The present study suggests that genetic factors are associated with susceptibility to develop symptomatic dental abscesses.

Increased co-immunostaining of CD31 and VEGF-3 in vessels associated with human dental pulp inflammation occurred, which suggests lymphangiogenesis.

A simple, economic, and sparing method for isolation of cardiomyocytes from adult rat heart is proposed. Ultrastructure of cardiomyocytes from suspension of freshly isolated cells was studied by light and transmission electron microscopy. The isolated cardiomyocytes were viable, had characteristic shape and size, and retained their normal structure.

The effects of Amiodarone and Nibentan on the postextrasystolic and postrest reactions were studied with normal rat myocardium and (for Amiodarone only) with myocardial strips isolated from patients with coronary heart disease (CHD). One-third of the patient samples displayed spontaneous activity that could be effectively suppressed by Amiodarone. All other samples displayed postrest inotropic effects of two types, with 30 or 70% decreases in the parameters of the contraction-relaxation cycle. Amiodarone did not influence the reaction of the first type but increased the postrest inotropic response of the second type. Both Amiodarone and Nibentan decreased the postextrasystolic inotropic response of the normal rat myocardium and simultaneously increased the postextrasystolic contraction. In addition, these drugs nearly doubled postrest potentiation. In the patient myocardium samples, however, Amiodarone did not decrease the amplitude of the extrasystolic contraction but increased postextrasystolic potentiation. It was supposed that, in the myocardium of some CHD patients (as well as in the rat myocardium), Amiodarone increases the ability of the sarcoplasmic reticulum to accumulate calcium ions. The same was supposed for the effects observed for Nibentan in tests with the rat myocardium. This phenomenon may contribute to the suppression of abnormal activity of the myocardium and strengthen the direct antiarrhythmic effect of Amiodarone.

Function of sarcoplasmic reticulum was studied in rat papillary muscles treated with amiodarone. An extra stimulus (0.5 Hz) was delivered to the muscle 0.225 sec after application of a regular stimulus. Postextrasystolic potentiation was evaluated in control myocardial samples and samples treated with amiodarone. The preparation significantly increased all the parameters of postextrasystolic contraction. It was concluded that amiodarone potentiates the ability of sarcoplasmic reticulum to accumulate Ca2+ ions.

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