The control of the external secretion of the pancreas in cats

SUMMARY1. Cooling the cervical vagi of the anaesthetized splanchnectomized cat to 2 TC caused a 54-4 + 8-8 % inhibition of pancreatic electrolyte secretion stimulated submaximally with pure secretin.2. On rewarming the vagi there was a prolonged increase in secretion rate over and above the control rate which existed before cooling. The increase lasted about 90 min.3. There were no changes in acid/base status due to interference of the lung inflation reflex which could account for the inhibition of secretion and the subsequent rebound.4. Cold block of the cervical vagi increased the transpancreatic electrical conductance, indicating that vasodilation had occurred and therefore eliminated a vasomotor cause for the inhibition.5. Electrolyte secretion was also inhibited by bilateral vagal section. 6. Atropine only partially prevented the inhibitory response to vagal cooling. A cholinergic mechanism, therefore, accounted for some but not all of the response to vagal cooling.7. It is concluded that even in the fasted, anaesthetized animal vagal impulses facilitate the action of secretin on the pancreas. This facilitation is only partially cholinergic; the major part of the response is due to some non-cholinergic transmitter substance. Such a mechanism may be necessary to potentiate the action of the very small amounts of secretin which appear to be released during a meal.

Section: Discussionmentioning

confidence: 99%

The response of the pancreas of the anaesthetized cat to secretin before, during and after reversible vagal blockade.

Grundy¹,

Hutson²,

Scratcherd³

1983

“…In these conditions it is difficult to detect a stimulation of enzyme secretion. Harper & Vass (1941) used casein and starch solutions in their experiments, and these may be ineffective as antral stimulants. More surprising in the light of our results is the claim of White, Lundh' & Magee (1960) that distension of pyloric pouches in dogs depressed pancreatic secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Hudock & Lawrence (1959) found that substances placed in a gastric pouch or isolated stomach had no effect on the volume or enzyme content of canine pancreatic juice. In cats, Harper & Vass (1941) observed that when protein or starch solutions were put into the stomach the enzyme content of secretin-stimulated pancreatic juice did not increase until the solutions began to pass into the duodenum. From all this evidence it was concluded that there was no gastric phase of pancreatic secretion.…”

Section: Introductionmentioning

confidence: 99%

A gastric phase of pancreatic secretion

Blair¹,

Brown²,

Harper³

et al. 1966

Self Cite

SUMMARY1. Extracts of antral mucosa increase the output of pancreatic amylase. They do not stimulate the resting pancreas of the anaesthetized cat to secrete juice, but have a slight 'secretin-like' effect on a pancreas already responding to endogenous or exogenous secretin.2. In animals with the vagus and splanchnic nerves cut instillation of meat extracts or acetylcholine into the antrum stimulates gastric acid and pancreatic amylase secretion. These responses can be prevented by injection of atropine or cocainization of the antral mucosa.3. In animals with the splanchnic nerves cut but the vagus nerves intact, distension of the body or antrum increases the output of amylase. After vagal section distension of the body has no effect on the pancreas, but the response to antral distension is still present.4. It is concluded that there is a gastric phase of pancreatic secretion which, in the cat, is almost entirely a stimulation of enzyme output. A vago-vagal reflex pathway is required for the pancreatic response to mechanical stimulation of the body of the stomach, and may be involved in the response to antral stimulation. Chemical and mechanical stimulation of the antrum produces a hormonally mediated increase in pancreatic enzyme secretion. The effects of atropine and cocaine on this response are consistent with the view that the release of the antral stimulant depends on a local cholinergic reflex pathway in the antrum.

“…The most obvious effect of stimulating the splanchnic nerves is inhibition of secretion, an effect which has been attributed to the accompanying vasoconstriction (Francois-Franck & Hallion, 1896;May, 1904;Edmunds, 1909; Anrep, 1916;and Gayet & Guillaumie, 1930), or to the direct action of the nerves on the secretary cells (Harper & Vass, 1941). On anatomical evidence, Richins (1945) concluded that as all sympathetic fibres are distributed to blood vessels the secretary effects of splanchnic stimulation must be due entirely to vascular changes.…”

Section: Introductionmentioning

confidence: 99%

“…E. BARLOW AND OTHERS As these effects could not be produced by adrenaline injections and were blocked by atropine they were presumably mediated by acetylcholine. In cats, Harper & Vass (1941) found that 5 min faradic stimulation of the splanchnic nerve reduced the enzyme output even when the flow of pancreatic juice was maintained by increasing the dose ofsecretin, and they concluded that the splanchnic nerves probably had a direct inhibitory effect on the enzyme secreting cells. They were unable to confirm the observations of Babkin et at., but suggested that this might have been due to the much shorter period of stimulation they employed.…”

mentioning

confidence: 99%

The influence of the splanchnic nerves on the external secretion, blood flow and electrical conductance of the cat pancreas

Barlow¹,

Greenwell²,

Harper³

et al. 1974

Self Cite

SUMMARY1. Electrical stimulation of the cut peripheral end of the splanchnic nerves results in a biphasic change in electrical conductance measured across the tail of the pancreas. A phase of decreased conductance is followed by a more prolonged phase of increased conductance.2. Simultaneous measurements of pancreatic blood flow indicate that the phase of decreased conductance occurs as a result of vasoconstriction, whilst the phase of increased conductance is due to vasodilatation.3. The initial phase of decreased conductance and vasoconstriction is abolished by ac-receptor blocking agents such as phenoxybenzamine and the phase of increased conductance blocked by f-receptor blocking agents such as pronethalol.4. Short periods of electrical stimulation applied to the splanchnic nerves result in a secretion of amylase and a reduction in the volume rate of secretion.5. When the vasoconstrictor response was abolished by phenoxybenzamine, nerve stimulation still reduced the rate of secretion, suggesting that the inhibitory effect is in part due to a direct action of the secretary cells.6. After bretylium tosylate, splanchnic nerve stimulation no longer produced vasomotor changes in the pancreas and the inhibitory effect on the volume response was converted to one of augmentation, but the secretion of enzymes was unaffected.7. The secretion of amylase on splanchnic stimulation was abolished by intravenous injection of atropine, suggesting that a cholinergic mechanism is involved.8. Noradrenaline did not mobilize pancreatic enzymes.