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The aim of this study was to investigate the influence of neurotensin on total microcirculatory blood flow, oxygen consumption, myoelectric activity and motility of the small bowel. The attempts were made to evaluate the role of L-Arginine, NO-system in the mechanism of action of this peptide on microcirculation, metabolism and motor-activity of the intestine. The experiments were performed in two experimental models--dogs and rats. In Vetbutal anesthetised animals the systemic arterial pressure, superior mesenteric artery blood flow, microcirculatory blood flow and myoelectric activity of the small bowel were continuously monitored. In experiments with dogs effective capillary index, arterio-venous oxygen difference and oxygen consumption were analysed. Neurotensin administered intraarterially caused a dose depended increase in total and microcirculatory blood flow in the small bowel in both groups of animals. The experiment with dogs showed the rise of effective capillary index and intestinal oxygen consumption. Administration of neurotensin changed the profile of myoelectric activity of the small bowel similar to that of postprandial hyperaemia. Inhibition of NO-synthase by the intravenous administration of L-NNA reduced significantly the amplitude of neurotensin hyperaemia. Pretreatment with L-Arginine, the substrate of NO-synthase reversed the hemodynamic, but not motility effects of neurotensin. The results presented proved the role of the L-Arginine-NO in circulatory mechanism, but not motility effects of neurotensin.

Examinations were carried out on 4 fasted dogs using chronic experimental model. In the animals the functional cholecystectomy was performed, 2 cannulas were inserted into the common bile duct and 9 pairs of electrodes were ++implanted from pyloric antrum till ileum. After the disconnection of the exteriorized tubes enterohepatic circulation of bile acid was interrupted. Then, sodium salts of taurocholic, taurodeoxycholic and taurochenodeoxycholic acids (at the concentrations 5, 20 and 50 mM) alone and in the combination were infused intraduodenally and myoelectric activity was continuously recorded. During control experiments the enterohepatic circulation was preserved. Application of individual bile acids at higher concentrations and their combinations caused significant (about 60 min) prolongation of cycle intervals changing fundamentally duration of both phases I and II along with the alteration of their relative proportion. In the control group duration, of both phase I and II as measured in mid jejunum lasted 47 +/- 3 and 38 +/- 2 min, respectively (ratio 1.24). During administration of 50 mM Na-taurodeoxycholate these values were respectively equal to 6 +/- 2 (P less than 0.01) and 122 +/- 31 min (P less than 0.05), respectively, and the ratio was 0.05. Infusions of primary bile acids resulted in the greater percentage of phases III which originated from the stomach. Propagation velocity of phase III as measured in the jejunum was about 50-100% faster, mainly during the infusion of dihydroxy bile acids. The results have suggested that bile acids are responsible for majority of alterations of the myoelectric cycle induced by intraduodenal bile administration. These changes could be interpreted as the disappearing tendency of the cycle but their mechanisms still remain to be elucidated.

In 4 dogs functional cholecystectomy was performed, 2 cannulas were inserted into the common bile duct and 9 pairs of the electrodes were implanted in the stomach and small intestine. During chronic experiments exteriorized tubes were disconnected for both monitoring of biliary secretion and intraduodenal infusions of buffer, standard bile, Na-taurocholate, Na-taurodeoxycholate and Na-taurochenodeoxycholate used in 3 various concentrations as well as mixtures of these salts. During other experiments Na-taurocholate was infused intravenously. In the control group biliary tubes were not opened. The interdigestive myoelectric activity was recorded simultaneously and blood samples were taken for motilin and PP radioimmunoassays. Biliary secretion and motilin release were the highest during phase III of the myoelectric cycle. During both bile acid depletion and intravenous infusion no clear fluctuation of biliary secretion was observed. Bile and bile acid infusions resulted in the increased motilin release about 20-50% depending on bile acid concentration and in more than 50% inhibition of PP release. Plasma level of PP fluctuated in relation to the phase of the cycle entirely during bile acid depletion. The results suggest that the regulation of myoelectric cycle by bile acid secretion can be mediated by motilin and PP as well as confirm the important role of small intestine in the modification of PP release.

The motoricity of an isolated intestinal loop under the influence of cholesterol before and after blocking the cholinergic or adrenergic receptors was recorded in 8 rabbits in chronic experiments. The adrenergic receptors wereblocked by intravenous administration of phentolamine and propranol, whereas cholinergic ones by atropine. At the same time the total level of cholesterol in vesicular bile was determined by the method of Zlatkis in 10 rabbits, and that in the wall of the jejunum by the method of Lieberman and Burchart. It was shown that cholesterol caused decrease of pressure in the intestinal loop, which was 1.3-4.1 kPa, resulting from dilatation of the intestines, if its concentration reaches 1.3-5.2 mmol/l. After blocking the adrenergic receptors and administration of cholesterol, its dilatating effect on the intestines was not observed, but most often a pressure increase in the intestinal loop by 2.3 kPa. The total cholesterol level in vesicular bile was 33.3 mmol/l, while 55.9 mg/g of tissue in the wall of the jejunum. The above studies showed that cholesterol at certain concentrations has a dilatating effect on the intestines. The dilatating mechanism of cholesterol is connected with adrenergic receptors. The concentrations of cholesterol decreasing the motoric activity of intestines are found in the organism, e.g. in bile, blood or in the intestine wall itself.

