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

Metabolic disturbances in the canine liver during warm ischemia by Pringle's method for 60 minutes and the role of Coenzyme Q10 (CoQ10), Prostaglandin E1 (PGE1) and ONO-3708, TXA2 receptor antagonist, were studied. Mongrel dogs were divided into five groups; control group, group of liver ischemia without drugs, groups of liver ischemia with CoQ10, PGE1 and ONO-3708 pretreatment. Metabolic rates of PGI2, TXA2, insulin, glucagon and glucose and production of lipid peroxides in the five groups were measured at the points before Pringle's procedure, 5 minutes, 60 minutes and 120 minutes after declamping. In the group of ischemia without drug administration, the hepatic metabolism of PGI2, TXA2, insulin and glucose were decreased after declamping. The metabolism of glucagon, however, was not disturbed by warm ischemia. The production of lipid peroxides increased at 5 minutes after declamping. In the groups of CoQ10, PGE1 and ONO-3708 pretreatment, changes of PGI2, TXA2 and insulin metabolism in the liver were improved, and an increased production of lipid peroxides by warm ischemia was normalized. This study suggests that CoQ10, PGE1 and ONO-3708 protect liver damage by warm ischemia as results of improvement of metabolic disturbances of PGI2, TXA2, insulin and suppression of lipid peroxides production.
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PMID:[Assessment for protective effects of CoQ10, PGE1 and TXA2 receptor antagonist (ONO-3708) on warm ischemic liver]. 138 60

Nineteen hepatic resections with continuous liver ischemia exceeding one hour (60 to 85 min, m = 68 +/- 8 min) are reported. Surgery was undertaken for 15 malignant tumors, mainly metastatic, and 4 benign tumors. In 16 out of 19 cases, a major hepatic resection was necessary to remove massive and central lesions. Vascular clamping was a Pringle maneuver (9 cases), associated with inferior vena cava clamping-complete hepatic vascular exclusion (10 cases). 2050 +/- 2000 ml of packed red cells were infused peroperatively. No operative nor hospital mortality was recorded. Major complications developed in 6 patients: 3 intraperitoneal haemorrhages leading to complementary hemostasis of the raw surface of the liver in the first 24 hours, 1 erosive gastritis, 2 subphrenic abscesses treated by percutaneous drainage. Severe liver failure developed after left trisegmentectomy on a steatotic liver and led to emergency transplantation on the 17th day with success. Except this case, biochemical liver tests demonstrated slight and transitory alteration. Magnetic resonance imaging confirmed the rapidity of the regenerative process and liver biopsies at 6 and 12 months did not show any late changes. There is no relation between the duration of liver ischemia in the limits of this study and post operative morbidity rate, which is more influenced by the magnitude of the resection and the quality of the liver remnant.
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PMID:[Is ischemia of the liver, lasting longer than an hour, a severity factor in hepatectomies? Apropos of 19 cases]. 181 33

Crushing of the hepatic parenchyma with hepatic clamps to minimize blood loss during resection of the liver leads to mechanical damage of hepatocytes. Pringle's maneuver may precipitate liver failure by hepatic warm ischemia as well. Therefore, we controlled bleeding from the surface of the resection by using light compression on the hepatic parenchyma with a band while applying a hepatic arterial clamp at the hepatic hilus. This vascular control method can be done because the portal pressure is about one-tenth of the hepatic artery pressure and provides an efficient and harmless transection of the liver.
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PMID:Modified technique of Pringle's maneuver in resection of the liver. 184 45

Liver resections are usually performed under occlusion of the hepatoduodenal ligament (Pringle manoeuvre) in order to limit operative blood loss. The maximal ischemic tolerance, although individually different, is generally accepted to be 60 min. Resections of centrally located tumors require precise preparation, sometimes combined with vascular reconstructions. In such cases a prolonged ischemic time is inevitable. A save prolongation of the ischemic tolerance could be useful for extensive liver resections. In an experimental study in pigs ischemic tolerance of the liver was studied under hypothermic protection with the HTK solution of Bretschneider during 2 and 3 h. Deterioration of liver function was compared with a warm ischemia during 2 h. Results showed significantly less serum transaminase activities and better hepatic blood flow (ICG test) after an ischemia under protection with the HTK solution compared to a warm ischemia during 2 h. A prolonged ischemia during 3 h under protection with the HTK solution was well tolerated. First clinical applications of hypothermic hepatic protection during resection were successful.
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PMID:[In situ protection of the liver with Bretschneider HTK solution]. 190 77

