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)

Although the liver is relatively resistant to normothermic ischemia, prolonged periods of inflow occlusion have produced evidence of hepatocyte injury. We have developed an animal model of liver ischemia using the pig and maintaining subtotal inflow (hepatic artery and portal vein) occlusion, allowing mesenteric portal decompression via patent portal veins through the caudate lobe, obviating the need for portosystemic shunting. This produced biochemical [aspartate transaminase (AST), lactate dehydrogenase (LDH)] and histopathologic evidence, using a microscopic grading system, of hepatocyte necrosis after 2 hr of normothermic ischemia. By administration of prostaglandin E1 (PGE1) prior to and during inflow occlusion, we have produced a statistically significant reduction in LDH (1085.9 +/- 413.5 U/liter compared to 669.1 +/- 161.4 U/liter) and AST (236.5 +/- 80.4 U/liter compared to 85.1 +/- 39.7 U/liter) (P < 0.05) between control and PGE1 animals 24 hr after reperfusion. Moreover, using the blinded microscopic grading system for hepatocellular necrosis, we have found significantly less (2.86 +/- 0.90 compared to 1.57 +/- 1.13, P < 0.01) necrosis when control and PGE1 animals were compared. Our experimental model supports the hypothesis that PGE1 exerts a cytoprotective effect during prolonged normothermic hepatic ischemia but does not aid in elucidating a mechanism for this effect.
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PMID:Evidence for cytoprotection by prostaglandin E1 with normothermic hepatic ischemia. 815 23

To reduce ischemia-reperfusion injury, a number of clinical lung transplant programs employ prostaglandin E1 (PGE1) or prostacyclin (PGI2) before donor lung flush and harvest. The effect of prostaglandins on the reperfusion component of this ischemia-reperfusion complex is unknown. We investigated the effect of PGE1 given only during the period of reperfusion, on ischemic lung injury in an in situ rabbit model. To examine the mechanisms involved, we measured pulmonary hemodynamics as well as myeloperoxidase, circulating platelet, and tumor necrosis factor (TNF) values. Two hours of warm ischemia of the left lung was produced in anesthetized New Zealand white rabbits. The animals were randomly allocated into four groups based on treatment received only during reperfusion: PGE1, PGI2, nitroprusside (NP), or no treatment (controls). After 2 h of reperfusion, PaO2 in the PGE1 group was significantly higher (423 +/- 52.7 mm Hg) than in all other groups (PGI2, 239 +/- 43.4, p < 0.05; NP, 146 +/- 14.2 p < 0.01; controls, 74 +/- 19.1 mm Hg, p < 0.01), despite similar pulmonary vascular resistance in the PGE1 and NP groups. Although lower than in the PGE1 group, PaO2 in the PGI2 group was still significantly higher than that in controls. Wet/dry lung weight ratios were significantly lower in the PGE1 and PGI2 groups (6.5 +/- 0.2 [p < 0.01] and 6.9 +/- 0.6 [p < 0.05], respectively, versus 8.2 +/- 0.1 in controls). There were no significant differences in plasma TNF levels, platelet sequestration across the lungs, or lung myeloperoxidase activity in the four groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration of post-ischemic lung reperfusion injury by prostaglandin E1. 821 43

The potential usefulness of somatosensory evoked potential monitoring during aortic cross-clamping is slowly being realized. In addition, the protection of endangered spinal nervous tissue during aortic cross-clamping has not been sufficiently evaluated. To test the pharmacologic protective efficacy of various agents, we recorded spinal evoked somatosensory potentials (bipolar epidural catheter) in dogs under controlled conditions (N2O/O2-enflurane anesthesia) following clamping of the aorta for 1 hour. There were 5 groups of animals: those treated with different medications, such as prostaglandin E1 (PGE1), prostacyclin (PGI2), superoxide dismutase (SOD), and PGE1 plus SOD for pharmacologic protection during ischemia, and the controls. The time to recovery of evoked potentials during the reperfusion period was 36 minutes in the controls, 15.9 minutes in the SOD group (p < 0.01), 12.5 minutes in the PGE1 group (p < 0.001), 10.8 minutes in the PGI2 group (p < 0.001), and 3.8 minutes in the combination group (p < 0.001). In addition, treatment resulted in a better neurologic outcome on the seventh postoperative day when compared with the control group. While in the control group only 1 animal could walk (9%), 7 of 12 in the PGE1 group (58%), 4 of 12 in the SOD group (33.8%), 8 of 12 in the PGI2 group (66.7%), and all animals in the combination group (100%) could walk. We computed an exponential correlation that related the mean time of potential recovery during reperfusion with Tarlov scoring (grade 0 = paraplegia; grade 1 = paraplegia with little movements; grade 2 = paraparesis; grade 3 = paraparesis with some problems; grade 4 = normal motor function) in the various groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Somatosensory evoked potential, a prognostic tool for the recovery of motor function following malperfusion of the spinal cord: studies in dogs. 834 72

