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Biomedical subjects

H Sarles

Publications and source records attributed to H Sarles.

At least 271 records · Page 15Linked to original sources

[Pathogenesis of chronic pancreatitis (author's transl)].

The earliest change during chronic pancreatitis seems to be precipitation of proteic material consisting apparently of the normal components of pancreatic juice, as demonstrated by pathology studies. Similar changes could be induced in animal experiments. There seems to be a causal relationship between increased protein concentration in pancreatic juice and protein precipitation. The cause of the disease in most cases is alcoholism combined with a diet rich in fat and proteins, or malnutrition in infants. The mechanism of action was clarified in dogs and rats: An increase of cholinergic stimulation influencing pancreatic secretion directly seems to be involved as well as an indirect stimulation of pancreatic secretion by gastroduodenal hormones.

Alcoholism↗

Evidences for duodenopancreatic reflexes and an anti-CCK factor with lidocaine infused intravenously and sprayed topically on pancreatic papilla in nonalcoholic and alcohol-fed dogs.

In 14 duodenal Thomas fistula dogs, four of them alcohol-fed for two years, lidocaine, applied topically to the duodenal pancreatic papilla, inhibited secretin-induced pancreatic secretion probably by interrupting duodenopancreatic reflexes that contribute to the "pancreon's" cholinergic tone. Opposite effects were observed with lidocaine administered against a CCK plus secretin background stimulation of the pancreas. The significant rising of volume and protein output above plateau levels were enhanced by chronic alcohol feeding. Lidocaine infused intravenously did not change secretin-induced pancreatic secretion but raised CCK and secretin evoked plateau secretion levels. Chronic alcoholism enhanced these latter effects. Atropine perfusion superimposed on CCK and secretin stimulation did not prevent but raised the intravenous lidocaine-induced pancreatic secretion changes. It is postulated that the modifications elicited by lidocaine sprayed topically and infused intravenously on CCK plus secretin evoked pancreatic secretion plateau levels are due to depression of an anti-CCK factor secreted by the small intestine mucosa.

Administration, Topical↗

Reserpine-induced dissociation of canine pancreatic secretion.

In five dogs, provided with chronic pancreatic and gastric fistulas (Thomas' cannula), the effects on exocrine pancreatic secretion of an intravenous continuous perfusion of gastrin (Eurorga, hog gastrin I-II, 6 mug./kg./hr.) and secretin (GIH, 0.5 C.U./kg.hr.) was studied before and after 48 hours of reserpine treatment (0.1 mg./kg./24 hr.). When compared with the pretreated plateau levels, reserpine induced a significant pancreatic secretion dissociation, a depressive of the alkaline and a rising of the protein component. The former phenomenon suggests a participation of a catecholamines in the secretin-elicited pancreatic electrolyte secretion. The latter, an enhanced sensitivity of intranpancreatic and/or acinar cells of the "pancreon" to gastrin stimulation.

Animals↗

Some aspects of human and canine macroscopic pancreas innervation.

Both vagus nerves and the celiac ganglion complex are the main source of the pancreatic gland innervation. In both man and dog there is a distinct difference in the number of fibers ending in the different segments of the gland. In the former, the macroscopic innervation is primarily concentrated in the pancreas head and isthmus. In the latter most of the nerves enter through the upper part of the right limb (uncinate process). Both vagus nerves send direct fibers to the gland but in most of the nerves, that course in general along the different branches of the celiac and mesenteric arteries, the parasympathetic and adrenergic fibers are intermingled. The anterior hepatic plexus, continued down by the gastroduodenal, completes a nervous circle, at the lower edge of the pancreas, with the branches arising from the splenic plexus. In human pancreas most of the nerves, with the exception of the branches given off by the gastroduodenal network, enter the gland by its periphery, either through its superior or inferior border. The gastroduodenal plexus is the pathway for the duodenopancreatic and the duodenogastric arc reflexes and for the "pancreatic type" of pain triggered by some posterior penetrating duodenal ulcers.

Animals↗

Diurnal changes of bile lipid concentration in hepatic bile of cholecystectomized man.

Diurnal variations of bile lipid concentration were studied in ten patients with a tube in the main bile duct following a cholecystectomy. 5-6 bile samples per 24 h were collected from each patient during 3-40 days. The enterohepatic cycle was not significantly modified since total bile samples did not exceed 40 ml/day. Significant diurnal variations were observed in cholesterol concentration. Changes in lecithin concentration seemed to be similar in seven patients but did not reach the level of significance in any individual patient. Maximal values were observed between 4 and 8 a.m. and minimal values at 4 p.m. Bile salt concentration varied without any circadian periodicity. Mean bile lipid concentration was calculated for each patient. The patients with highest cholesterol concentrations have also the highest mean lecithin concentration. Mean bile salt concentration does not differ much from one patient to another.

