[Echinococcosis in a thoroughbred horse imported from Ireland].
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Biomedical subjects
Publications and source records attributed to W Murmann.
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The present paper describes spontaneous pathological findings including etiological aspects in digestive tracts of kangaroos, which have been detected in 166 necropsies during the last 20 years. Protozoan - infections, herpes virus infections, gastroenteritis of unknown etiology and especially the occurrence of the so called "lumpy-jaw" turned out to be of special importance. These findings are discussed with reference to the literature, completed as well by short literature reviews, sub-divided into the different organs and the variable etiology of the diseases, as by a brief description of digestive tract physiology and anatomy in marsupials.
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The effects on plasma lipids and nicotinic acid concentrations of a single dose of 2-(3-pyridinecarbonylamino)-2-deoxy-1,3,4,6 dihydrogen-D-glucose tetra-3-pyridinecarboxylate (LG 13979) compared with the effects of nicotinic acid and of its known derivatives niceritrol and sorbinicate, at the same doses, were studied in the fasted rat. Results show that LG 13979 has more prolonged activity on plasma free fatty acids and triglycerides, with longer lasting and more intense activity on plasma cholesterol than these three reference standards. Free fatty acid rebound occurs after administration of nicotinic acid and niceritrol, but not after LG 13979. This pharmacodynamic profile may be explained on the basis of the kinetics of nicotinic acid plasma concentrations, which are low, constant and lasting after LG 13979 administration.
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A derivative of nicotinic acid, D-glucitol hexanicotinate (sorbinicate, SN), was investigated in rats for gastrointestinal absorption, hydrolysis to free nicotinic acid and plasma kinetics of nicotinic acid following oral administration. All the data obtained in several test conditions, suggest that SN is absorbed unhydrolysed in the first segment of the intestinal tract after being rendered at least partially soluble by the gastric HCl and subsequently hydrolysed to free nicotinic acid by several tissues. The hydrolysis is so rapid that the plasma nicotinic acid after a dose of SN is practically all in the free form. There are large species differences in the plasma kinetics of nicotinic acid after an oral dose of SN but in all species the plasma nicotinic acid levels are always much lower and more constant than after an equidose of nicotinic acid.
The study was designed to elicit any interference on the part of dipyrone with the antispasmodic activity of 2-(diethylamino)-1-methylethyl cis-1-hydroxy(bicyclohexyl)-2-carboxylate (rociverine) and on the part of rociverine with the analgesic activity of dipyrone. No evidence of any reciprocal inhibition of the specific pharmacodynamic activities of the two drugs emerged. Further, dipyrone exerted remarkable antispasmodic effect which in some experimental conditions supplements that of rociverine. The nature of this antispasmodic effect contributed by dipyrone could not be identified from the in vivo work, though in in vitro tests dipyrone revealed appreciable antihistaminic activity and weak muscle-relaxant activity. The value of an association in which neither activity is diminished and one is actually augmented is obvious.
The gastric secretion pattern resulting from histamine, pentagastrin and carbachol infusion was studied in lumen-perfused anesthetised male Wistar rats. The differences between the results of this study and other published results and among the latter demonstrate the necessity of knowing the acid secretion patterns in given laboratory conditions before attempting to assess the antisecretory activity of any drug.
A study on variables influencing the gastric secretory response of pylorus-ligated Wistar rat, shows that: 1. 24 h is a sufficient fasting period for satisfactory emptying of the stomach, periods of up to 48 h yielding no advantage; 2. between 2 and 4 h is the most appropriate pyloric ligation time because in this range there are no variations in volume of gastric secretion, concentration and output of acid per unit of ligation time; 3. sex has no influence on any of the parameters; 4. animals should be age-selected because only above a given age threshold the gastric secretory response per unit of bodyweight is constant.
A systematic study in vitro and in vivo of the antispasmodic agent 2-(diethylamino)-1-methylethyl cis-1-hydroxy (bicyclohexyl)-2-carboxylate (rociverine) showed that its activity is both antimuscarinic and directly muscle-relaxant. The antimuscarinic activity is weaker than that of atropine, N-butylscopolammonium bromide and dicyclomine whilst the direct muscle-relaxant activity is equal to or greater than that of papaverine. The peculiarly balanced ratio of the neurotropic and myotropic components ensures that the antispasmodic effect is the outcome of both, without one prevailing over the other. This not only rules out major atropine-like side-effects but renders rociverine potentially effective on spasm of the different viscera, of particular interest in viscera in which there is only minor involvement of cholinergic structures. The muscle-relaxant activity of rociverine is achieved by inhibiting the availability of Ca2+ at contraction site and not through an antiphosphodiesterasic mechanism, which might explain the absence of muscle-relaxant effects on the smooth musculature of the blood vessels.
D-Glucitol hexanicotinate (sorbinicate), when given orally to fasted rats, depresses the plasma free fatty acids (FFA) and triglycerides. The depression is about equal in intensity and duration to that induced by corresponding doses of nicotinic acid as such, but occurs in the presence of nicotinic acid plasma levels far lower than those obtained with nicotinic acid. In fact, sorbinicate is absorbed more slowly and more smoothly than is the case with nicotinic acid and the bioavailable nicotinic acid after oral sorbinicate administration is thought to be not more than 3--4% of the dose given. At the dose closest to that in clinical use sorbinicate exerts a more lasting effect than nicotinic acid both on FFA and on triglycerides, and at all the doses tested, contrary to nicotinic acid, sorbinicate did not induce plasma FFA rebound. This particular type of bioavailability, which differentiates sorbinicate from nicotinic acid, might explain the better effect on the plasma lipids as well as the absence of the side-effects that occur with nicotinic acid administration.
A sulfomucopolysaccharide complex extracted from bovine pancreas displayed marked inhibitory activity against every one of a broad series of experimental inflammation models. No standard antiinflammatory drug has such all-inclusive action. The complex also exerts intense anticomplement activity in vitro. The potential antiatherosclerotic interest of this type of activity is suggested, in the light of recent hypotheses regarding the relevance of inflammatory and immune factors to the etiopathogenesis of atherosclerosis.
The effects of cis-2-hydroxy-2-phenylcyclohexanecarboxilic acid (cicloxilic acid) on the liver damage produced by a choline-free, high-fat low-protein diet (Handler's diet) were studied in rats. Treatment with cicloxilic acid significantly counteracted the increase in liver weight, hepatic lipids, serum transaminase and ornithine carbamoyl transferase activities, caused by the unbalanced and deficient diet. Histological examination of the liver showed a near-normal structure of the hepatic cells in the cicloxilic acid-treated animals. Other antihepatotoxic and choleretic drugs, with which cicloxilic acid was compared, showed either much less protective activity or none at all. Furthermore, while cicloxilic acid (which exhibits choleretic activity) did not alter the hepatic glycogen content, another choleretic drug, 1-phenyl-1-hydroxypentane (PC 1), caused marked depletion. It is concluded that the protective activity exerted by cicloxilic acid on the liver is separable from its choleretic activity.