The postischemic acute renal failure is one of the most important and frequent complications after surgery for renal artery and thoracoabdominal aortic diseases. In a canine model we studied the possible beneficial effects of Prostaglandin E1 (PGE1), Diltiazem and Superoxiddismutase (SOD) on postischemic renal function. 46 dogs were exposed to 3 hours ischemia. In 35 dogs PGE1 (n = 10), Diltiazem (n = 10), Superoxiddismutase (n = 10) or both PGE1 and SOD (n = 5) were given intravenously. 11 dogs treated with normal saline served as controls. Glomerular filtration rate, renal plasma flow, plasma creatinine, blood urea nitrogen, urine volume, free water clearance and renovascular resistance were calculated before and after renal ischemia. Radionuclide studies were performed on the third postoperative day. Two weeks later clearance measurements were repeated and kidneys were removed for histology. PGE1, Diltiazem and SOD significantly attenuated the post-ischemic fall in glomerular filtration rate and renal concentrating ability as well as the postischemic changes of tubular epithelium on histology.
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PMID:[The role of pharmacologic kidney protection in preventing post-ischemic renal failure in animal experiment]. 837 23

To clarify the influence of clamping of aorta on ischemic heart, 235 patients who underwent abdominal aortic surgery from 1980 to 1989 were studied. One hundred and twenty patients underwent resection of abdominal aortic aneurysm, and 115 patients underwent operation for aortoiliac occlusive disease. Myocardial infarction occurred in 8 patients, and 4 patients died. The onsets of the myocardial infarction were later than the 3rd post operative day in every patient but one. There were no significant differences in the incidence of myocardial infarction between the patients of nonruptured abdominal aortic aneurysm and of aortoiliac occlusive disease. To clarify the hemodynamic changes during abdominal aortic procedure, following experiments were performed using dogs. The dogs were divided into 6 groups, Groups 1, 3, 5; normal control groups, Group 2, 4, 6; groups with coronary stenoses. The infrarenal aorta were cross-clamped in groups 1, 2, 3, 4. In groups 3 and 4, PGE1 were administrated continuously into the infrarenal aorta below the clamping sites. In groups 5 and 6, descending thoracic aorta were cross-clamped. In group 6, one dog developed ventricular fibrillation at 60 minutes after aortic cross-clamping. Moreover ECG of the other dog of group 6 demonstrated myocardial ischemia during aortic clamping. But there were no significant differences in hemodynamic variables between groups, 1, 3, 5 and 2, 4, 6. These results indicate that aortic clamping can induce the myocardial ischemia, but that ischemia is not the chief cause of postoperative myocardial infarction.
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PMID:[Clinical and experimental study of hemodynamic changes during aortic surgery]. 837 62

During the last decade intensive work on the relationships between the liver and the arachidonic acid cascade has greatly expanded our knowledge of this area of research. The liver has emerged as the major organ participating in the degradation and elimination of arachidonate products of systemic origin. The synthesis in the liver of arachidonate products derived from the cyclooxygenase, lipoxygenase and cytochrome P450 system pathways has been demonstrated. The participation of leukotriene B4 and cysteinyl-leukotrienes as mediators of liver damage and the possible therapeutic usefulness of prostaglandins (PGs) in acute liver injury has attracted the interest of clinicians. This article reviews the essential features regarding the role of arachidonate metabolites in liver disease and specially focuses on the cytoprotective effects on the liver displayed by PGE2, PGE1, PGI2 and synthetic PG analogs in experimental models of liver damage induced by ischemia-reperfusion injury, carbon tetrachloride, bacterial lipopolysaccharide and viral hepatitis and on the possible mechanisms underlying liver cytoprotection in these experimental models. The therapeutic usefulness of PGs in clinical practice is critically analyzed on the basis of available evidence in patients with fulminant hepatic failure and primary graft nonfunction following liver transplantation.
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PMID:Liver cytoprotection by prostaglandins. 841 74

The effect of PGE1 and PGF2 alpha in the ischemic intestinal tract were examined. In 40 mongrel dogs, we studied ischemic models of small intestine. PGE1 or PGF2 alpha was injected into the anterior mesenteric artery after reperfusion according to each occlusion time, and the tissue blood flow was measured on both mucosal and serous sides of small intestinal loop by laser flowmeter to examine the relation to the extent of tissue damage. Tissue blood flow of the ischemic intestine after the injection of PGE1 increased by 148-208% in the 3-5 hr occlusion group and by 86-110% in the 7-10 hr occlusion group. Tissue blood flow after the injection of PGF2 alpha decreased by 39-59% in the 3-5 hr occlusion group and by 1-15% in the 7-10 hr occlusion group. These results indicate that the effect of PGE1 and PGF2 alpha in the ischemic intestine would be available up to 3-5 hr of ischemia. Histological examination revealed that viability of the remaining crypt was high in the PGE1 injection group but low in the PGF2 alpha injection group. These findings suggest that PGE1, if try at the early stage, would be effective for the treatment of ischemic lesion.
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PMID:[The effect of prostaglandin E1 and prostaglandin F2 alpha in the ischemic small intestine of dogs]. 846 67

