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R Albertini

Publications and source records attributed to R Albertini.

95 records · Page 6Linked to original sources

Transition-metal complexes of isatin-beta-thiosemicarbazone. X-ray crystal structure of two nickel complexes.

Manganese, iron, cobalt, nickel, copper and zinc complexes of isatin-beta-thiosemicarbazone (H2L) have been synthesized and spectroscopically characterized The X-ray crystal structures of two nickel complexes, namely [Ni(HL)2]. EtOH (1) and [Ni(HL)2]. 2DMF (2), reveal a distorted octahedral coordination with the monodeprotonated ligand that behaves as an O,N,S terdentate. Different packing interactions are determined by the presence of different crystallization solvents, i.e., ethanol in 1 and dimethylformamide (DMF) in 2. 1H and 13C NMR studies of the ligand and zinc complexes in solution were carried out and a complete assignment for the ligand was made by homodecoupling, gradient assisted 2D 1H-13C HMQC and HMBC NMR spectroscopy. Biological studies, carried out in vitro on human leukaemic cell lines U937, have shown that the free ligand and the copper (II) complex are more active in the inhibition of cell proliferation than the nickel complexes. No compound was able to induce apoptosis.

Apoptosis↗

Angiotensin and sodium balance: their role in chronic two-kidney Goldblatt hypertension.

The purpose of this study was twofold: 1) to determine whether the failure of rats with chronic renovascular hypertension to respond to the angiotensin II antagonist (AIIA) with a decrease in mean blood pressure (BP) was dur to the agonistic effect of the antagonist; and, 2) if this was not the case, to examine whether a positive sodium balance impaired the reversal of the hypertension, after unclamping, in the rats that did not respond to angiotensin inhibitors. For this purpose, rats with chronic, two-kidney Goldblatt hypertension (one renal artery clamped and contralateral untouched) were tested for their BP response to the AIIA (1-Sar-8-Ala-angiotensin II) and to the converting enzyme inhibitor (CEI) SQ20,881, which is devoid of agonistic effect. Approximately 50% of the rats responded to both inhibitors either with no change or with a decrease in BP of less than 20 mm Hg (nonresponders). The other 50% had a decrease in BP of 20 mm Hg or greater (responders). The decrease in BP produced by the AIIA and the CEI correlated significantly (r = 0.76). Nonresponders to both inhibitors were unclamped or sham unclamped. A positive sodium balance was produced before surgery by injecting either 400 or 1000 microEq of sodium and was maintained for 12 hours. Direct BP significantly decreased 12 hours after surgery in the unclamped rats despite a continuous positive sodium balance. In the sham unclamped rats, BP did not change. These data indicate that the failure to respond to the AIIA is not due to the agonistic effect of this peptide. Furthermore, these data suggest that a positive sodium balance is not a major pathogenetic factor in maintaining the high BP in the nonresponder rats, since a positive sodium balance failed to maintain the hypertension after unclamping.

Angiotensins↗

Exchangeable sodium in angiotensinogenic and nonangiotensinogenic renovascular hypertension.

Previous studies have suggested that angiotensin II and sodium can act as alternative mechanisms in maintaining high blood pressure in chronic renovascular hypertension, In the present study, exchangeable sodium was measured in rats in which angiotensin II has been confirmed or excluded as the main cause of the hypertension. To determine the degree of participation of angiotensin II in the maintenance of the high blood pressure, we studied the mean blood pressure response to an angiotensin antagonist (1-Sar-8-Ala-angiotensin II) and to a converting enzyme inhibitor (SQ20,881). Rats with a decrease in blood pressure of less than 20 mm Hg, in response to both inhibitors, were classified as nonresponders; those with a decrease of 20 mm Hg or more, as responders. Fifty percent of the rats with two-kidney hypertension were nonresponders, and they had lower blood pressure and plasma renin activity than the responders. Further, these two-kidney, hypertensive, nonresponder rats had normal exchangeable sodium. The two-kidney hypertensive responders, on the other hand, had significantly higher exchangeable sodium than both the two-kidney, hypertensive nonresponders and the two-kidney control rats. These results suggest that angiotensin II and exchangeable sodium do not play a major role in the maintenance of the high blood pressure in the two-kidney hypertensive nonresponders. However, there appears to be an abnormal relationship between renin and exchangeable sodium in the two-kidney hypertensive responders that could contribute to the maintenance of the hypertension.

Angiotensin I↗

Effect of renal nerve stimulation on urine and tissue kininogenase activity in cats.

The effect of electrical stimulation of efferent renal nerves on urine and renal tissue kininogenase activity was studied in cats. Handling renal nerves before crushing produced a significant increase is mean blood pressure (BP) in intact animals. After crushing, stimulation of efferent fibers (15 V, 0.5 msec, and 25 Hz) by 15-second train duration and at 2.45-minute intervals did not alter the average renal blood flow (RBF) or BP over 30 minutes. Glomerular filtration rate, water, and potassium excretion rates did not change significantly in either kidney. Sodium excretion in the ipsilateral kidney decreased significantly (p less than 0.05) in both intact and adrenalectomized cats. In intact animals, the kininogenase activity of urine (UK) also decreased significantly in both kidneys during nerve stimulation. In adrenalectomized animals it decreased significantly (p less than 0.05) only in the ipsilateral kidney, and UK of the ipsilateral kidney was significantly lower than in the contralateral (p less than 0.05). In both groups of cats, UK returned to control values during the recovery period of 30 minutes after stimulation. Adrenergic blockade abolished the effect of nerves stimulation on sodium and UK. Renal tissue kininogenase activity (RK) per gram of wet tissue was significantly lower in adrenergically blocked animals. No differences were detected when comparing RK content of ipsilateral vs a release of adrenal and peripheral nerve ending catecholamines.

Adrenalectomy↗

Acute polyradiculoneuropathy occurring after hymenoptera stings: a clinical case study.

Hymenoptera stings may be responsible for both local and systemic reactions; these can be immediate or delayed, depending on the time between the sting and the development of signs or symptoms. Delayed clinical reactions have been reported, although unusual, due to serum sickness and/or affecting organs or systems generally not involved in the immediate reaction, such as heart, kidneys, central and peripheral nervous systems. This paper describes the clinical and immunological findings in a 51-year-old subject, who, after two stings of paper wasps, the second one after the third venom immunotherapy (VIT) injection, presented immediate large local and systemic allergic reactions which quickly improved after e.v. methylprednisolone administration. About 40 hours later, he developed acute polyradiculoneuropathy with muscle weakness, paresthesia, difficulties in standing up and walking. Skin tests and specific IgE determination showed allergy to paper wasp. The activation, by wasp venom, of peripheral blood mononuclear cells in primary culture, evaluated by tritiated thymidine incorporation proliferation assay, showed an important hypersensitivity to wasp venom. Therefore our results suggest the hypothesis that the polyradiculoneuritis causative etiopathogenetic mechanism might be a delayed immunological response to wasp antigens followed by an allergy-triggered autoimmune reaction, as previously suggested by other authors; they found lymphocytic infiltrates in demyelinization areas and at perivascular levels, by histologic examination of autoptical and bioptical material of patients with nervous system lesions after hymenoptera stings.

Acute Disease↗