Marked sinus tachycardia and overdrive suppression.
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Biomedical subjects
Publications and source records attributed to C Castillo.
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Liver injury produced by CCl4 depends on its metabolism by the liver cytochrome P450 enzyme system to a highly reactive intermediate (CCl3.). Cimetidine impairs cytochrome P450 and stimulates regenerative processes acting on DNA synthesis. This work was performed to investigate whether cimetidine may prevent CCl4-induced liver cirrhosis. Male Wistar rats were used: animals in group 1 received CCl4 (0.04 g per 100 g, i.p.) three times a week for 8 weeks; group 2 was treated with CCl4 plus cimetidine (120 mg kg-1, p.o.) three times a week for 8 weeks; group 3 received CCl4 for 8 weeks and then cimetidine for 4 weeks. Alkaline phosphatase, gamma-glutamyl transpeptidase (gamma-GTP) and alanine aminotransferase (ALT) activities, as well as protein and bilirubin, were measured in serum; collagen and lipoperoxidation were quantified in liver. Intoxication with CCl4 increased (P < 0.05) serum activities of alkaline phosphatase, gamma-GTP and ALT, and bilirubin concentration; liver collagen and lipoperoxidation were also increased. Cimetidine treatment prevented or reverted the increases in the three enzyme activities and in bilirubin content and the fall in proteins. It is worth noting that cimetidine co-treatment completely prevented both the increase in collagen content and the lipid peroxidation. The protective effect of cimetidine can be attributed to a reduction in cytochrome P450. However, it could also stimulate regenerative processes.
Drug-addicted patients (N = 435) admitted for treatment in different clinical settings were studied. Patients were classified according to their self-report of consumed drugs and to the results of urine screening tests. Of the patients, 77.8% were active consumers, 9.6% were included in a methadone maintenance program, and 12.6% were abstinent. In the active consumer patients, positive urine screening results surpassed by far the information provided in the self-reports. Most patients tested positive to several drugs, while only 8.7% tested negative to all screened drugs. These results indicate that the information provided by drug-dependent patients lacks reliability when an analytical screening method is used simultaneously.
The case of a patient with a cystic partially differentiated nephroblastoma (CPDN) is reported. Careful histological study is essential to distinguish CPDN and other types of multicystic kidneys (specially cystic nephroma or multilocular cyst of the kidney). Because of the rare potential for aggressive behavior of this tumor, nephrectomy alone is the therapy of choice. However, its relationship with Wilm's tumor is an indication for a regular clinical follow up.
Many exogenous and endogenous vasodilator substances produce their effects by stimulation of guanylate cyclase in vascular smooth muscle and increasing cyclic 3',5'-guanosine monophosphate (cGMP) levels. Activation of such enzyme leads to vasodilatation. Possibly as a consequence of a change in the pattern of protein phosphorylation, including dephosphorylation of the light chain myosin and of a decrease in the bioavailability of free calcium. Guanylate cyclase exists in two different forms in the vascular smooth muscle cells: a cytosolic (soluble) and the other associated to membranes (particulate). The nitro vasodilators and vasodilators with endothelium-dependent activity, act by main stimulation of the soluble guanylate cyclase, while the atrial natriuretic factor acts specifically on the particulate form of the enzyme. Guanylate cyclase represents the final path in the vasodilatation induced by diverse endogenous and exogenous substances, an aspect that has created a great interest among investigators due to its possible physiological, physiopathological and therapeutic implications. The more relevant aspects related with the mechanism of action of this numerous group of drugs are deeply analyzed in the present review.