Melatonin reduces early changes in intramitochondrial cardiolipin during apoptosis in U937 cell line.

Cardiolipin (CL) is found exclusively in the inner mitochondrial membrane. CL deficiency leads to an alteration in the stability of mitochondrial membranes, to an increased permeability as well as a decreased respiratory rate, and therefore to mitochondria which are completely dysfunctional. It is known that reactive oxygen species (ROS) cause a decrease and a variation in CL content, concomitantly the formation of the mitochondrial permeability transition pore facilitates the release of cytochrome c (cyt c) into the cytosol. Melatonin (Mel), the secretory product of the pineal gland, is a potent and efficient endogenous radical scavenger. It has been shown to protect, various biomolecules, such as DNA, membrane lipids, and cytosolic proteins from oxidative damage. To evaluate the protective role of Mel, we have studied U937 cells treated with UV-B irradiation. In our model, the administration of 1mM Mel before UV-B irradiation showed a significant protection from apoptotic cell death, in particular, mitochondrial structure and function were preserved through apoptotic pathways when cells were preincubated with 1mM Mel before UV-B exposure. The cardiolipin-sensitive probe 10-nonyl acridine orange (NAO) was used to monitor changes in mitochondrial lipids. Our data suggest that the Mel treatment protects CL from ROS and this suggests a possible link with the reduction of the apoptotic phenomenon.

[Antiarrhythmic treatment with mexiletine in acute myocardial infarction (author's transl)]. / Trattamento antiaritmico con mexiletina nell'infarto acuto.

The effect of an introduced i.v. bolus of 250 mg of mexiletine was checked in cases of acute myocardial infarction with ventricular premature beats. On the 19 observed subjects 17 are male and 2 female: 18 cases with acute myocardial infarction and 1 with acute coronary failure. The introduction of the bolus was followed by an infusion of 0.75 mg/m for the successive four days. After 60 m' no significant changes in arterial pressure and in the heart rate were recorded. The Extrasistolies decrease from 11 +/- 3 to 3 +/- 2/m' (-71%, p less than 0.01); PQ and QT variations were not significant. After four days of infusion, systolic arterial pressure decrease from 135 +/- 4 to 121 +/- 3 (-10%; p less than 0.01), sinusal rate drops from 90 +/- 4 to 80 +/- 3 (-12%, p less than 0.05). The changes of diastolic arterial pressure, PQ and QT were not significant. Extrasistolies disappears entirely. A comparison between a mexiletine and a xilocaine i.v. bolus showed that mexiletine performs a higher antiarrhythmic activity.

[Therapeutical comparison between atenolol and nifedipine in effort angina (author's transl)]. / Comparazione terapeutica fra atenololo e nifedipina nell'angina da sforzo.

In order to assess the therapeutical efficacy of atenolol in stable angina pectoris of effort, we studied 40 patients with a positive exercise stress test. Our double-blind study included a first group of 20 patients treated with atenolol, 100 mg once daily, and a second group of 20 subjects, treated with nifedipine (10 mg 3 times daily). The exercise test was performed before the treatment, after one month of placebo and after one month of therapy with nifedipine or atenolol. The variables examinated were the frequency of anginal chest pain, the quantity of nitroglycerin taken by the patients, the arterial pressure, the heart rate and the double product at the peak of the exercise testing. Differences between the results obtained in the two groups weren't statistically significant.