Canine Exocrine Pancreatic Secretory Changes Induced by an Intragastric Ethanol Test Meal

In five dogs with chronic gastric fistulas (Thomas cannula) and a new type of chronic pancreatic fistula which permits collection of pure nonactivated pancreatic juice after ingestion of a test meal, the following series of experiments were performed: In the first series, a test meal (400 gm. canned dog meat) was given with 200 ml. saline simultaneously infused through the gastric cannula. In response to this stimulus, the 20-minute peak pancreatic flow rate and bicarbonate output were respectively 33% and 34%, of the maximal secretion of the pancreatic gland obtained with secretin in six control dogs provided with gastric and the classical Thomas duodenal fistula. The 20-minute peak protein output represented 84% of the maximal secretory capacity attained with dose-response curves to CCK in the same group of control animals.
In the second series either 1.5 or 2.0 gm./kg. ethanol were given instead of saline. Intragastric ethanol induced a dissociation of pancreatic secretion: a significant inhibition of flow rate, of bicarbonate concentration and output and a significant rise of protein concentration; protein output remaining unchanged.
It is postulated that ethanol, acting on the stomach and duodenojejunum, evokes, independently of its gastrin-releasing capacity', an unknown humoral or nervous mechanism that counteracts the ethanol-elicited cholinergic-mediated inhibition of pancreatic protein secretion which has been previously described.     

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.     

DISSEMINATED AMERICAN CUTANEOUS LEISHMANIASIS

Background. While studying cutaneous leishmaniasis in the central part of western Venezuela, we found four cases of disseminated American cutaneous leishmaniasis, three from the Lara State and one from Portuguese State. Methods. A clinical history was taken for each of these patients, followed by microscopic examination of the Giemsa-stained smears from their cutaneous lesions and by a Montenegro skin test. Serum from a skin lesion were grown in Novy-MacNeal-Nicolle medium (nnn). Hamsters were inoculated with suspension of tissues taken from the patient's lesions. Biopsies were taken for histopathologic examination. Isolates from cultures on nnn medium and from hamsters were subcultured in Schneider's medium for parasite identification, using molecular techniques. Treatment with injections of N-methyl glucamine antimonate, 25 mg/kg/day was precribed for each patient for 20 consecutive days and, after a week of rest, a second course of injections was administered. Results. Patients had disseminated papular, ulcerous, nodular, and ulceronodular lesions on the skin. Smears of the skin lesions from all of the patients showed abundant amastigotes within histiocytes or free in the tissues. The skin test was negative in two patients. On histopathologic examination of skin lesions, mainly numerous vacuolated histiocytes filled with amastigotes were observed. Isolates from all the patients were identified as Leishmania venezuelensis. One of the patients healed after treatment with N-methyl glucamine antimonate. The others were resistant to this therapy. Conclusions. Diffuse cutaneous leishmaniasis can be caused also by Leishmania venezuelensis. Patients with nodular lesions who presented a negative Montenegro skin test were more resistant to treatment with specific pentavalent antimonials.     

Blocking of Protein Pancreatic Secretion by Maximal Secretion Infusion in the Dog

In conscious chronic gastric and pancreatic fistula dogs (Thomas cannula), secretin was perfused for three hours with a submaximal (GIH, 1.0 C.U./kg.) and a maximal dose (GIH, 8.0 C.U./kg.), according to the following schedule: 1. First hour submaximal stimulus; 2. second hour maximal stimulus; 3. third hour submaximal stimulus.
The alkaline and protein components of pancreatic secretion were analyzed in 20-minute sample collections throughout the three hours.
The same protocol was followed in anesthetized dogs subjected to a mid line laparotomy. A biopsy of the pancreatic gland was taken before (control) and at the end of each perfused dose. The secretion showed a significant increase of protein concentration and output when passing from the maximal to the last submaximal secretin perfusion dose. These findings correlate well with the piling up of zymogen and prozymogen granules in the apical zone of the acinar cells during maximal secretin perfusion, with their subsequent discharge into the acinar lumen upon abrupt reversal to the initial secretin submaximal dose.
The study confirms that secretin influences pancreatic protein secretion and indicates in addition, that pharmacologic doses of the hormone, have the capacity to block acinar cell zymogen granule release.     

Atropine and Exocrine Pancreatic Secretion in Alcohol-fed Dogs

In dogs provided with chronic pancreatic and gastric fistulas (Thomas cannula), one of them vagotomized and alcohol-fed for 17 months with 50% (v/v) intragastric ethanol (2.0 gm./kg.), an atropine perfusion (1.0 mg./hr.) superimposed on a continuous i.v. injection of secretin (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. ethanol-induced excitatory effect on "pancreon" is exerted through a cholinergic mechanism, elicited at the hypothalamic bulbar centers and/or the intrapancreatic ganglia.