Pathophysiology of acute pancreatitis: Evaluation of the effects and mode of action of indomethacin in experimental pancreatitis in dogs

Studley, J. G. N.; Lee, James B.; Schenk, Worthington G.

doi:10.1016/0022-4804(82)90140-8

Cited by 22 publications

(15 citation statements)

References 10 publications

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“…In the present study, indomethacin prophylaxis could not prevent the decrease in cardiac output, although the initial blood pressure was restored. It has been shown that indomethacin significantly decreases pancreatic blood flow in experimental AHP in dogs [14]. It is thus possible that filling of the left ventricle is impaired, i.e., venous return is decreased leading to decline in cardiac output.…”

Section: Discussionmentioning

confidence: 99%

Indomethacin in canine acute hemorrhagic pancreatitis

et al. 1988

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The effects of indomethacin administration on hemodynamics were investigated in canine acute hemorrhagic pancreatitis (AHP). Thirteen mongrel dogs were randomly divided into a fluid treatment group, an indomethacin prophylaxis group (IMP), and an indomethacin therapy (IM) group. Indomethacin (5 mg/kg) was administered as a bolus dosage 30 min before the induction of AHP in the IMP group. In the IM group, indomethacin was also given as a bolus (5 mg/kg) in 5 min starting 30 min after the induction of AHP. AHP was induced with a mixture of trypsin and sodium taurocholate infused into the pancreatic duct. Hemodynamics were monitored during the 4.5 h of surveillance time. Heart rate did not change significantly between the groups. Indomethacin prophylaxis maintained mean arterial pressure at a significantly higher level (P less than 0.05) and prevented the initial fall in blood pressure when compared to the fluid treatment or IM group. Indomethacin increased cardiac output (P less than 0.05) in the IM group, but did not differ significantly in the IMP group in comparison with the fluid treatment group. In conclusion, the inhibition of the initial fall in blood pressure by indomethacin in AHP suggests prostaglandins to play a role in hemodynamic changes and pancreatic shock to be "septic" as evaluated by hemodynamic changes.

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Section: Discussionmentioning

confidence: 99%

Indomethacin in canine acute hemorrhagic pancreatitis

et al. 1988

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“…With progressing inflammation and increasing hypovolemia, more vasodilatation is obviously needed to compensate vasoconstriction, both at the systemic level and locally in the pancreas. Studley et al [19] suggested that prostaglandins are released during pancreatitis to maintain blood flow and showed that indomethacin, a prostaglandin synthesis inhibitor, decreased pancreatic blood flow. In the pancreas, high levels of PGI2 could compensate both the vasoconstriction caused by TXA2 and some other factors, such as the function of the sympathetic nervous system and catecolamines.…”

Section: Discussionmentioning

confidence: 98%

“…In the pancreas, high levels of PGI2 could compensate both the vasoconstriction caused by TXA2 and some other factors, such as the function of the sympathetic nervous system and catecolamines. As early as 1963, Anderson suggested that toxic products are important in changing the edematous form of pancreatitis to a necrotic one [1] and Studley [18] speculated that vasoconstrictory substances are released into the pancreatic circulation during severe pancreatitis. Recently, it has also been shown that pancreatic juice from patients with pancreatic cancer activates platelets to produce TXB2.…”

Section: Discussionmentioning

confidence: 99%

The behaviour of prostanoids during the course of acute experimental pancreatitis in rats

Kiviniemi

Rämö

1986

Res. Exp. Med.

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The behavior of two vasoactive prostanoids was studied in experimental acute pancreatitis (AP) in rats. The stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TXA2), 6-keto-PGF1 alpha and TXB2, respectively, were measured during the course of experimental AP. Blood samples were taken at 3, 6, and 8 h after the induction of AP. In AP both plasma 6-keto-PGF1 alpha plasma TXB2 and serum TXB2 increased up to 6 h simultaneously (6-keto-PGF1 alpha from 271.1 +/- 77.2 pg/ml (mean +/- SD) to 459.4 +/- 192.6 pg/ml, plasma TXB2 from 752 +/- 350 pg/ml to 3640 +/- 2160 pg/ml and serum TXB2 from 22.3 +/- 14.8 micrograms/ml to 140.8 +/- 52.8 micrograms/ml). After 6 h 6-keto-PGF1 alpha remained elevated, whereas serum TXB2 dropped significantly. We suggest that in AP the balance of PGI2 and TXA2 is initially maintained, but later on an imbalance appears to favor vasodilatory PGI2. These agents may contribute to the regulation of the blood flow in the pancreas and thus play a role in the pathophysiology of AP.

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“…Some studies support the hypothesis that one of the impor tant pathophysiological events in this disease is acute ischaemia of the pancreas [6,12,13]. However, opinion on this point is divided, since other studies show increased pancreatic blood flow [1,5,13] and yet others show a decrease [3,5,6,12], These discrepancies are very likely due to the different models of experimental pancreatitis and the different methods used for determination of pan creatic blood flow.…”

Section: Introductionmentioning

confidence: 96%

Pancreatic Blood Flow and Contrast Enhancement in Computed Tomography during Experimental Pancreatitis

Schröder

Kivisaari

Standertskjöld‐Nordenstam

et al. 1985

Eur Surg Res

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The pancreatic blood flow and contrast enhancement in computed tomography (CT) were studied in 10 piglets weighing 17–25 kg with experimental pancreatitis. Each animal served as its own control. CT and blood flow measurements were made both before induction of pancreatitis and 5–6 h after the onset of the disease. Cardiac output was measured by thermodilution, and was kept constant throughout the study by infusion of dextran and saline. Although the pancreatic blood flow remained constant in this experiment, CT showed a significant decrease in contrast enhancement.

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Pathophysiology of acute pancreatitis: Evaluation of the effects and mode of action of indomethacin in experimental pancreatitis in dogs

Cited by 22 publications

References 10 publications

Indomethacin in canine acute hemorrhagic pancreatitis

Indomethacin in canine acute hemorrhagic pancreatitis

The behaviour of prostanoids during the course of acute experimental pancreatitis in rats

Pancreatic Blood Flow and Contrast Enhancement in Computed Tomography during Experimental Pancreatitis

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