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.
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Lovett WL, Wangesteen SL, Glenn TM, Lefer AM (1971) Presence of a myocardial depressant factor in patients in circulatory shock. Surgery 70:223–230
Bradley EL, Hall JR, Lutz J, Hammer L, Lattouf O (1983) Hemodynamic consequences of severe pancreatitis. Ann Surg 198:130–133
Warshaw AL, Lesser PB, Rice M, Cullen DJ (1975) The pathogenesis of pulmonary edema in acute pancreatitis. Ann Surg 182:505–510
Ito K, Ramirez-Schon G, Shah PM, Agarwal N, DelGuercio LRM, Reynolds BM (1980) The myocardial depresant factor (MDF) in acute hemorrhagic pancreastitis. Trans Am Soc Artif Intern Organs 26:149–152
Goldfarb RD, Tambolini W, Nightingale L, Lefkowitz M, Kish P, Loegering DJ, Weber PB (1985) Canine left ventricular function during experimental pancreatitis. J Surg Res 38:125–133
Carey LC (1970) Low molecular weight dextran in experimental pancreatitis. Am J Surg 119:197–199
Okada M (1979) A digital filter for the QRS complex detection. IEEE Trans Biomed Engin BME-26:700–703
Marble AE, McIntyre CM, Hasting-James R, Hor CW (1981) A comparison of digital algorithms used in computing the derivative of left ventricular pressure. IEEE Trans Biomed Engin BME-28:524–529
Urschel CW, Vokonas PS, Henderson AH, Liedtke AJ, Horwitz LD, Sonnenblick EH (1981) Critical evaluation of indeces of myocardial contractility derived from the isovolumic phase of contraction. Cardiology 65:4–22
Holt JP (1966) Indicator-dilution methods: indicators, injection, sampling and mixing problems in measurement of ventricular volume. Am J Cardiol 18:208–225
Kettunen R (1985) The thermodilution technique in on-line computation of the left ventricular volumes on anaesthetized dogs. Cathet Cardiovasc Diagn 11:25–40
Yang SS, Bentivoglio LG, Maranhao V, Golberg H (1978) Assessment of ventricular function. In: Yang SS (ed) From cardiac catheterization data to hemodynamic parameters. Philadelphia: Davis 233–358
Jaffe JH, Martin WR (1975) Narcotic analgesics and antagonists. In: Goodman LS, Gilman A (eds) The pharmacological basis of therapeutics. New York: MacMillan, pp 245–283
Halinen MO, Hakumäki MOK, Sarajas HSS (1978) Suppression of autonomic postganglionic discharges by pentobarbital in dogs, with or without endotoxemia. Acta Physiol Scand 104:167–174
Weber KT, Janicki JS, Shroff SG (1986) Measurement of ventricular function in the experimental laboratory. In: Fozzard HA, Haber E, Jennings RD, Katz AK, Morgan HE (eds) New York: Scientific Foundations, Raven Press, pp 865–886
Parmley WW, Talbot L (1979) Heart as a pump. In: Geiger SR, Sperelakis N, Berne RM (eds) Handbook of physiology, Section 2: The cardiovascular system, Vol I: The heart. Baltimore: Williams & Wilkins, pp 429–460
Anderson MC, Scoenfeld FB, Iams WB, Suwa M (1967) Circulatory changes in acute pancreatitis. Surg Clin N AM 47:127–140
Wulff K, Sjöström B (1974) Influence of acute pancreatitis on central hemodynamic, regional blood flow distribution and arteriovenous shunting in the dog. Eur Surg Res 6:354–363
Takada Y, Appert HE, Howard JM (1976) Vascular permeability induced by pancreatic exudate formed during acute pancreatitis in dogs. Surg Gynecol Obstet 143:779–783
Tagnon HJ (1945) The nature and mechanism of the shock produced by the injection of trypsin and thrombin. J Clin Invest 24:1–10
Kettunen R, Kouvalainen E, Timisjärvi J, Rämö P, Linnaluoto M (1986) The automatic computation of pressure derived maximal shortening velocity (Vmax) of the unloaded contractile element in the intact canine heart left ventricle. Acta Physiol Scand 127:467–475
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Rämö, O.J., Rämö, P., Karhunen, M. et al. Impaired venous return causes circulatory failure in experimental pancreatitic shock in dogs. Intensive Care Med 15, 111–115 (1989). https://doi.org/10.1007/BF00295987
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DOI: https://doi.org/10.1007/BF00295987