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World J Gastrointest Pharmacol Ther. Feb 6, 2010; 1(1): 9-14
Published online Feb 6, 2010. doi: 10.4292/wjgpt.v1.i1.9
Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis
Mónica García, José Julián Calvo
Mónica García, José Julián Calvo, Department of Physiology and Pharmacology, Campus Miguel de Unamuno, Universidad de Salamanca, 37007 Salamanca, Spain
Author contributions: García M and Calvo JJ contributed equally to this paper.
Supported by University of Salamanca, Consejería de Sanidad Junta de Castilla y León, Solórzano Foundation
Correspondence to: José Julian Calvo, PhD, Department of Physiology and Pharmacology, Campus Miguel de Unamuno, Universidad de Salamanca, 37007 Salamanca, Spain.
Telephone: +34-923-2944001941 Fax: +34-923294669
Received: November 24, 2009
Revised: December 25, 2009
Accepted: January 1, 2010
Published online: February 6, 2010

Acute pancreatitis (AP) is a common and potentially lethal acute inflammatory process. Although the majority of patients have a mild episode of AP, 10%-20% develop a severe acute pancreatitis (SAP) and suffer systemic inflammatory response syndrome (SIRS) and/or pancreatic necrosis. The main aim of this article is to review the set of events, first localized in the pancreas, that lead to pancreatic inflammation and to the spread to other organs contributing to multiorganic shock. The early pathogenic mechanisms in SAP are not completely understood but both premature activation of enzymes inside the pancreas, related to an impaired cytosolic Ca2+ homeostasis, as well as release of pancreatic enzymes into the bloodstream are considered important events in the onset of pancreatitis disease. Moreover, afferent fibers within the pancreas release neurotransmitters in response to tissue damage. The vasodilator effects of these neurotransmitters and the activation of pro-inflammatory substances play a crucial role in amplifying the inflammatory response, which leads to systemic manifestation of AP. Damage extension to other organs leads to SIRS, which is usually associated with cardiocirculatory physiology impairment and a hypotensive state. Hypotension is a risk factor for death and is associated with a significant hyporesponsiveness to vasoconstrictors. This indicates that stabilization of the patient, once this pathological situation has been established, would be a very difficult task. Therefore, it seems particularly necessary to understand the pathological mechanisms involved in the first phases of AP to avoid damage beyond the pancreas. Moreover, efforts must also be directed to identify those patients who are at risk of developing SAP.

Keywords: Severe acute pancreatitis, Cardiovascular impairment, Systemic inflammatory response syndrome, Hypotension, Substance P, Cytosolic calcium homeostasis