusion.
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PMID:Improvement of currently used methods for lung preservation with prostacyclin and University of Wisconsin solution. 149 28

Functionally similar ischemic acute renal failure (ARF), as estimated by glomerular filtration rates (GFR), was induced by renal artery clamping (RAC) or intrarenal norepinephrine (NE) in rats and renovascular reactivity was examined at 1 week. With RAC-ARF induction there was total renal ischemia followed by abrupt return of renal blood flow (RBF). With NE-ARF induction there was subtotal ischemia (10-15% of basal RBF) with RBF recovery over several hours. Renovascular resistance (RVR) did not change to renal perfusion pressure (RPP) reduction in the autoregulatory range in RAC-ARF but paradoxically increased in NE-ARF. There was an exaggerated response to renal nerve stimulation in NE-ARF but no response in RAC-ARF. There was a vasoconstrictor response to intrarenal norepinephrine in the former but a negligible response in the latter. There was no vasodilation to acetylcholine in either group, but there was a normal response to prostacyclin in NE-ARF. Smooth muscle necrosis was found in 46% of resistance arterial vessels in RAC- but in only 8% of NE-ARF (p less than .001). When mean arterial pressure was reduced to 90 mm Hg for 4 h at 1 week, recurrent azotemia and fresh ischemic injury were noted in NE- but not RAC-ARF. It is concluded that different models of ischemic ARF induction result in different patterns of abnormal postischemic vascular reactivity. Differences in vascular smooth muscle and endothelial injury are due to differences in initial ischemia or rates of postischemic reperfusion.
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PMID:Renal vasculature and ischemic injury. 150 62

Despite omental wrap and avoidance of prophylactic administration of corticosteroids in the early postoperative phase, ischemic bronchial complications still represent an important source of early morbidity and mortality following lung transplantation. In a retrospective analysis, the effect of pharmacological enhancement of pulmonary collateral flow on bronchial healing was investigated. Thirty-nine consecutive unilateral or bilateral transplant procedures (Tx) were analyzed. Immunosuppression consisted of rabbit antithymocyte globulin (RATG), cyclosporine A, and azathioprine. In group 1 (10 Tx, 12 anastomoses) routine immunosuppression was employed and the anastomoses wrapped with an omental or pericardial pedicle. In group 2 (29 Tx, 41 anastomoses) PGI2 (4 ng/kg per min x 48 h), heparin (200 U/kg per day), and prednisolone (0.5 mg/kg per day) were added to the therapeutic regimen. The 2 groups were comparable with respect to age and sex of the patients, primary diagnosis, type of transplant, intraoperative use of extracorporeal circulation, graft ischemia, duration of mechanical ventilation, and mortality. Bronchoscopic evidence of a significant bronchial ischemia (extending more than 1 cartilaginous ring beyond the anastomosis) was seen in 8 of 12 anastomoses in group 1 vs 14 of 53 anastomoses in group 2 (P = NS). In group 1, significant bronchial stenosis required implantation of an endobronchial silicone stent in 6 of 12 anastomoses, whereas in group 2, no significant bronchial stenosis occurred (P less than 0.01). No negative effects possibly related to the prophylactic administration of corticosteroids could be observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased incidence of bronchial complications following lung transplantation. 158 91


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