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Notes: Summary A disturbed renal circulation due to an imbalance between vasoconstrictor catecholamines and a vasodilator such as acetylcholine, caused by a decrease in acetylcholine, has been postulated as the basic mechanism of hemorrhagic degeneration of the kidneys in choline deficiency. In previous works from our laboratory we have shown a marked increased in the levels of renal catecholamines in choline-deficient rats in comparison to choline supplemented animals, while the content of acetylcholine remained unchanged. Since the changes in tissue catecholamines occurred before there were kidney lesions, we have suggested that an autonomic imbalance, due to an excess of catecholamines, plays an important role in the pathogenesis of renal injury in choline-deficient rats. A series of experiments were then planned to explore this theory further by administering adrenergic blocking agents (alpha-methyldopa and reserpine) attempting to prevent the development of the renal injury in choline deficiency. Young male Wistar rats from our outbred colony were allocated into two experiments. In experiment I the animals were divided at random in 4 groups: group CS-I, was fed a cholinesupplemented diet; group CSD-I, was fed a choline-supplemented diet and treated with alpha-methyldopa; group CD-I, was fed a choline-deficient diet; and group CDD-I, was fed a choline deficient diet and treated with alpha-methyldopa. Groups CSD-I and CDD-I received daily intraperitoneal injections of alpha-methyldopa (300 mg/kg of body weight). In experiment II the animals were divided at random in 4 groups: group CS-II, was fed a choline-supplemented diet; group CSR-II, was fed a choline-supplemented diet and treated with reserpine; group CD-II, was fed a choline-deficient diet; and group CDR-II, was fed a choline-deficient diet and treated with reserpine. The appropriate groups received daily intraperitoneal injections of reserpine (0.4 mg/kg of body weight). The kidneys of all surviving rats were studied grossly and histologically, and the levels of noradrenaline and adrenaline determined. All animals from controls groups (CS-I, CSD-I, CS-II and CSR-II) showed essentially normal kidneys on gross and light microscopic examination. On the other hand, while CD-I and CD-II rats showed severe hemorrhagic degeneration of the kidneys, the renal lesions of animals given alpha-methyldopa (CDD-I) and reserpine (CDR-II) were significantly less pronounced. The total content of noradrenaline and adrenaline in the kidneys of CDD-I and CD-I rats were not statistically different, although the CDD-I animals tended to have lower levels of catecholamines. The content of noradrenaline and adrenaline of rats from group CD-I was significantly higher than the corresponding values in CS-I rats. Besides, the total content of renal noradrenaline of CDD-I animals was found to be unaltered when compared to CS-I rats, while their content of adrenaline was found to be higher than the corresponding value in CS-I group. The noradrenaline levels of CS-I and CSD-I rats were similar, but the latter group had a higher renal adrenaline content than the former. The total content of noradrenaline and adrenaline of the group CDR-II was lower than that of the group CD-II and did not differ than that of the group CS-II. Besides, the total content of noradrenaline in the kidneys of CSR-II animals was lower than that of the CS-II animals, while the content of adrenaline did not differ in these groups. The findings of the present investigation, besides confirming our previous observations, clearly show that alpha-methyldopa and reserpine afforded a protective effect against the renal injury of choline deficiency, thus giving strong additional support to the theory that the kidney hemorrhagic necrosis of choline deficiency in young rats is in all probability due to an autonomic imbalance.

Notes: Summary A disturbed renal circulation due to an imbalance between vasoconstrictor catecholamines and a vasodilator such as acetylcholine, caused by a decrease in acetylcholine, has been postulated as the basic mechanism of hemorrhagic degeneration of the kidneys in choline deficiency. To explore this hypothesis further a group of male weanling Wistar rats was fed on a choline-deficient diet for 10 days (group CD). A control group was fed on the same basal diet supplemented with choline (group CS). Food intake and body weights were registered. The kidneys of choline-supplemented and choline-deficient rats were studied grossly and histologically. The levels of catecholamines (noradrenaline and adrenaline) and acetylcholine were determined. Pathological changes of the kidneys were present in 30 out 57 choline-deficient rats, permitting the separation of data obtained from deficient rats into those not associated with renal injury (CDa rats) and those associated with renal injury (CDb rats). A marked increase in the levels of renal catecholamines was observed in both CDa and CDb rats. On the other hand, the content of acetylcholine remained unchanged. It is noteworthy that the changes in tissue catecholamine levels occurred before there were changes in kidney weight and morphology. The findings support the concept that an imbalance between sympathetic and parasympathetic systems plays an important role in the pathogenesis of the renal injury of choline-deficient weanling rats; and this imbalance would be the result of an excess of catecholamines in the kidneys.

