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)

Studies were carried out to investigate the effects of prostaglandin E1 (PGE1) pretreatment on normothermic liver ischemia. Mixed-breed dogs were divided into three groups: a control group, a group with induced liver ischemia, and a group pretreated with PGE1 followed by induced liver ischemia. Liver ischemia was induced by the Pringle procedure for 60 min. PGE1 was administered intravenously to some dogs at a dose of 0.5 microgram/kg/min for 30 min prior to the Pringle procedure. Sham operations were performed without induction of liver ischemia in control animals. Insulin, glucagon, and glucose metabolic clearance rates were examined before and after the Pringle procedure in the control and experimental groups. Insulin and glucose metabolic clearance rates decreased 5 min after declamping in the ischemic group, while the glucagon metabolism was not affected, and lipid peroxide production increased. In contrast, hepatic insulin metabolism improved, and lipid peroxide production normalized in the ischemic group which was pretreated with PGE1. This study suggests that PGE1 prevents hepatic metabolic disturbances due to warm ischemia and subsequent reperfusion.
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PMID:Prostaglandin E1 protects liver from ischemic damage. 807 86

Hepatic regeneration of cirrhotic liver following partial hepatectomy was evaluated in the rats following portal triad cross clamp (Pringle's maneuver). Cirrhotic rats were induced by repeated intraperitoneal injection of thioacetamide. Sixty eight percent of partial hepatectomy was performed under general anesthesia with or without total hepatic normothermic ischemia. Pringle's maneuver consisted of 4 times repetition of the combination of 15-minute ischemia and 15-minute reperfusion. Rats were sacrificed on 1, 7, and 28 postoperative days. The increasing rate of regenerated liver, the labeling index (LI) by histochemical measurement of BrdU positive hepatocyte, biochemical tests of the blood were evaluated in non cirrhotic and cirrhotic rats. Cirrhotic rats tolerated Pringle's maneuver well, without portal congestion as observed in non cirrhotic rats, suggesting the formation of porto-systemic shunt in cirrhotic rats. The inhibition in DNA synthesis and hepatic regeneration rate was observed in liver cirrhosis. However, no statistical significant difference in hepatic regeneration was observed in cirrhotic rats with or without Pringle's maneuver. In conclusion, the rat with cirrhotic liver tolerated Pringle's maneuver well and the maneuver itself was not harmful for hepatic regeneration following the partial resection.
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PMID:[Effect of ischemia and reperfusion on hepatic regeneration following partial hepatectomy in cirrhotic rat liver]. 831 1

This report describes a simple and improved inflow control technique for resection of a hepatic tumor that lies across the right and left hepatic lobes. With alternate hemihepatic inflow control by en masse occlusion of Glisson's sheath of each hemipedicle at the bifurcation, hepatic resection across the two hepatic lobes is completed. Compared with Pringle's maneuver, this technique eliminates splanchnic congestion and reduces warm ischemia of the remnant liver, while maintaining a comparable hemostatic effect.
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PMID:Alternate hemihepatic vascular control technique for hepatic resection. 779 3

The onset of warm ischemia and reperfusion injury in the liver was investigated in a canine model through changes in parenchymal markers [isozyme class V of lactate dehydrogenase (LDH) and alanine aminotransferase (ALT)], endothelial markers [purine nucleoside phosphorylase (PNP) and hyaluronic acid clearance], and the liver metabolism (ketone body ratio) in warm ischemia induced by inflow occlusion using Pringle's maneuver and subsequent reperfusion. In this in vivo model, a PNP assay system and a model were designed so as to exclude the influence of wide localization of PNP possibly originating in erythrocytes or the intestine, and to discriminate between PNP of endothelial cells and that of parenchymal cells in the liver. After 45 min of warm ischemia, reperfusion resulted in damage only to endothelial cells, as seen by significant increase in PNP alone (3.6 +/- 0.1 U/liter at the end of warm ischemia to 6.8 +/- 0.5 U/liter at 5 min after reperfusion, P < 0.01) and significant decrease in hyaluronic acid clearance compared to the 30-min warm ischemia group in which no increase in either marker for parenchymal and endothelial cells was noted. By contrast, after 60 min of warm ischemia, reperfusion resulted in damage to parenchymal cells along with damage to endothelial cells, as seen by significant increases in LDH(V) and ALT (93 +/- 4 U/liter and 32 +/- 2 IU/liter at the end of warm ischemia to 239 +/- 17 U/liter and 165 +/- 27 IU/liter at 5 min after reperfusion, respectively), as well as a marked increase in PNP and deterioration of hyaluronic acid clearance compared to the 45-min warm ischemia group. Reperfusion after 120 min of warm ischemia did not show recovery of metabolic function of the liver as evaluated by hepatic mitochondrial redox state. It is suggested that a time lag occurs in the onset of injury between parenchymal cells and endothelial cells and that endothelial cells are temporally earlier in failing than parenchymal cells when the liver is exposed to short-term warm ischemia and subsequent reperfusion.
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PMID:Difference in onset of warm ischemia and reperfusion injury between parenchymal and endothelial cells of the liver. Evaluation by purine nucleoside phosphorylase and hyaluronic acid. 860 98