Adult↗

Action of intragastric ethanol on the pancreatic secretion of conscious rats.

A surgical procedure has been disigned which permits injection in the stomach and the duodenum by separate catheters, collection of the pancreatic juice during the experiments, recirculation of the pancreatic juice into the duodenum between experiments, and a normal circulation of bile in rats. Experiments were performed in conscious rats given either 20% ethanol or water. In rats submitted to daily ethanol consumption for 13 months, the intragastric injection of 2 g/kg 20% ethanol considerably increased the pancreatic secretion of protein and, to a lesser extent, of water. In control non-alcoholic rats, a short period of increased secretion is followed by a major inhibition of pancreatic secretion, this reverse reaction to ethanol of pancreatic secretion according to whether or not rats are adapted to regular ethanol consumption is similar to what has been previously observed in dog. In chronic alcoholic rats, the release of secretin is probably not very different from controls.

Animals↗

Experimental lymphatic obstruction and fat absorption in the rabbit.

Using a previously published procedure of experimental abdominal lymphatic duct obstruction, we were unable to confirm increased faecal fat excretion after the operation. Nevertheless, the completeness of the obstruction and the huge dilatation of the lymph ducts of the villi have been verified. A spontaneous seasonal variation of faecal fat excretion has been observed in the rabbit with a maximum in October and November.

Animals↗

Atropine and exocrine pancreatic secretion in alcohol-fed dogs.

In dogs provided with chroinic pancreatic and gastric fistulas (Thomas canula), one of them vagotomized and alcohol-fed for 17 months with 50% (v/v) intragastric ethanol (0.2gm./kg.), an atropine perfusion (1.0 mg./hr.) superimposed on a continuous i.v. injection of secretion (GIH, 1.0 CU./kg./hr.) and CCK (GIH, Crick, Harper 3.0 U./kg./hr) prevents the excitatory effects on pancreatic secretion of an acute i.v. ethanol infusion (1.3 gm./kg.). In alcohol-fed dogs, the i.v. ehtanol-induced excitatory effect on 'pancreon' is exerted through a cholinergic mechanism, elicited at the hypothalamic bulbar centers and/or the intrapancreatic ganglia.

Animals↗

Analysis of the mechanism of action of calcium-induced exocrine pancreatic secretory changes in the dog.

In conscious dogs, provided with gastric and duodenal fistulas (Thomas cannula), the effect of an acute i.v. calcium infusion (10 mg./kg./hr.) on the plateau levels of secretin-induced (GIH, 1 CU./kg./hr.) pancreatic juice parameters were analyzed without or with previous cholingergic blockade by a continuous atropine perfusion (1.5 mg./hr.). In the former condition, i.v. calcium raised all pancreatic juice parameters, mainly protein concentration (148%) and output (173%). During atropine blockade, i.v. calcium changed neither flow rate nor bicarbonate output of secretin-induced pancreatic secretion. On the other hand, i.v. calcium exerted a reduced but still evident effect on protein concentration (85%) and output (40%). Intravenous calcium enhances secretin-induced pancreatic secretion plateau values through two mechanisms, mainly by raising the cholinergic tone of the whole "pancreon" and, partially, through a direct stimulus-secretion coupling effect on the acinar cells. Acute hypercalcemia induces the formation of protein plugs in the pancreatic secretion. They are excreted in the course of many days in both basal and secretin-stimulated pancreatic juice.

Animals↗

Lactoferrin in the duodenal juice of patients with chronic calcifying pancreatitis.

We have shown the presence of lactoferrin in the pancreatic juice of patients with chronic calcifying pancreatitis (CCP) and its absence in controls. In this work, lactoferrin has been found in saliva, but neither in gastric juice nor in bile. Therefore, a technique for collecting the human duodenal juice with a rubber tube and preventing its contamination with saliva is described. In the duodenal juice of 15 patients with CCP, 52 controls without evident pancreatic diseases, and 9 cases of pancreatic diseases other than CCP, lactoferrin has been searched for by immunological methods before and after an intravenous injection of CCK-PZ (3 U CHR) + secretin ( C U). The lactoferrin test in positive in 5, inconclusive in 6, and negative in 41 cases, and in the 9 cases of non-CCP pancreatic diseases it is negative. The use of this test in the diagnosis of CCP is proposed.

Adolescent↗

Chronic alcoholism and endogenous gastrin.

Gastirn blood levels after the ingestion of a meat meal, either alone or associated with ethanol (1.0 gm./kg.), are higher and better sustained in dogs treated chronically with alcohol than in control animals. This greater gastrin-releasing capacity of the dog gastric antrum would be responsible for the increased parietal cell mass and gastric acid secretion shown by animals subjected to chronic alcohol intoxication.

Alcoholism↗