Notes: Summary The levels of noradrenaline, adrenaline, and serotonin in the jejunum and ileum of weanling rats fed protein-free (deficient) and high-protein (control) diets were analyzed. The concentration of noradrenaline of the deficient rats was markedly increased, both in the jejunum (0.430±0.039μg/g vs. 0.188±0.019μg/g in the control animals, +228%, P〈0.001) and in the ileum (0.492±0.041μg/g vs. 0.212±0.014μg/g in the control rats, +232%, P〈0.001). However, the levels of adrenaline and serotonin were unaltered in deficient rats as compared to controls, both in the jejunum (0.049±0.009μg/g of adrenaline and 1.233±0.178μg/g of serotonin vs. 0.047±0.006μg/g of adrenaline and 1.364±0.131μg/g of serotonin in the controls) and in the ileum (0.027±0.005μg/g of adrenaline and 0.902±0.150μg/g of serotonin vs. 0.038±0.006μg/g of adrenaline and 1.118±0.192μg/g of serotonin in the controls). In view of these results, it can be speculated that the abdominal distension and the reduced intestinal motility usually seen in the states of protein malnutrition could be caused, at least in part, by the accumulation of noradrenaline in the intestine.

Notes: Summary Catecholamine levels and weight of heart were studied in rats subjected to protein-calorie malnutrition and after a period of nutritional rehabilitation. Rats given a protein deficient diet (4% protein) for periods of 6 and 12 weeks showed a severe restriction of body weight gain. Nevertheless, even though the measured heart weight of deficient rats was significantly lower than the respective controls (16% protein), the deficient rats incurred “real” cardiac enlargement since the mean heart weight of the equal body weight controls was significantly different from that of the deficient animals. The mean heart weight of rats fed a high-protein diet for 6 weeks thereupon a 6-week period of protein deprivation was still less than that of controls, and the heart ratio was still greater than that of controls. However, the heart weight of rehabilitated rats was not significantly different from that of equal body weight controls. Serum protein and albumin levels in deficient rats were significantly decreased in comparison to rats fed a high-protein diet. While the serum protein levels of rehabilitated rats were lower than those of controls, the albumin levels were not different. The protein-calorie malnourished rats, which received a low-protein diet for 6 and 12 weeks, showed a significant increase in myocardium noradrenaline concentration. After a period of nutritional rehabilitation this change did not persist. These catecholaminergic alterations in heart may be responsible, at least in part, for the different cardiac abnormalities described as a result of protein-calorie dietary deficiency. It may also explain the “real” cardiac enlargement observed in deficient rats, according to the hypothesis that noradrenaline may be the ultimate myocardial hypertrophy hormone.

Notes: Abstract By means of transthoracic contrast echocardiography, the prevalence of a patent foramen ovale (PFO) was studied, in a continuous series of 48 patients aged less than 50 years with a recent episode of acute cerebral ischemia. A PFO was found in 11 subjects (23%). In the subgroup of younger patients (aged less than 30 years), the prevalence was much higher than in those aged 30 or more (58% against 11%, p=0.0022). In the 19 patients with clear evidence of extracardiac causal factors of cerebral ischemia, there was no PFO; of the remaining 29 subjects, a PFO was present in 11 (38%) (p=0.0015). In conclusion, the possibile presence of a PFO must be carefully investigated in subjects with cerebral ischemia aged less than 30, as well as in subjects aged between 30 and 50 in whom there is no acceptable explanation for their cerebral ischemic episode.

Notes: Zusammenfassung Bei normaler Ernährung und täglichem Trinken von beliebigen Mengen 40% igem Zuckerrohrschnaps wurden bei weissen Laboratoriumsratten diverse anatomische und ultrastrukturelle Lungenveränderungen nachgewiesen: Hypertrophie und Hyperplasie der Pneumocyten vom Typ 2, Anhäufung intraalveolärer Makrophagen und Verdickung der Alveolarwände.

Notes: Summary Chronic administration of alcohol to well-nourished rats led to striking changes in the small intestinal cell population. The present experiments corroborate the view that alcohol is directly toxic to the small intestine.

Notes: Zusammenfassung Elektronenoptischer Nachweis, dass Skorpiongift (Tityus serrulatus) nach i.p. Verabreichung an der quergestreiften Muskulatur der Küchenschabe eine starke nekrosierende Wirkung ausübt.

Notes: Zusammenfassung Bei Ratten, die während 4 Monaten ad libitum 40% igen Zuckerrohrschnaps getrunken hatten, wurden tiefgreifende Degenerationserscheinungen des adrenergischen Nervenplexus der Atrioventrikularklappen festgestellt.

Notes: Summary The effect of long-term alcohol ingestion on the norepinephrine concentration of the heart was investigated in rats. The alcoholic animals showed a highly significant increase in cardiac norepinephrine concentration as compared with the corresponding controls. It is further suggested that continued exposure to high levels of norepinephrine may play a role in the development of cardiomyopathy in chronic alcoholism.