The effects of hepatic warm ischemia and portal pooling on the viability of the liver were investigated with respect to hepatic energy metabolism by performing intermittent portal triad cross-clamping (Pringle's maneuver) on dogs with or without portosystemic shunt. The dogs were divided into two groups of five: Group 1, non-shunt group, underwent Pringle's maneuver performed for 30 min and declamping for 30 min, a process that was repeated five times; and Group 2, shunt group, underwent the same procedure as Group 1, except for portosystemic shunt using a heparinized hydrophilic catheter between the splenic and jugular veins. The shunt was opened during Pringle's maneuver and was closed immediately at declamping. In the non-shunt group, portal pooling increased and systemic blood pressure decreased when Pringle's maneuver was performed, but in the shunt group portal and systemic blood pressures remained within the normal range. In the non-shunt group, the initial velocity of arterial blood ketone body ratio (KBR) recovery after each declamping significantly (P less than 0.01) decreased from 0.122 +/- 0.016 (per min) after the first declamping to 0.028 +/- 0.017 (per min) after the fifth declamping. Hepatic energy charge [= (ATP + 1/2 ADP)/(ATP + ADP + AMP)] decreased from 0.840 +/- 0.003 before ischemia to 0.749 +/- 0.003 30 min after the fifth declamping (P less than 0.001). The concentrations of lactate and total amino acids in arterial blood increased. On the other hand, in the shunt group, the initial velocity of KBR recovery and hepatic energy charge showed little change even after the fifth declamping (0.081 +/- 0.016 per min and 0.851 +/- 0.009, respectively). The concentrations of lactate and total amino acids showed almost no increase. The impairment of hepatic energy metabolism by intermittent portal triad cross-clamping is mainly due to reinflow of pooled-portal blood to the previously ischemic liver, rather than hepatic warm ischemia. The KBR may be useful for determining the degree of impairment of hepatic energy metabolism.
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PMID:Is the deterioration of liver viability due to hepatic warm ischemia or reinflow of pooled-portal blood in intermittent portal triad cross-clamping? 322 58

Juxtahepatic venous injuries are usually fatal. The optimal method of dealing with these injuries remains controversial, but most experience has been with the insertion of an atriocaval shunt. However, the mortality rate with atriocaval shunting remains prohibitively high (60% to 100%). The experience at the Bellevue Hospital Trauma and Shock Unit during a 9-year period revealed a 50% mortality rate in four consecutive patients who underwent atriocaval shunting. As such, a different approach was used in the following five patients, all of whom survived. One additional patient died in the operating room before any definitive repair could be undertaken. Four steps are considered essential to the successful management of these patients: (1) compression of the injury site until adequate resuscitation has been achieved; (2) early recognition that a juxtahepatic venous injury exists, as indicated by failure of the Pringle maneuver to adequately arrest hemorrhage; (3) prolonged portal triad occlusion with hepatocyte protection by means of large doses of steroids and topical hypothermia (portal triad occlusion time in the nonshunted group ranged from 20 to 64 minutes with a mean occlusion time of 46 minutes; although a transient rise in liver function test results seemed to correlate with the length of ischemia time, neither hepatic dysfunction nor hepatic necrosis occurred; and (4) extensive finger fracture of the liver to the site of vascular injury for primary repair or ligation; the extent of the finger fracture varied from 15 to 30 cm in length and from 5 to 15 cm in depth. The successful results achieved in five consecutive patients who sustained juxtahepatic venous injuries treated without a shunt serve as a basis for recommending this operative approach.
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PMID:The management of juxtahepatic venous injuries without an atriocaval shunt: preliminary clinical observations. 351 6

Temporary occlusion of hepatic inflow, namely, the Pringle maneuver, was adopted for 15 patients with liver cirrhosis who underwent partial hepatectomy. The warm ischemia time ranged from 2 to 32 minutes with an average of 19 minutes. The procedure did not cause any harmful effects on systemic hemodynamic and postoperative liver function. The results in our patients were compared with those of 15 comparable control patients who had been operated on over the same period of time without inflow obstruction. The Pringle maneuver significantly diminished the estimated blood loss during surgery, intraoperative and postoperative complications, and suppressed the operative mortality rate from 20 percent to 0.
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PMID:Tolerance of the cirrhotic liver to normothermic ischemia. A clinical study of 15 patients. 673 91

