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Biomedical subjects

S N Joffe

Publications and source records attributed to S N Joffe.

At least 73 records · Page 4Linked to original sources
PubMed1983

In vitro and in vivo technique for assessing vagus nerve regeneration after parietal cell vagotomy in the rat.

This study determined if the vagus nerve can regenerate and/or reinnervate the gastric parietal cell mass after parietal cell vagotomy (PCV) and examines tests for assessing vagus nerve regeneration in rats. Microscopic dissection of the neurovascular bundle allowed the vagus nerve to be divided at the gastric body with preservation of the antropyloric nerve and gastric vasculature. Gastric secretory tests were performed under basal and stimulated conditions using secretagogues and insulin hypoglycemia. The candidate hormone, pancreatic polypeptide, was measured in plasma following a mixed meal, insulin hypoglycemia and i.v. secretin. Rats were killed weekly for 9 weeks and the vagal nerve distribution examined by both light and electron microscopy. Stimulated gastric acid output fell from 164 to 26 mumol/h immediately after operation (P less than 0.001). One week following PCV, the nerves were swollen with fibroblast infiltration and collagen around axon groups showed degeneration. By the third week after PCV, the axons were more densely packed with neurofilaments and acid output had increased to 183 mumol/h. In the fourth and fifth weeks, the enlarged Schwann cell processes had more axons and acid output rose to 262 mumol/h. By the seventh week, both large and small axons were identified and the acid output was 93% higher than the preoperative level (P less than 0.001). PCV and antrectomy also was followed by reinnervation of the gastric mucosa. Pancreatic polypeptide concentration in plasma was virtually unchanged following ingestion of food, insulin hypoglycemia or secretin. In rats, following PCV, gastric secretory tests and electron microscopy seem to be the most reliable methods of assessing vagus nerve regeneration.

Animals↗
PubMed1983

Pain provocation test in peptic duodenitis.

Controversy exists as to whether or not duodenitis alone can cause peptic ulcer symptoms. A modified provocation perfusion test has been performed in 10 symptomatic patients with duodenitis confirmed by endoscopy and histology. The test was conducted without the patient being aware of whether 0.1 N hydrocholoric acid, normal saline, or 8.5% sodium bicarbonate was being perfused directly on the area of duodenitis through the endoscopic irrigation cannula at a fixed rate of 10 ml/min for 10 min. The test was also performed in eight patients with dyspepsia alone and in five patients with chronic duodenal ulceration. Intraduodenal infusion of acid reproduced the epigastric pain in all patients with peptic duodenitis and duodenal ulcer patients, including the feeling of nausea in several which was partially relieved by bicarbonate infusion. In patients with dyspepsia but no peptic duodenitis, the symptoms were not reproduced. It would appear that "peptic duodenitis" can cause symptoms and that this "pain provocation test" may prove useful in its diagnosis.

Bicarbonates↗
PubMed1983

Cyclic changes of plasma pancreatic polypeptide and pancreatic secretion in fasting dogs.

Fasting conscious dogs, each with a gastric fistula, Heidenhain pouch and Thomas duodenal fistula, were used. Basal pancreatic secretion showed periodic increases in phase with the periodic contraction of the stomach and duodenum. Periodic increases of plasma pancreatic polypeptide (PP), but not of gastrin, were observed in phase with the periodic contraction and secretion of the gut. Ganglion blockade abolished the cyclical activity, both secretory and motor, of the gut and of plasma PP. Intraduodenal infusion of lidocaine suppressed the spontaneous increase of pancreatic secretion and plasma PP. It is concluded both that the cyclical release of PP and the increase in pancreatic secretion are under the control of the intrinsic nerves of the duodenum.

Animals↗
PubMed1983

Increased lithogenicity of the bile after jejunoileal bypass in the rat.

Increased formation of biliary calculi is a complication of jejunoileal bypass (JIB) in man. We investigated the biliary lipid composition and bile flow rate in the rat 42 days after a JIB or sham operation. In the bile of the bypassed rats, the percentage cholesterol saturation and the concentration of phospholipids were significantly increased, while the concentration of bile acids and the lithogenic index (bile acids + phospholipids/cholesterol) were markedly decreased. The concentrations of cholesterol in the bile and in the liver were unchanged. These results suggest an increase in lithogenicity of the bile with decreased bile flow after JIB in the rat.

