Biomedical subjects
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We investigated the effect of gallopamil administration during a cold pressor test (CPT) in 18 patients suffering from chronic angina (CA) and in 21 healthy subjects. CA patients showed increased basal levels of beta-thromboglobulin and thromboxane B2 compared to control patients and normal plasma levels of catecholamines. CPT caused plasma catecholamines, beta-thromboglobulin and TxB2 levels to rise. This rise was greater in CA patients than in control patients. Administration of gallopamil (50 mg kg-1 three times a day for 30 days) reduced plasma levels of catecholamines, beta-thromboglobulin and TxB2 blood concentrations either under basal conditions or after CPT. Our data suggest that gallopamil is able to modulate the response induced by adrenergic stress.
BACKGROUND: Most respiratory diseases involve the heart and can lead to acute or chronic pulmonary heart in the most serious cases. The common pathogenetic element is pulmonary arterial hypertension which es secondary to the resistance of the pulmonary circulation together with hypertrophy and/or dilatation of the right ventricle, caused mainly by chronic hypoxia. METHODS AND RESULTS: In order to verify the effects induced on pulmonary circulation and right heart by BA or COPD the cardiac function was assessed by mono and bidimensional Doppler echocardiography in 10 patients with BA (group A), 10 with COPD (group B) and 10 healthy control subjects (group C). At the M-mode echocardiography examination no significant difference was observed among the three study groups. By Doppler pw the peak velocity of early tricuspidal flow (VmaxE) was significantly higher in the group A when compared to the group B (p = 0.03). No subject had pulmonary hypertension. The pulmonary acceleration time (PAT) using pw Doppler technique was similar in groups A and B but it was significantly different when compared to group C (p = 0.006:A vs C; p = 0.03:B vs C). CONCLUSIONS: Our results suggest in patients either with BA or COPD, an early involvement of the right heart even if they had a clinical stable condition and no pulmonary hypertension.
Thirty-two patients, nineteen males and thirteen females, mean age 59.4 +/- 11.9 years, 18 with peripheral arteriopathy Fontaine stage II and 14 with cerebral vasculopathy were submitted to treatment with picotamide, 900 mg/die. In basal conditions and after 30 and 60 days of treatment, we evaluated some blood clotting parameters concerning both platelets (circulating platelet aggregates, beta-thromboglobulin, TxB2, 6-keto-pgF1 alpha) and plasma (fibrinogen, plasminogen, ATIII, Factor VIII-C and VIII Ag, prothrombin time, activated thromboplastin time) and some instrumental parameters such as walking distance and Doppler with a post-ischaemic hyperaemia test in patients with peripheral arteriopathy and Doppler of epiaortic vessels with resistance and pressure-perfusion index evaluation in patients with cerebral vasculopathy. Treatment with picotamide significantly reduced circulating platelet aggregates, beta-TG and TxB2 levels, without change of 6-keto-PGF-alpha values, with reduction of F VIII-C and slight increase of plasminogen and ATIII levels. In patients with peripheral arteriopathy after two months, a significant increase in distance and an improvement of arteriolar reactivity were observed, as shown by increase of the perfusion-index and by reduction of the post-ischaemic recovery time. These observations, together with the good tolerance of the drug, justify the use of picotamide in the treatment of patients with atherosclerotic vasculopathy at different localizations.