Effect of somatostatin on pancreatic enzyme secretion

The effect of somatostatin (SS) on the pancreatic enzyme secretion was studied in a perfusion system using dispersed pancreatic rat acini in vitro. In addition the effect of SS on pancreatic secretion in vivo was also studied in conscious rats for comparison. In an in vitro study, 6 x 10(-7) M SS-14 caused no significant change in amylase release when added 20 min before stimulation by 10(-5) M carbamylcholine (Cch), 10(-6) M A23187, 5 x 10(-7) M secretin and 2 mM dibutyryl cyclic AMP. The addition of 6 x 10(-7) M SS-28 also caused no significant change in amylase release stimulated by 10(-5) M Cch. High performance liquid chromatographic examination indicated that no degradation of either SS-14 or SS-28 occurred after reaction with dispersed acini. In an in vivo study SS-14 caused marked inhibition of basal pancreatic secretion and stimulated pancreatic secretion by bile-pancreatic juice diversion. These results indicate that SS has no direct inhibitory action on rat pancreatic secretion, and that SS may inhibit the pancreatic secretion by indirect mechanisms.     

Effects of dithiocarbamates on testicular toxicity in rats caused by acute exposure to cadmium.

N-Benzyl-D-glucamine dithiocarbamate (BGD), N-p-isopropylbenzyl-D-glucamine dithiocarbamate (PBGD), and diethyl-dithiocarbamate (DED) were compared for their protective effects against the testicular toxicity in rats induced by acute exposure to cadmium. Rats were injected subcutaneously with 109CdCl2 (3 mg Cd and 74 kBq of 109Cd/kg) and 30 min later, they were injected intraperitoneally with the chelating agents (0.4 or 3 mmol/kg). Cadmium injection increased lipid peroxidation and concentrations of hemoglobin and Ca in the testes, decreased the testicular weight, and caused sterility. The treatment with BGD (0.4 mmol/kg) did not satisfactorily protect against the testicular toxicity of cadmium. The administration of PBGD or DED at a dose of 3 mmol/kg significantly prevented the increase in the lipid peroxidation and hemoglobin concentration in the testes, the decrease in the testicular weight, and the sterility caused by cadmium. PBGD and DED significantly decreased the cadmium concentration in the testes, but DED increased the cadmium concentration in the kidney and brain. Only DED significantly prevented the increase in the testicular Ca concentration after cadmium. These results indicate that PBGD and DED protect against the sterility caused by cadmium in rats and that the effect of DED to increase the brain level of cadmium is more dangerous than the lack of effect of PBGD to prevent the increase in the testicular Ca level. The protective effects of PBGD and DED against the cadmium-induced testicular toxicity presumably result from a decrease in the cadmium concentration in the testes.     

Successfully treated intraoperative coronary artery spasm in a patient with type B dissecting aortic aneurysm: a case report]

A 65-year-old man with chronic type B dissecting aortic aneurysm, complicated by variant from of angina pectoris without any coronary artery obstructed disease on preoperative angiogram was operated upon through left posterolateral thoracotomy under the left heart bypass with Bio-pump system using preoperative Ca antagonists and intraoperative nitroglycerin infusion. Shortly before the end of operation the patient suddenly developed shock status definitely due to coronary artery spasm, associated with ST-elevation in II, III, aVF and bradycardia, then ventricular tachycardia, finally cardiac arrest. The patient was resuscitated by cardiac massage and administration of nifedipine and nitroglycerin. Such attacks repeated five times at ten or twenty minutes intervals. The coronary artery spasm could be successfully suppressed with the additive use of noradrenaline infusion. The patient had no attacks at all postoperatively and was discharged with good success. This case suggests that the prevention of intraoperative coronary artery spasm is essential, but if it occurs, additive use of noradrenaline infusion is effective for the cessation of coronary artery spasm.     

Changes in plasma and duodenal cholecystokinin concentrations after pancreatic duct occlusion in rats

The changes in plasma and duodenal cholecystokinin (CCK) concentrations after pancreatic duct occlusion were examined in rats. The rats were sacrificed 1, 3, 7, 10, 14, and 30 days after occlusion of the duct. Histological examination showed acute inflammation on days 1 and 3 after duct occlusion, interstitial fibrosis and regenerative changes on days 7, 10, and 14, and pancreatic atrophy on day 30. The plasma CCK concentration increased from 0.45 pM to 2.0 pM after the occlusion and then remained high throughout the observation period. In contrast to the stable increase in plasma CCK concentration, the CCK content in the duodenum increased on days 1 and 3, decreased on day 7, increased on day 10, reaching over the control level on day 14, and then returned to the control level on day 30. Administration of boiled and 10-fold concentrated rat pancreatic juice or human pancreatic secretory trypsin inhibitor for seven days after pancreatic duct occlusion reversed the decrease in duodenal CCK content. The major molecular forms of duodenal CCK were CCK-8, -33, and -58. These results indicate that (1) basal plasma CCK concentration did not reflect the duodenal CCK content, (2) duodenal CCK content was well correlated with a decrease in inflammation in the pancreas, and (3) a nonenzymatic component in the pancreatic juice reversed the decrease in duodenal CCK content and body weight caused by pancreatic duct occlusion.     

Estimation of passive smoking during pregnancy by cotinine measurement and its effect on fetal growth

Maternal cigarette smoking has been associated with some complications of pregnancy, including low birth weight and increased morbidity. Recently, it has been reported that maternal passive smoking also affects the fetal environment and causes fetal growth disturbance. In this study, we aimed to investigate the effects of maternal passive smoking on pregnant women and their fetuses by measuring cotinine concentrations in maternal urine and umbilical cord blood. The results were as follows: 1) Among 259 pregnant women, 17 cases (6.6%) were active smokers. The women who were not aware of passive smoking at all, were only 39 cases (15.1%). More than 80% of the pregnant women smoked either passively or actively each day. 2) Cotinine concentrations in both maternal urine and umbilical cord blood increased with the increase in passive smoking. Those in maternal serum, however, did not correlate with the increase in passive smoking. 3) The relative birth weight (R.B.W.) of the newborn infants delivered by the mothers whose cotinine concentration was more than 9.0ng/ml (This value represented the mean +1.5SD of the cotinine concentration in the urine from the mother who did not passively or actively smoke) was significantly lower than that of the mothers whose cotinine concentration was less than 9.0ng/ml. It is concluded that the measurement of the cotinine concentration in maternal urine or umbilical cord blood is very useful in estimating the effects of passive smoking on pregnant women. And passive smoking as well as active smoking also has a harmful effect on the fetal growth mechanism.