It has been questioned whether the Pringle maneuver induces complete ischemia of the liver. We examined changes in liver blood flow (LBF) in sixty patients who underwent liver resection, under conditions of prolonged inflow occlusion. The ischemia period ranged from 30 to 75 minutes. All patients tolerated the procedure. To better understand the metabolic consequences of ischemia, 10 female mongrel pigs were divided into two groups treated with hepatic inflow occlusion or total vascular exclusion for one hour (n = 5, each). Clinical and experimental data showed approximately 10% of residual LBF under the Pringle maneuver. Only one out of five animals tolerated complete ischemia (total vascular exclusion) in terms of 7-day survival while all pigs treated with the Pringle method survived. This was attributed to the lower serum transaminase levels and attenuation of liver adenosine triphosphate (ATP) decline in the inflow-occluded group. Our data indicate that the Pringle maneuver induces partial rather than full ischemia of the liver and hepatic vein "back flow" is likely to be the cause. The clinical implications of hepatic inflow occlusion for liver surgery are discussed.
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PMID:The Pringle maneuver induces only partial ischemia of the liver. 767 66

The effect of a thromboxane (Tx) A2 receptor antagonist, ONO 3708, on cholestasis and injury related to ischemia and subsequent reperfusion (I-R) was investigated in the dog liver by assessing changes in insulin and glucagon metabolism. The left hepatic duct was ligated for 4 weeks to create a cholestatic lobe. Sixty-minute ischemia was induced by Pringle's procedure. ONO 3708 (200 micrograms/kg/min) was initiated 60 min before induction of ischemia and continued throughout the experiment. The rate of insulin metabolism was higher in the right noncholestatic lobe than in the left cholestatic lobe. There was no significant difference in the rate of glucagon metabolism between the right and left lobes. After induction of I-R, the rate of insulin metabolism, but not glucagon metabolism, decreased. The lipid peroxide level was higher and the glutathione level was lower in the cholestatic lobe than in the noncholestatic lobe. There was no significant difference in the alpha-tocopherol level between lobes. After induction of I-R, the lipid peroxide level increased and the alpha-tocopherol level decreased. There was no change in the glutathione level. I-R accelerated the release of 6-keto-prostaglandin (PG) F1 alpha, a stable metabolite of PGI2, and of TxB2, a stable metabolite of TxA2, from the liver. After I-R, cholestasis accelerated the release of TxB2, but not 6-keto-PGF1 alpha. I-R also increased the TxB2/6-keto-PGF1 alpha ratio. ONO 3708 reduced these metabolic changes in the cholestasis and after I-R. These findings suggest that ONO 3708 protects liver function, especially in the cholestatic lobe, from I-R-related injury by reducing peroxidation of lipids and the TxA2/PGI2 ratio, which predicts cellular damage, and by increasing levels of alpha-tocopherol and glutathione.
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PMID:Thromboxane A2 receptor antagonist (ONO 3708) protects from liver damage induced by cholestasis and ischemia-reperfusion. 778 41

The rapid changes in extracellular oxygenation and intracellular oxidation during ischemia and reflow were measured in deep liver tissue by a novel method combining tissue near-infrared spectroscopy with multicomponent curve-fitting analysis. This method enabled us to make real-time measurements of oxygen saturation (SO2) and amount (THB) of hemoglobin in the liver sinusoid as parameters of extracellular oxygenation state and of redox transition of cytochrome aa3 as intracellular oxidation state. Clamping of the hepatic artery in rabbit decreased the THB with a transient fall of SO2. Clamping of the portal vein decreased both SO2 and THB. The decreases of SO2 and THB caused by Pringle's maneuver were larger than the sum of decreases by hepatic artery and portal vein. These changes in SO2 were correlated with intramitochondrial oxidation state as measured by cytochrome aa3. These results indicate the presence of an interrelationship of oxygen supply by hepatic artery and portal vein. This method was clinically applied during and after clamping of hepatic artery and portal vein in 19 cases of hepatic resection with or without chronic hepatic diseases. The decrease in SO2 values before and after clamping (SO2D) and the slope of SO2 recovery (SO2R) after release were calculated. SO2D and SO2R values of the portal vein in cirrhotics were significantly higher and lower, respectively, than those in the normal liver. These data indicate that the present method provides a rapid and reliable method of quantifying hepatic oxygenation during liver surgery and its perioperative management.
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PMID:Interrelationship of oxygen supply by hepatic artery and portal vein: rapid analysis of ischemia-reflow-induced changes in hepatic oxygenation in experimental and clinical subjects by tissue near-infrared spectroscopy. 785 60


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