The effects of OKY-046, a thromboxane A2 synthetase inhibitor, on hepatic dysfunction produced by liver cell ischemia were studied in an experimental model of rats with obstructive jaundice. The experiments were performed 7 days after the rats underwent bile duct ligation. Warm total ischemia of the liver was induced by Pringle's method over a 20-min period and the animals were divided into two groups according to whether or not OKY-046 was administered. The reperfusion time was 30 min in each group. OKY-046 was administered via the femoral vein at a rate of 100 micrograms/kg per min from 15 min before the blockade to the end of the experiment. The level of ATP in the liver tissue of the OKY-046 group was elevated slightly, but not significantly, compared to that of the control group. The ratio TXB2/6-keto PGF1 alpha in the liver tissue was lower in the OKY-046 group than in the control group, and significant differences were found between the two groups in the water content of the liver and the mitochondrial score as examined by transmission electron microscopy. Thus, it was observed that an improvement in the balance of TXA2 and PGI2 associated with OKY-046 administration proctected the cellular structure of the mitochondria in the rat liver.
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PMID:The effects of thromboxane A2 synthetase inhibitor (OKY-046) on complete hepatic ischemia in rats with obstructive jaundice. 868 Jan 15

Abdominal aortic aneurysms are rare in children. Causes include mycotic aneurysms, vasculitides (eg, Takayasu's arteritis), connective tissue diseases (eg, Marfan's syndrome, Ehlers-Danlos syndrome, and tuberous sclerosis) and traumatic false aneurysms. Four cases are described. Case 1 was a 12-year-old boy who presented with an acute unheralded rupture of the subdiaphragmatic aorta accompanied by lower limb paralysis and ischemia. Attempted repair failed because of extensive friability of the large arteries. Histological evaluation confirmed cystic medial necrosis despite Marfanoid phenotype. Cases 2 and 3 were boys aged 12 and 11 with Takayasu's arteritis who presented with hypertensive encephalopathy and heart failure. Although both had involvement of the origins of the renal arteries, one aneurysm was predominantly suprarenal and the other infrarenal. Currently both children are being managed successfully with antihypertensive therapy. Case 4 was a 5-year-old girl who presented with hypertension and a pulsatile abdominal mass after treatment of infective endocarditis 18 months previously. Arteriography and three-dimensional computed tomography confirmed an aneurysm (6 x 5 x 4 cm) arising from the aorta and involving the right renal artery. Aneurysmectomy, removal of a small ischemic right kidney, and Gore-Tex grafting resulted in cure of the hypertension and uneventful recovery. The present series confirms that rupture is a fatal complication, renovascular complications are common, and medical control of hypertension is an essential part of management. Management strategies need to be highly individualized, and may be successful without surgical intervention. Close clinical and ultrasound follow-up of those managed nonoperatively is essential.
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PMID:Abdominal aortic aneurysms in children. 898 73