In 3 rabbits in chronic experiments motor activity of the innervated and vascularized pouch of jejunum was frequently registered under the influence of vitamins C, B1, B6 and folic acid before and after the blockade of cholinergic or adrenergic receptors. Vitamins B1, B6 and C decreased the motor activity of intestines but B2 and folic acid increased it. Decreased motor activity of intestines under the effect of vitamin C is probably connected with the stimulation of adrenergic receptors. Adrenergic and cholinergic receptors did not participate in the motor activity of intestines occurring under the influence of group B vitamin. In chronic experiments the intestines excitability to group B vitamin and to that of vitamin C does not differ much.

The studies were carried out on 33 chickens of the broiler breed in chronic experiments and in vitro. In the chronic experiments the motility of the jejunum under the influence of vitamins of group B and vitamine C was recorded in 8 chickens. The vitamins were used at concentrations from 10 mg/l to 2.5 x 10(3) mg/l. In the experiments in vitro, the motility of the isolated segment of the jejunum was recorded by the method of Magnus. In this part of experiments the chickens were divided into 3 groups, of which group I (15 chickens) were fed with DKA finischer mixture, group II (5 hens) received, besides the mixture, per os 200 mg of vitamin C for 2 weeks, group III (5 hens) received the mixture and for 2 weeks intraperitoneally 200 mg of vitamin C. The effect of vitamins of group B in vitro was determined in chickens of group I, whereas that of vitamin C in chickens of group I, II and III. At the same time the level of vitamin C in the wall of the jejunum was determined by the method of Roe-Kuenther. It was shown that vitamin B2 and folic acid caused stimulation of intestine motility in the chickens, while vitamin B1, B6 and C decreased the motoric activity. Increased level of vitamin C in the intestinal wall resulted in increased intestine sensitivity. Chicken intestines sensitivity to vitamins was 10 times stronger to vitamins than that of the intestines of rabbits.

In chronic experiments and in vitro the motoricity of jejunum in rabbits was recorded under the influence of vitamins soluble in fats - A, D3 and E before and after blocking adrenergic or cholinergic receptors. In chronic experiments the vitamins were used at concentrations of 2 - 500 micrograms/ml, whereas in vitro 0.1 - 30 mg/ml. It was shown that vitamins A, D3, and E inhibited the motoric activity of the intestines, but the influence of the vitamins was stronger in chronic experiments than in vitro. The strongest action inhibiting the motoricity was shown by vitamin D3, then A and a very weak action by vitamin E. Neither adrenergic nor cholinergic receptors were shown to participate in the mechanism of action of the vitamins on intestine motoricity, which is likely to be connected with direct influence of the vitamins on smooth muscular coat of the intestines.

The effect of interruption of enterohepatic circulation of bile acids on the interdigestive electrical activity of gastrointestinal tract was studied on 6 dogs. Animals underwent the functional cholecystectomy and cannulation of common bile duct. 9 bipolar electrodes were then implanted into the stomach and small intestine. Electrical activity was recorded during 2-3 and 4-10 hr periods of bile diversion with and without intravenous infusion of sodium taurocholate and also during intraduodenal bile acid infusions. In control group the enterohepatic circulation of bile acids was maintained. During longer bile diversion intervals of the myoelectric cycle increased from 104 +/- 7 min in control group till 133 +/- 8 min (P less than 0.05) mainly due to the prolongation of phase II. During the latter period a specific pattern of spike bursts (bile diversion myoelectric pattern, BDMP) was observed. This phenomenon was induced by the lack or deficiency in bile acids in the intestinal lumen (the bile acid depletion pattern, BADP) and it was inhibited during bile acid administration. When the biliary drainage was continued, 82% of an activity fronts originated in the jejunum. Their propagation velocities in upper jejunum were 9 +/- 1 cm.min-1 as compared to the control value, 6 +/- 0.05 cm.min-1 (P less than 0.05). These changes were approximate to those observed during intravenous taurocholate infusion. However, the cycle duration lasting 90 +/- 9 min was not significantly altered and BADP was less frequently recorded. The results obtained confirm the significant role of bile and bile diversion in modification of the myoelectric activity of stomach and small bowel in dogs.