Relationship between pancreatic secretion and pancreatic blood flow

Goodhead, B; Himal, H. S.; Zanbilowicz, J

doi:10.1136/gut.11.1.62

Cited by 49 publications

(17 citation statements)

References 21 publications

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“…They concluded that there was no adequate data to establish association between pancreatic secretion and an increase in blood flow to the pancreas. Eichelter and Schenk (26) and Goodhead et al (27) suggested an association between secre tion and increased blood flow, but such a postulation is not in agreement with the drug responses observed in the experiments herein. As presented in Fig.…”

Section: Discussioncontrasting

confidence: 55%

Secretory and Vascular Response to Various Biogenic and Foreign Substances of the Perfused Canine Pancreas

1974

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Japan. Abstract-Secretoryand vascular responses to various biogenic and foreign sub stances of the isolated blood-perfused canine pancreas were investigated. The ma jority of cholinergic drugs such as acetylcholine, methacholine, carbachol, bethanechol pilocarpine, neostigmine, lobeline, nicotine, TMA and McN-A-343, and gastroin testinal hormones such as secretin, pancreozymin, gastrin, glucagon caused an increase of output of pancreatic juice with vasodilatation.Bradykinin and kallikrein in hibited the secretion with vasodilatation, and DMPP, physostigmine and dopamine increased the secretion with vasoconstriction.Dibutyryl cyclic AMP, histamine, nitroglycerin and methylxanthines such as caffeine, theophylline and theobromine also caused a secretion with vasodilatation.Vasopressin inhibited the secretory rate of pancreatic juice with vasoconstriction.Most adrenergic drugs such as nor adrenaline, adrenaline, phenylephrine, methoxamine, ephedrine, tyramine and iso prenaline except dopamine, had no effect on secretion. Vascular responses of the pancreas to various drugs were found to be similar to those of the mesenteric vessels. Since the secretion of pancreatic juice did not change in parallel with the rate of local blood flow, the mechanism of pancreatic secretion appears to be independent of the blood supply to the pancreas.Since secretin was discovered by Bayliss and Starling in 1902 (1), little attention has been given to the nervous control of pancreatic secretion. About twenty years later, Mal lanby (2) suggested that the vagus nerves regulated enzyme output, while secretin con trolled the flow of pancreatic juice. This theory found general acceptance until Harper and Raper (3) discovered another pancreatic hormone, pancreozymin, in 1943. Thus, it has been assumed that the external secretory activity of the pancreas is mainly controlled by these hormones, while the secretory nerve plays a relatively subsidiary role. Recently, however, Hickson (4, 5) showed in the pig, that either stimulation of the vagus nerve or intra-arterial injection of acetylcholine produced a profuse flow of pancreatic juice rich in bicarbonate and poor in enzymes. He suggested that the parasympathetic, secretory nerve supply exerted a quantitatively greater influence on the external secretion of the pan creas. On the other hand, it is accepted that the sympathetic nerve supply and also sym

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Section: Discussioncontrasting

confidence: 55%

Secretory and Vascular Response to Various Biogenic and Foreign Substances of the Perfused Canine Pancreas

1974

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“…Doses of secretin comparable to those used in the present study have been reported to significantly increase pancreatic and superior mesenteric artery blood flow with little effect on gut motility (4,5,8). Burns and Schenk (4) found that in conscious dogs intravenous injections (1.5 U/kg) produced a sus tained (38 %) increase in superior mesenteric artery flow.…”

Section: Discussionmentioning

confidence: 84%

Hepatic, Vascular and Biliary Responses to Infusion of Gastrointestinal Hormones and Bile Salts

Post

Hanson²

1975

Digestion

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The effects of secretin, cholecystokinin, synthetic pentagastrin, sodium dehydrocholate and sodium taurocholate on hemodynamics of the canine liver were studied in a total of 57 dogs. Bile flow was also measured. Dehydrocholate and cholecystokinin significantly decreased systemic arterial pressure while the other substances did not. Hepatic arterial vessels were dilated by pentagastrin and the bile salts; however, flow was not increased in the latter case. Intrahepatic portal venous resistance was decreased by pentagastrin and increased by the bile salts. Portal flow was decreased by the bile salts and increased by pentagastrin. Apart from this, mean changes in portal venous flow and portal pressure were not statistically significant. All were potent choleretic agents except pentagastrin which produced only a relatively small transient increase in bile flow.

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“…The characteristic changes in the RER, zymogen granules and the increased appear ance of autophagic vacuoles during the devel opment of acute pancreatitis have been at tributed to either metabolic factors or isch emia. Previous studies have shown that acute pancreatitis is associated with a reduction in pancreatic blood flow [2,6,11,18,26,27]. If this reduction in blood flow and its subse quent lowering of tissue oxygen tension is responsible for the early changes in the exo crine pancreas, the lack of a protective effect of PGE| is not surprising at this stage of development of pancreatitis.…”

Section: Discussionmentioning

confidence: 93%

Prostaglandin E<sub>1</sub>Treatment in Experimental Acute Pancreatitis in the Rat

Crocket¹,

Brackett²,

Crocket³

et al. 1984

Eur Surg Res

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Prostaglandin E₁ (PGE₁) was tested for cytoprotective activity against the development of experimental acute pancreatitis in the rat induced by the closed duodenal loop technique. Sham-operated, untreated and PGE₁-treated pancreatitic rats were investigated. All rats received an initial bolus of 3 ml 5% dextrose in normal saline (D5NS) via jugular catheter 30 min prior to surgery, and a continuous subcutaneous infusion of 35 ml D5NS over 24 h. Each treated rat received 10 µg/kg PGE_l· in the initial bolus and a maintenance dosage of 10 µg/kg/h via the infusate. Serum amylase rose significantly in all pancreatitic rats with no significant difference between treated and untreated. Pancreatic edema was more pronounced in PGE₁-treated than in untreated rats. The ischemic and autolytic damage to acinar cells and vascular endothelial cells typical of untreated pancreatitis was delayed by PGE₁. Mortality rates were unaffected by PGE₁.

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Relationship between pancreatic secretion and pancreatic blood flow

Cited by 49 publications

References 21 publications

Secretory and Vascular Response to Various Biogenic and Foreign Substances of the Perfused Canine Pancreas

Secretory and Vascular Response to Various Biogenic and Foreign Substances of the Perfused Canine Pancreas

Hepatic, Vascular and Biliary Responses to Infusion of Gastrointestinal Hormones and Bile Salts

Prostaglandin E<sub>1</sub>Treatment in Experimental Acute Pancreatitis in the Rat

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