Sánchez-Vicente C, Rodríguez-Nodal F, Minguela A, García L J, San Román J I, Calvo J J, López M A
Department of Physiology and Pharmacology, University of Salamanca, Spain.
Pancreas. 1995 Jan;10(1):93-9. doi: 10.1097/00006676-199501000-00013.
The response of the exocrine pancreas to intraduodenal perfusion of acetic and lactic acids in normal and previously atropinized rats was studied. Secretin and vasoactive intestinal peptide (VIP) plasma levels in portal plasma were also measured. Intraduodenal perfusion of both acetic and lactic acids significantly stimulated flow rate (from 0.29 +/- 0.03 microliters/min to a maximum of 1.06 +/- 0.08 microliters/min after acetic and from 0.35 +/- 0.05 microliters/min to a maximum of 1.13 +/- 0.12 microliters/min after lactic acid perfusion) and protein output (from 11.16 +/- 2.33 micrograms/min to a maximum of 35.1 +/- 7.4 micrograms/min after acetic and from 8.98 +/- 0.95 micrograms/min to a maximum of 22.5 +/- 1.3 micrograms/min after lactic acid perfusion). Atropine treatment significantly inhibited pancreatic flow rate and protein output after acetic acid perfusion, but no inhibition of flow rate and a slight decrease in the protein output after lactic acid perfusion were seen. With respect to plasma peptide concentrations, significant increases in secretin and VIP levels were found after perfusion of both organic acids; atropine administration significantly decreased plasma secretin levels after acetic acid administration although it did not affect plasma VIP concentrations. By contrast, atropine significantly increased plasma secretin levels, but significantly lower values of plasma VIP concentrations were observed after lactic acid perfusion. Therefore, cholinergic mechanisms are involved in the release of secretin and VIP and different types of control of exocrine pancreatic secretion occur, depending on the features of the intraduodenal stimulant.
研究了正常大鼠和预先用阿托品处理过的大鼠的外分泌胰腺对十二指肠内灌注乙酸和乳酸的反应。还测量了门静脉血浆中促胰液素和血管活性肠肽(VIP)的血浆水平。十二指肠内灌注乙酸和乳酸均显著刺激了流速(乙酸灌注后从0.29±0.03微升/分钟增至最高1.06±0.08微升/分钟,乳酸灌注后从0.35±0.05微升/分钟增至最高1.13±0.12微升/分钟)和蛋白质输出量(乙酸灌注后从11.16±2.33微克/分钟增至最高35.1±7.4微克/分钟,乳酸灌注后从8.98±0.95微克/分钟增至最高22.5±1.3微克/分钟)。阿托品处理显著抑制了乙酸灌注后的胰腺流速和蛋白质输出量,但乳酸灌注后未观察到流速受抑制,蛋白质输出量略有下降。关于血浆肽浓度,两种有机酸灌注后促胰液素和VIP水平均显著升高;乙酸给药后,阿托品给药显著降低了血浆促胰液素水平,尽管它不影响血浆VIP浓度。相比之下,阿托品显著提高了血浆促胰液素水平,但乳酸灌注后观察到血浆VIP浓度显著降低。因此,胆碱能机制参与了促胰液素和VIP的释放,并且根据十二指肠内刺激物的特性,外分泌胰腺分泌存在不同类型的控制。