Stimulation of pancreatic afferents reflexly increases cardiovascular function via sympathetic pathways, suggesting a mechanism for cardiovascular changes during acute pancreatitis.
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Suggests a pancreatic sympathetic reflex mechanism for CV instability in pancreatitis; leaves open translation to human disease.
Chemical stimulation of afferents from the stomach and gallbladder has been shown reflexly to activate the cardiovascular system. It is not known, however, whether stimulating afferents from the pancreas evoke similar reflex activity. Therefore we recorded the cardiovascular responses in cats anesthetized with methoxyflurane, while we applied capsaicin (200 micrograms/ml) and bradykinin (0.001-1,000 micrograms/ml) to the surface of the pancreas. Topically applying these algesic substances evoked cardiovascular responses that included increases in systemic arterial pressure, heart rate, left ventricular dP/dt at 40-mmHg developed pressure and systemic vascular resistance. Bilateral vagotomy at the level of the diaphragm did not diminish the cardiovascular responses evoked by capsaicin or bradykinin. In contrast, removal of the celiac and superior mesenteric ganglia abolished the cardiovascular responses demonstrated previously when capsaicin or bradykinin was applied to the pancreas. We conclude that afferent endings in the pancreas can be stimulated reflexly to increase cardiovascular function in cats. This reflex activation represents a potential mechanism for eliciting the cardiovascular changes observed during acute pancreatitis, particularly the marked vasoconstriction that may lead to renal failure.
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Ordway et al. (1983) studied this question. Topical application of capsaicin and bradykinin to the pancreas was evaluated on Cardiovascular responses including systemic arterial pressure, heart rate, left ventricular dP/dt, and systemic vascular resistance.
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