The effect of prostaglandin E1 on liver adenine nucleotides and cytoplasmic enzymes in a porcine model of normothermic hepatic ischemia

Abstract

The liver has been judged relatively resistant to ischemia, but prolonged inflow occlusion at normothermic conditions can produce evidence of reversible or irreversible hepatocellular damage. Cytoprotective agents have been used both experimentally and clinically to afford extended viability of hepatocytes under reduced perfusion. One agent, prostaglandin E1, has been described clinically as effective in sustaining liver function under ischemic conditions. We have sought to verify this observation in an experimental model using prolonged normothermic inflow occlusion. Twenty miniature pigs were anesthetized and subjected to subtotal normothermic hepatic inflow occlusion (portal vein, hepatic artery, choledochal vessels) to allow for sufficient splanchnic decompression. Half of the animals received pretreatment with prostaglandin E1 (alprostadil) 500 micrograms intravenously. Inflow occlusion was maintained for 2 hours followed by reperfusion and killing 24 hours later. As a measure of functional preservation, the tissue adenine nucleotides adenosine monophosphate, diphosphate, and triphosphate (AMP, ADP, ATP) were measured in ischemic liver by freeze-clamping and high-performance liquid chromatography during occlusion and after reperfusion. Cytosolic enzyme determinations (aspartate transaminase, alanine transaminase, lactate dehydrogenase) were also made before occlusion and after reperfusion. As a possible indicator of cellular injury, blood ionized Ca++ was measured before inflow occlusion and after reperfusion. Although no difference was found in levels of AMP and ADP between prostaglandin E1 and control animals, ATP levels rose significantly higher during recovery in prostaglandin E1 animals at 60 minutes and 24 hours after reperfusion (13.97 +/- 1.29 and 13.60 +/- 0.91 mumoles/gm dry weight prostaglandin E1 vs. 9.25 +/- 0.97 and 9.80 +/- 0.85 mumoles/gm dry weight co control, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

High-Intensity Focused Ultrasound (HIFU)-Assisted Hepatic Resection in an Animal Model

“…The median number of HIFU lesions needed to obtain coagulative necrosis of the resection line was 8.9 lesions. [5][6][7][8][9][10][11][12] All vessels \5 mm in diameter were sealed successfully using HIFU precoagulation. Surgical clips were used to control vessels [5 mm in diameter.…”

“…Vascular clamping is a time-critical technique, since higher morbidity results if it lasts more than 45 min. 9,10 Hepatic resection techniques have been improved using devices such as bipolar forceps, water jet dissectors, ultrasonic cutting systems, argon coagulation, and others. 11 These techniques are both expensive and time consuming.…”

Study of rat hepatocytes in primary culture submitted to hypoxia and reoxygenation: action of the cytoprotectors prostaglandin E1, superoxide dismutase, allopurinol and verapamil

“…NAKANO et al (41) observed in a model of primary culture of hepatocytes under exposure to superoxide radicals that Prostaglandin I 2 analogues prevented the increase of intracellular calcium in a dose-dependent manner. HELLING et al (22) questioned the relation between PGs and calcium balance. These authors worked with a pig liver ischemia model, and they did not find a significant difference in the ionized calcium blood level in the animals that received PGE1 transfusion.…”

“…The prostaglandin E1 (PGE1), superoxide dismutase (SOD), allopurinol (ALO) and verapamil (VERA) were evaluated in this study. Prostaglandins (PGs) and prostacyclin have been studied in various injury models such as isolated hepatocytes under anoxia, liver perfusion ischemia, fulminant hepatitis, hepatic necrosis, liver lesion by drugs, among others (1,2,21,22,31,37,52,53,54,58) . However, there are few studies employing PGs in primary culture of hepatocytes (3) .…”

Effect of Oral Sub-Lethal Dose of Abamectin in the Rat: Serum ALT, AST, Urea, Creatinine and Histopathological Changes

“…Since some hepatic changes are irreversibly satisfactory [17], a higher AST may make the liver more susceptible to other pathological diseases [18,19]. Aspartate aminotransferase (AST) is an important indicator of liver damage in clinical studies.…”