There is a rapid growth of interest in heart transplantation therapy during early infancy. From 10% to 25% of the infants who are listed for transplantation annually have died while awaiting a donor heart. There has been no significant trend in this variable. Since November 1985, 140 consecutive orthotopic transplantation procedures were performed in 139 infants who were from 3 hours to 12 months of age. Indications for transplantation included hypoplastic left heart syndrome (63%), other complex structural anomalies (29%), myopathy (6.5%), and tumors (1.5%). Most recipients had ductus-dependent circulation and received continuous infusion of prostaglandin E1. Heart donors were usually victims of trauma, sudden infant death, or birth asphyxia. A donor-recipient weight ratio of 4.0 or less was found to be acceptable. The amount of time the graft underwent cold ischemia, ranged from 64 to 576 minutes. The procurement process was facilitated by a single dose of cold crystalloid cardioplegic solution and cold immersion transport. Profound hypothermic circulatory arrest was used for graft implantation. One hundred twenty-four (89%) recipients survived transplantation and were discharged from the hospital. There were 9 late deaths, which resulted in an 83% overall survival. The 5-year actuarial survival is 80%. The survival among newborn recipients (n = 60) at 5 years is 84%. Chronic immunomodulation was cyclosporine-based and steroid-free. Surveillance was noninvasive and relied heavily on echocardiography, electrocardiography, and clinical intuition. There was one documented late lethal infection, tumor was not encountered, and coronary occlusive disease was known to exist in only one long-term survivor. We concluded that transplantation results in excellent life quality and is a highly effective and durable therapy when applied during early infancy.
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PMID:Bless the babies: one hundred fifteen late survivors of heart transplantation during the first year of life. The Loma Linda University Pediatric Heart Transplant Group. 848 60

The binding of leukocytes to intercellular adhesion molecules expressed on endothelial surfaces during ischemia and subsequent reperfusion initiates leukocyte-mediated reperfusion injury. Interruption of this leukocyte-endothelium interaction may therefore prevent reperfusion injury. In an isolated, ventilated, blood-perfused rabbit lung preparation, we studied the effect of a monoclonal anti-intercellular adhesion molecule antibody on lung function during reperfusion. Lungs were harvested with 50 ml/kg cold Euro-Collins flush and 30 micrograms prostaglandin E1 before storage for 18 hours at 4 degrees C. Experimental groups received low-dose (100 micrograms) or high-dose (200 micrograms) anti-intercellular adhesion molecule antibody added to the pulmonary flush at harvest and to the initial reperfusate. Eighteen-hour control preparations were preserved for 18 hours and received saline solution vehicle. Immediate control preparations were harvested and immediately reperfused. The oxygen tension in the recirculated pulmonary venous effluent was measured after 30 minutes of reperfusion. Histologic specimens were graded by blinded observers for degree of leukocyte infiltration (0, normal, to 4, severe infiltration). The mean oxygen tensions (+/-standard error of the mean) were 138.29 +/- 6.23, 58.86 +/- 9.14, 86.87 +/- 11.32, and 139.33 +/- 16.15 mm Hg in immediate control preparations, 18-hour control preparations, low-dose antibody group, and high-dose antibody group, respectively (p = 0.0001). The leukocyte grades (mean +/- standard error of the mean) were 1.5 +/- 0.723, 3.0 +/- 0.955, 1.9 +/- 0.899, and 1.2 +/- 0.834, respectively (p = 0.0002). We conclude that anti-intercellular adhesion molecule antibody added to the pulmonary flush and initial reperfusate results in a dose-dependent enhancement of the reperfused lung's ability to oxygenate blood, possibly as a result of decreased leukocyte sequestration.
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PMID:Enhanced isolated lung function after ischemia with anti-intercellular adhesion molecule antibody. 862 17

We treated 14 patients suffering from critical limb ischemia (CLI) as defined by the Consensus Document, and in whom possibilities of surgical or percutaneous arterial reconstruction were excluded, by PGE1 60 micrograms i.v. daily during 3 weeks. Effects were evaluated by clinical, macrocirculatory and microcirculatory parameters during a follow-up of 1 year. After treatment with PGE1, we noted a significant reduction in analgesic use and in pain score. The average tcpO2 values on the forefoot in the supine and sitting positions, with or without inhalation of O2 through a face mask, showed a significant improvement after 3 weeks, as well as capillary stage. Laser Doppler flux did not change, but was significantly higher in diabetic patients than in nondiabetics with CLI. In 4 patients (28%) no improvement could be found after 3 weeks' treatment. Although in 6 patients the improvement lasted for up to 4 months, the legs eventually deteriorated. In 4 patients (28%) the legs were preserved after 1 year without further active therapy. No patient with initial tcpO2 values above 40 mm Hg in the supine and 100 mm Hg in the sitting positions during O2 inhalation lost a leg. Although other effects like local care could have influenced the outcome favorably, we noticed a beneficial albeit transient effect of PGE1 for the majority of our patients with CLI. TcpO2 measurements with O2 inhalation might be a valuable predictor of a positive long-term result.
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PMID:Acute and long-term effects of prostaglandin E1 assessed by clinical and microcirculatory parameters in critical limb ischemia: a pilot study. 873 8


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