Effect of prostaglandin E1 on hepatic cyclic AMP activity, carbohydrate and lipid metabolism

Levine, Robert A.

doi:10.1016/s0090-6980(74)80061-4

Cited by 11 publications

(2 citation statements)

References 9 publications

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“…However, neither the splanchnic oxygen consumption nor ethanol elimination increased, in contrast to the effects of glucagon and dibutyrylic cyclic AMP (Krarup & Larsen, 1974a;Krarup, Larsen & Munck, 1975). This may indicate, that the prostaglandins do not affect the hepatocellular cyclic AMP level, in accordance with findings in the perfused rat liver (Levine, 1974).…”

Section: Discussionsupporting

confidence: 78%

Secretin‐like choleretic effect of prostaglandins E1 and E2 in cats.

Krarup¹,

Larsen²,

Munck³

1976

The Journal of Physiology

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SUMMARY1. The effects of intraportal and hepatic arterial infusion of prostaglandins E1 and E2 on liver function and circulation was studied in fasting chloralose anaesthetized cats. 2. Infusion of the prostaglandins at rates of 0 1, 1 0 and 5 0 jtg/kg. min caused a 35-40 % increase in bile flow. This may be explained by a decrease in the reabsorption or a secretion of sodium ions by the ductular cells. The canalicular bile production and bile acid excretion was not affected by the prostaglandins.3. Infused at rates of 1 0 and 5 0 jug/kg. min the prostaglandins caused a transient decrease in mean arterial blood pressure and mesenteric vascular resistance. The resistance in the intrahepatic arterioles and lowpressure vessels was not affected.4. The prostaglandins did not influence the splanchnic uptake of oxygen and ethanol, whereas a slight increase in the splanchnic glucose output occurred.5. The effects of the two prostaglandins were identical and not related to the route of administration.

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Section: Discussionsupporting

confidence: 78%

Secretin‐like choleretic effect of prostaglandins E1 and E2 in cats.

Krarup¹,

Larsen²,

Munck³

1976

The Journal of Physiology

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“…Although several studies have demonstrated hyperglycaemic effects ofprostaglandins in vivo [32][33][34], studies in vitro have furnished apparently conflicting results. Whereas some studies have demonstrated glycogenolytic responses to prostaglandins in isolated hepatic systems [34][35][36], others have shown no effect [37][38][39][40] or inhibition [41] of hepatic glycogenolysis by E-series prostaglandins, leading to the suggestion [40] that the hyperglycaemia observed in response to prostaglandins in vivo may be secondary to changes in hormonal status [42][43][44]. It is clear from the present study that prostaglandin E2 has glycogenolytic effects in the perfused rat liver.…”

Section: (A) Menmentioning

confidence: 54%

Glycogenolytic and haemodynamic responses to heat-aggregated immunoglobulin G and prostaglandin E2 in the perfused rat liver

Buxton¹,

Fisher²,

Briseno³

et al. 1987

Biochemical Journal

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Infusion of heat-aggregated immunoglobulin G (HAG) into perfused livers from fed rats caused transient increases in hepatic glycogenolysis and portal-vein pressure, accompanied by a transient increase in hepatic glycogen phosphorylase alpha content. The hepatic responses to HAG were inhibited by indomethacin (2 microM). In contrast, HAG was without effect on phosphorylase alpha content and glucose output in isolated hepatocytes. HAG infusion caused a transient decrease in hepatic cyclic AMP. Lowering the extracellular Ca2+ concentration to 6 or 50 microM attenuated markedly the glycogenolytic and haemodynamic responses to HAG; efflux of Ca2+ from the liver was not observed in response to HAG. Co-infusion of the specific platelet-activating-factor antagonist U-66985 (1-O-octadecyl-2-O-acetyl-sn-glycero-3-phosphoric acid 6'-trimethylammoniumhexyl ester) did not attenuate the glycogenolytic response to HAG. Infusion of prostaglandin E2 caused increases in glucose output, portal-vein pressure and the reduction state of the cytosolic NAD(H) redox couple similar to those seen with HAG. The present study suggests that the glycogenolytic activation after HAG infusion may be an indirect consequence of the haemodynamic response of the hepatic vasculature to stimulation of the reticuloendothelial cells of the liver.

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The effects of intraportal prostaglandin E1 administration on hepatic warm ischemia and reperfusion injury in dogs

et al. 1995

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To determine the route of prostaglandin E1 (PGE1) administration which would have the greatest protective effect against hepatic warm ischemia, two experiments were performed using dogs. The pharmacokinetics of PGE1 were investigated in a preliminary study, after which, the effects of PGE1 in a 90-min warm ischemic liver model were examined. The dogs were divided into three groups of ten, according to the treatment given: group A was an untreated control group, group B received PGE1 intravenously, and group C received PGE1 intraportally. The PGE1 was infused continuously at a rate of 0.02 microliters/kg/min before and after ischemia. All the dogs in groups A and B died within 24 h of induced ischemia. Whereas, six of the ten dogs in group C survived for over 3 days. The arterial ketone body ratio was not maintained in groups A and B, but it was in group C. Furthermore, in group C the serum lipid peroxide level, which reflects hepatocellular membrane damage, was maintained at a lower level than that in the other groups after ischemia. Electron microscopy revealed sinusoid destruction and changes in both the plasma membrane and parenchymal cell mitochondria in groups A and B, while in group C these structures were well preserved. These findings confirmed that intraportally administered PGE1 improved the hepatic microcirculation and stabilized the hepatocellular membranes. Our results indicate that intraportal administration of PGE1 has a greater protective effect than intravenous administration against warm ischemic liver injury.

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Effect of prostaglandin E1 on hepatic cyclic AMP activity, carbohydrate and lipid metabolism

Cited by 11 publications

References 9 publications

Secretin‐like choleretic effect of prostaglandins E1 and E2 in cats.

Secretin‐like choleretic effect of prostaglandins E1 and E2 in cats.

Glycogenolytic and haemodynamic responses to heat-aggregated immunoglobulin G and prostaglandin E2 in the perfused rat liver

The effects of intraportal prostaglandin E1 administration on hepatic warm ischemia and reperfusion injury in dogs

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