Animals↗
PubMed1983

Pre-operative localisation of parathyroid tumours using neck vein catheterisation and radioimmunoassay for parathyroid hormone: the Glasgow experience.

Reliable pre-operative localisation of parathyroid tumours can be of value in surgery for primary hyperparathyroidism, and particularly so where re-exploration of the neck is required. Neck vein catheterisation and parathyroid hormone radioimmunoassay have been suggested as a sensitive means of tumour localisation, and we report our experience of the technique over the last five years. A total of 46 patients with primary hyperparathyroidism had 50 studies performed with positive localisation and a pre-operative prediction made on 38 occasions (76%). Forty-two operations were carried out and a parathyroid tumour confirmed in 39 cases for a localisation efficiency of 69 per cent. No negative neck exploration followed a positive localisation. Twelve studies were performed in patients with renal osteodystrophy and localisation to a single site was achieved on only three occasions. It is concluded that neck vein catheterisation and parathyroid hormone assay can correctly localise parathyroid tumours in most cases of primary hyperparathyroidism, but it is suggested that its use be restricted to selected cases such as those subjects with previous negative neck exploration or patients for whom prolonged or repeated surgery may be a particular hazard.

Adenoma↗
PubMed1983

The prevalence of gastrinomas in recurrent peptic ulceration.

The prevalence of gastrinomas and the Zollinger-Ellison syndrome is unknown. In order to examine a high risk group of patients, basal and secretin-provoked plasma gastrin levels were determined in 50 consecutive patients, predominantly from the west of Scotland. All had endoscopically proven recurrent peptic ulceration following duodenal ulcer surgery. This resulted in three cases strongly suspected of having a gastrinoma. Further investigations including exploratory laparotomy were unable to demonstrate a gastrinoma in two, but the evidence suggested an occult tumour in one. In this remaining unoperated patient, the serum gastrin returned to normal. The reference range for both basal and secretin stimulated gastrin response and percentage change has been determined in normal control subjects (n = 10) and in primary ulcer patients (n = 20). It is concluded that in this study, gastrinomas had a less than 2 per cent prevalence in patients presenting with recurrent peptic ulceration. As the diagnosis of a gastrinoma changes the surgical approach, conducting screening tests still seems warranted.

Adolescent↗
PubMed1983

Nodular adrenal hyperplasia and Cushing's syndrome.

Clinical, biochemical, operative, and postmortem findings have established nodular adrenal hyperplasia as a clinicopathologic entity and a cause of Cushing's syndrome. The possibility exists that there is a relationship among the various forms of adrenal and pituitary diseases that lead to hyperadrenocorticism. This may include a continuous sequence from bilateral adrenal hyperplasia to micronodular and macronodular hyperplasia to a unilateral adrenocortical adenoma and even carcinoma. We report the investigation and management of six patients with Cushing's syndrome caused by bilateral nodular adrenal hyperplasia who were treated by operation at the Glasgow Royal Infirmary, Scotland from 1975 to 1979. Investigations included a variety of biochemical and radioimmunoassay tests on plasma and urine, provocative and inhibition tests, scanning (ultrasonography, computed tomography, and iodocholesterol), arteriography, and selective venous sampling. All patients underwent a bilateral adrenalectomy by the posterior approach. The adrenal glands varied in size from 4.9 to 18 gm and histology showed that they had the features of bilateral nodular adrenal hyperplasia. Five patients did well after operation; they are presently receiving replacement steroid therapy, and at a 3- to 7-year follow-up there was no evidence of Nelson's syndrome. Advances in drug therapy (medical adrenalectomy) with aminoglutethimide, metyrapone, and O,p-DDD should not at present cause a change in our surgical approach to this condition.

Adrenal Glands↗
PubMed1982

Morphologic and functional evidence of reinnervation of the gastric parietal cell mass after parietal cell vagotomy.