The purpose of this study was to investigate whether extracellular MR contrast agents or intracellular liver-specific MR contrast agents may enable the assessment of liver reperfusion injury. Ischemia-related reperfusion was induced in 32 rats using Pringle's maneuver. Pringle's maneuver consisted of cross-clamping of the complete hepatoduodenal ligament for 45 minutes followed by 90 minutes of reperfusion. Two extracellular (gadopentetate dimeglumine and gadobutrol) and two intracellular gadoxetic acid and SH U 555 A) MR contrast agents were evaluated as model agents. Control animals and animals with liver ischemia were used to calculate changes in liver signal enhancement after Pringle's maneuver. Significant changes in liver signal after reperfusion injury were observed only with reticuloendothelial system (RES)-specific SH U 555 A. Liver signal enhancement after Pringle's maneuver with RES-specific SH U 555 A was decreased by 25.4% as compared with the control group. RES-specific contrast agents such as SH U 555 A seem to be more sensitive to ischemia-related dysfunction of the liver than hepatobiliary contrast agents such as gadoxetic acid or extracellular gadolinium chelates at different concentrations because Kupffer cells are more sensitive to liver ischemia than hepatocytes.
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PMID:Assessment of reperfusion injury by means of MR contrast agents in rat liver. 917 32

The arterial ketone body ratio (AKBR) has been proposed as an accurate indicator of liver mitochondrial redox potential. However, the efficacy of the AKBR as a biochemical marker has been recently called into question. To resolve this issue, we studied the effect of temporary vascular occlusion on the AKBR during hepatectomy. Twenty patients undergoing hepatectomy were divided into two groups: those with hepatocellular carcinoma with a history of hepatic cirrhosis (n = 10; cirrhotic group) and those with liver disease without cirrhosis (n = 10; non-cirrhotic group). To minimize blood loss during hepatectomy, temporary vascular occlusion was applied using the Pringle maneuver. Acetoacetate and beta-hydroxybutyrate concentrations in the arterial blood and the AKBR were determined before and after vascular occlusion. In 25% of the two groups combined, the AKBR increased following normothermic ischemia, as compared with the levels prior to clamping; in 20% of cases in the cirrhotic group, it increased immediately following reperfusion, as compared with the levels prior to clamping. Changes in the AKBR during hepatectomy did not correlate with preoperative hepatocellular function. An AKBR of less than 0.7 prior to clamping which persisted during surgery was not a consistent risk factor for postoperative complications. The AKBR was not a useful predictor of liver viability in partial liver resection with temporary vascular occlusion.
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PMID:Arterial ketone body ratio during hepatectomy. 935 69

The aim of the study was to state consequence of 90 minutes occlusion of hepatoduodenal ligament and 24 hours reperfusion. Full liver ischemia was performed by a Pringle manoeuvre above temporary, internal portocaval anastomosis. Changes of the liver were analysed at the level of light microscope, and the activity of many enzymes participating in processes of energy production and distribution was measured using histochemical methods. It was stated, that hepatocytes included in zone I of the liver cluster possess the biggest regenerative opportunities.
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PMID:[Liver injury as a result of temporary occlusion of the hepatoduodenal ligament in the rat]. 944

Cells primed by sublethal stress transiently overproduce heat shock proteins (HSPs) and thereby develop tolerance to the next lethal stress. This response in organisms is called the stress response and involves the induction of HSPs. To assist the liver in developing tolerance for warm ischemia-reperfusion injury, which sometimes jeopardizes the patients after extended surgery for malignancies with vascular invasion in the liver, basic experiments to activate the stress response using stress preconditioning were performed. Heat shock preconditioning in rat livers has been shown to induce tolerance against warm ischemia-reperfusion injury in normal, fibrotic, and steatotic livers. Ischemic preconditioning using short-term Pringle's maneuver and pharmacological preconditioning using doxorubicin were also effective. In rats, heat shock preconditioning protected livers from free radical injury induced by the oral administration of carbon tetrachloride. The above data were supported by animal survival, suppression of serum transaminase levels, and improved energy status of the liver after intervention. Increased production of HSP72 was observed after preconditioning. In addition, the significance of HSP production as a stress parameter was demonstrated during the reperfusion of congested portal blood to the ischemic liver. The ill effect of congested portal blood could not be detected by conventional parameters but was detected by observing the increase in HSP72 production. Stress preconditioning seems to be a promising strategy to counter the damaging effect of hepatic warm ischemia during liver surgery and liver perfusion.
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PMID:Implications of heat shock proteins during liver surgery and liver perfusion. 967 Feb 77


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