Prostacyclin and thromboxane in acute hemorrhagic pancreatitis in dogs

Kiviniemi, Heikki; Rämö, Juhani; Ståhlberg, M; Laitinen, S; Jalovaara, P.; Viinikka, Lasse; Kairaluoma, Matti I.

doi:10.1016/0022-4804(87)90138-7

Cited by 18 publications

(15 citation statements)

References 14 publications

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“…The liberated PGH during AHP has been previously suggested to be of pancreatic origin [ 1 ], but there are also other organs rich in prostanoids, such as the lungs and kidneys, which may release the elevated prostanoid lev els measured in peripheral blood samples as has been reported earlier in this context [1][2][3]. It is obvious, how ever, that PGI2 measured in the blood samples collected from the portal vein in the present study was liberated mostly from the pancreas, as splenectomy was per formed prior to the induction of AHP to exclude the release of prostaglandins from that origin [10].…”

Section: Discussionmentioning

confidence: 76%

“…More over, PGH seems to dominate the prostanoid release in the splanchnic area and may thus be partly responsible for the hemodynamic changes observed during the early phase of AHP. It has been shown that in endotoxic and pancreatic shock the initial fall in blood pressure can be prevented by the administration of prostaglandin block ers [3,[16][17][18]. Plasma TXB2 seems to be liberated from various sources -possibly mainly from the lungs and kidneys.…”

Section: Discussionmentioning

confidence: 99%

“…The role of vasoactive substances in acute pancreati tis is not clear, but it has been proposed that they con tribute to pancreatic shock [4,5]. During experimental acute hemorrhagic pancreatitits (AHP), PGH and TXA2 have been reported to be released into the pancreatic venous blood [6], systemic circulation [1][2][3] and perito neal exudate [1,6], but the definite origin of released PGH and TXA2 in acute pancreatitis is, however, poorly known.…”

Section: Introductionmentioning

confidence: 99%

“…They are va soactive prostanoids and their plasma levels in systemic circulation have recently been reported to be elevated in different models of experimental acute pancreatitis [1][2][3]. The role of vasoactive substances in acute pancreati tis is not clear, but it has been proposed that they con tribute to pancreatic shock [4,5].…”

Section: Introductionmentioning

confidence: 99%

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Prostacyclin Is Released Mainly from the Splanchnic Region during the Early Phase of Acute Experimental Hemorrhagic Pancreatitis in Dogs

Rämö¹,

Rämö²,

Kiviniemi

1988

Dig Surg

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The release of 6-keto-prostaglandin F_1α (6-keto-PGF_1α) and thromboxane B₂ (TXB₂, the stable metabolites of prostacyclin (PGI₂) and thromboxane A₂ (TXA₂) during canine acute hemorrhagic pancreatitis (AHP) was studied using four different catheters in order to obtain simultaneous blood samples from (1) the abdominal aorta (2) the inferior vena cava (3) the right atrium of the heart and (4) the portal vein. Splenectomy was performed prior to the induction of AHP, which was performed with a mixture of trypsin and sodium taurocholate infused into the pancreatic duct. Sampling was performed before the induction of AHP (zero value) and thereafter up to 90 min. Plasma 6-keto-PGF_1α increased most in the samples collected from the portal vein, and was significantly higher already after 1 min of induction of AHP when compared to the zero value. Plasma TXB₂ increased significantly in all sites except in the inferior vena cava. Plasma TXB₂ levels decreased rapidly in the portal vein and the right atrium after the induction of AHP, whereas in the abdominal aorta TXB₂ levels remained high up to 90 min after induction compared to the zero value. In conclusion, the splanchnic area seems to be the main origin of the released PGI₂ during canine AHP and may also have a role in hemodynamic changes observed in AHP due to its vasoactive properties. TXA₂ is released from various sources – possibly mainly from the lungs and kidneys during experimental AHP.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prostacyclin Is Released Mainly from the Splanchnic Region during the Early Phase of Acute Experimental Hemorrhagic Pancreatitis in Dogs

Rämö¹,

Rämö²,

Kiviniemi

1988

Dig Surg

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“…TXA2 is generated (fourfold increase) in rats with acute pancreatitis (4,5,15), although not in dogs (16). In these rats thromboxane levels are reduced by treatment with inhibitors of thromboxane synthesis of flunarizine (5).…”

Section: Discussionmentioning

confidence: 99%

Significance of thromboxane A2 and prostaglandin I2 in acute necrotizing pancreatitis in rats

et al. 1990

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Plasma thromboxane concentrations were found to be significantly elevated in acute necrotizing pancreatitis in rats, whereas prostaglandin 12 levels were not. Prostaglandins play an important role in the pathophysiology of several diseases (1). They possess potent and diverse biological activities. Thromboxane A 2 (TXA2) is a vasoconstrictor and stimulates platelet aggregation (1). Prostaglandin 12 (PGI2) is a vasodilator and the most potent naturally occurring inhibitor of platelet aggregation yet discovered (2). These differences in biological activities have led to the development of new concepts in vascular and cellular homeostasis (3). Recently we demonstrated that the plasma levels of thromboxane B2, the stable end-product of TXA 2, were elevated in acute necrotizing pancreatitis (4, 5). The TXB z levels tend to rise dramatically compared with those of PGE 2 and I 2 (4). Simple inhibition of TXA2 synthesis and effects, however, did not alter survival time significantly (4), but with simultaneous administration of PGE2 a significant amelioration was encountered (6).In the present study we investigated the effects of iloprost (ZK 36 374, a stable PGI 2 derivate) (7-9) on the survival time of rats with acute pancreatitis. Iloprost was administered with and without simultaneous inhibition of TXA 2 synthesis. The synthesis of TXA 2 was inhibited by dazmegrel (10) and flunarizine. Flunarizine, a calcium entry blocker, decreases TXA 2 formation (5) and also inhibits the effects of raised TXA 2 concentrations (! 1).

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Changes of systemic prostacyclin and thromboxane A2 in sodium taurocholate-and cerulein-induced acute pancreatitis in rats

et al. 1993

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Systemic prostacyclin and thromboxane A2 production in rat experimental acute pancreatitis has been evaluated by measuring the urinary excretion of the 2,3-dinor 6-keto prostaglandin F1 alpha and 2,3-dinor thromboxane B2, respectively. Acute pancreatitis was induced by intraductal administration of 4.5% sodium taurocholate (0.1 ml/100 mg body weight) and intravenous cerulein perfusion (5 micrograms/kg/hr) for 6 hr, respectively. Urinary excretion of 2,3-dinor 6-keto prostaglandin F1 alpha and 2,3-dinor thromboxane B2 were much more important in sodium taurocholate- than in cerulein-induced acute pancreatitis. These data confirm an altered prostacyclin and thromboxane metabolism occurring in experimental acute pancreatitis. Phospholipase A2 activity and the effect of gabexate mesilate on the arachidonate metabolism were also evaluated.

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Prostacyclin and thromboxane in acute hemorrhagic pancreatitis in dogs

Cited by 18 publications

References 14 publications

Prostacyclin Is Released Mainly from the Splanchnic Region during the Early Phase of Acute Experimental Hemorrhagic Pancreatitis in Dogs

Prostacyclin Is Released Mainly from the Splanchnic Region during the Early Phase of Acute Experimental Hemorrhagic Pancreatitis in Dogs

Significance of thromboxane A2 and prostaglandin I2 in acute necrotizing pancreatitis in rats

Changes of systemic prostacyclin and thromboxane A2 in sodium taurocholate-and cerulein-induced acute pancreatitis in rats

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