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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 186 (1986), S. 449-453 
    ISSN: 1433-8580
    Keywords: Prostacyclin ; Thromboxane A2 ; Experimental pancreatitis ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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-PGF1α and TXB2, respectively, were measured during the course of experimental AP. Blood samples were taken at 3, 6, and 8h after the induction of AP. In AP both plasma 6-keto-PGF1α plasma TXB2 and serum TXB2 increased up to 6 h simultaneously (6-keto-PGF1α 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 µg/ml to 140.8 ± 52.8 µg/ml). After 6h 6-keto-PGF1α 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.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1238
    Keywords: Haemodynamics ; Cardiac performance ; Cardiac contractility ; Cardiac catheterization ; Cardiac preload ; Myocardial depressant factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The haemodynamic effects in the early phase of canine acute experimental pancreatitis (AP) were studied using a cardiac catheterization technique. AP was induced in anaesthetized dogs with an infusion of trypsin-sodium-taurocholate into the pancreatic duct. The initial haemodynamic measurements were performed after the preparation of the animal and 5 min after the induction of AP. Thereafter, pressure and volume parameters were measured at 10 min intervals. AP induced significant increases in heart rate, dP/dtmax and mean arterial pressure, but a decrease in Vmax 5 min after the induction of AP. After the initial phase, the heart rate remained significantly increased, while constant and significant decreases of stroke volume, cardiac output, enddiastolic volume and end-diastolic pressure developed. The parameters of the contractility of the left ventricle were not affected to the same extent. It is suggested that the circulatory failure observed in AP, characterised by a prompt reduction of cardiac output, was primarily due to a heavy reduction in preload. This supports the theory that cardiac output is primarily affected by impaired venous return with consequently decreased preload rather than by a loss of ventricular contractility. Hence, the existence of a myocardial depressant factor in the early phase of experimental AP does not gain support from the present results.
    Type of Medium: Electronic Resource
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