The incidence of recurrent ulceration after parietal cell vagotomy varies greatly and the cause is largely unknown. Whether the vagus nerve can regenerate or reinnervate the gastric parietal cell mass after parietal cell vagotomy was investigated. Careful microscopic dissection of the neurovascular bundle in 130 rats allowed the vagus nerve to be divided to the gastric body with preservation of the antropyloric nerve and gastric vasculature. Gastric secretory tests were performed under basal and stimulated conditions after secretagogue and insulin hypoglycemia stimulation. Rats were killed weekly and the vagal nerve distribution examined by electron microscopy. Stimulated gastric acid output decreased from 164 to 26 mumol/hour immediately after operation (p less than 0.001). One week after parietal cell vagotomy the nerves were swollen with fibroblast infiltration and collagen around axon groups showed degeneration. By the third week after parietal cell vagotomy, the axons were more densely packed with neurofilaments and acid output had increased to 183 mumol/hour. In the fourth and fifth weeks, the enlarged Schwann cell processes had more axons and acid output increased to 262 mumol/hour. By the seventh week, both large and small axons were identified and the acid output was 93 percent higher than the preoperative level (p less than 0.001). The sequential neuropathologic changes of vagus nerve degeneration, regeneration and functional reinnervation of the gastric parietal cell mass after parietal cell vagotomy are shown by this study. If this occurs in man, it may be an important cause of recurrent peptic ulceration after parietal cell vagotomy.

Animals↗
PubMed1982

The effect of cimetidine and 15(S) 15-methyl prostaglandin E2 on the healing of laser-induced gastric mucosal damage.

Delayed perforation, a complication of laser photocoagulation, could be reduced by accelerating healing and inhibiting gastric secretion. With the use of the Nd:YAG laser, a beam was passed through a single glass fiber (400 micrometer) with 10 degrees divergence at a constant power of 80 W for 1 sec at a 1-cm distance from the gastric mucosa. Rats were then randomly allocated to receive cimetidine (50 mg/kg), 15(S)15-methyl prostaglandin E2 (50 micrograms/kg), or saline intraperitoneally twice daily for 4 or 7 days. The surface area of ulceration at 4 days for the control rats and the cimetidine- and prostaglandin-treated rats was 29, 34, and 28 mm2, respectively, and was much larger than the initial lesion of 15 mm2. Histologically, all lesions showed the typical appearances of peptic ulceration with perforation in half the prostaglandin-treated rats. By 7 days, the surface area in the cimetidine-treated rats appeared to decrease, but the light microscopic changes were similar to the saline- and prostaglandin-treated rats. Neither cimetidine nor prostaglandin enhanced healing in this study.

Animals↗
PubMed1982

The effect of parenteral and enteral nutrition on portal and systemic immunoreactivities of gastrin, glucagon and vasoactive intestinal polypeptide (VIP).

To compare the effect of parenteral with enteral nutrition on gastroentero-pancreatic hormones, hypercaloric and hypocaloric nutrient preparations, commonly used clinically, were administered to rats either through cannulae in the jugular vein or gastrostomies. Control rats were fed orally ad libitum. Portal and aortic plasma was collected for radioimmunoassay with antibodies to C-terminal regions of gastrin and glucagon and to N-terminal-to-central regions of glucagon and VIP. Levels of all immunoreactivities were significantly lower in aortic than portal plasma. Apparent clearance of glucagon and gastrin by liver or lung both was enhanced by administration of the hypercaloric nutrient intravenously. Only intragastric hypercaloric nutrition maintained levels of VIP immunoreactivity close to those of control rats. Intragastric administration of either preparation appeared to maintain adequate levels of gastrin. Differences in the levels of glucagon immunoreactivities may be related to the stimulatory effects of metabolites in the lower gut and pancreas.

Animals↗
PubMed1982

Effect of jejunoileal bypass on plasma and brain amino acids in the rat.

Liver failure and coma are serious complications of jejunoileal bypass (JIB) in man. Rats underwent either a 90-95% JIB or a sham operation. Six weeks later all animals were sacrificed, and plasma and brain amino acids were determined. In the plasma of rats with JIB compared with sham operation, the concentrations of valine, leucine, isoleucine, lysine, tryptophan, and tyrosine were significantly lower, while in the brain, phenylalanine, tyrosine, histidine, and glutamine were significantly higher. These changes in the brain are similar to those resulting from portalsystemic shunting in the rat.

Amino Acids↗