A pilot study was conducted of males 40-45 years old from rural areas of three countries to study the long-term effects of dietary fats on the lipids of plasma, red blood cells (RBCs), and platelets. Differences were observed in cholesterol and phospholipid levels of plasma. Total phospholipids of RBCs and platelets were similar in all three countries. The pattern of individual phospholipids of RBCs in the Finnish and Italian samples differed from the American samples. In all plasma and RBC glycerolphospholipids, the monounsaturated fatty acids were highest in the Italian and the saturated fatty acids were highest in the Finnish samples; PUFAs were highest in the USA samples. Platelet glycerolphospholipids followed similar fatty acid patterns. We concluded that the fatty acid compositions of the glycerolphospholipids of plasma, RBCs, and platelets reflect the major dietary fatty acids.

Three-dimensional TTE and TEE are feasible and useful methods in identifying the location of MV prolapse. They were superior in the description of pathology in comparison with the corresponding 2D techniques and should be regarded as an important adjunct to standard 2D examinations in decisions regarding MV repair.

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Nifedipine (10 mg qid) and captopril (25 mg qid) were tested alone and in combination in 14 patients suffering from severe primary hypertension. Each study period was of 1 week's duration. Circulatory response was evaluated through hourly pressure and pulse rate readings. The fall in pressure after oral nifedipine was maximal within 1 hr or less and was generally accompanied by palpitation and increase in pulse rate; with a six hourly dosing regimen the tendency of blood pressure to recover after each dose was interrupted by the next dose, so that values remained significantly reduced throughout the 24 hr, although pressure fluctuations were evident. Promptness of the antihypertensive action of captopril was similar, but the magnitude and the duration of the fall in pressure were less pronounced. When the converting-enzyme inhibitor was combined with the calcium-channel blocker, pressure fluctuations were not abolished, but the antihypertensive response was definitely enhanced, so that normal blood pressure was maintained for several hours during the day. Additional positive effects of captopril were mitigation of the heart rate reaction and prevention of the ankle pitting or edema elicited by nifedipine. A balance in arteriolar and venular dilatation promoted by captopril is the suggested mechanism for these effects. With the two-drug combination the function of the left ventricle was not reduced and possibly improved; blood urea nitrogen and serum electrolyte and creatinine concentration were not affected. Plasma renin activity increased with captopril and reverted toward baseline with the addition of nifedipine, suggesting an interference of the calcium-channel blocker with the release of renin. Circulation 70, No. 2, 279-284, 1984. CALCIUM ANTAGONISTS block transmembrane Ca supply and reduce the contractile vascular muscle activity in a dose-related manner. However, the higher the wall tension is elevated above normal, the more relaxation is induced by a given concentration of Ca antagonist.' Because of this, the use of these compounds has been proposed in the management of hypertensive crises2 as well as in the treatment of essential hypertension.3 The hypotensive response to oral nifedipine is prompt, and a dosing regimen every 6 hr significantly lowers blood pressure over the 24 hr, although fluctuations are recorded owing to the rate of decay of the vasodilating effect.4 The reaction of pulse rate at the nadir of the hypotensive response to each

We evaluated in patients suffering from COPD-related pulmonary hypertension whether nifedipine therapy lowers acutely and chronically pulmonary vascular pressure and resistance and whether pulmonary transmural pressure may be further lowered by the combined use of nifedipine and oxygen. Changes of the pulmonary vascular tone were determined on the pulmonary driving pressure/flow curve, which was generated by upright exercise. Fifteen patients with COPD and mean pulmonary pressure greater than or equal to 20 mm Hg were studied at control (Week 0) and after 1 wk of nifedipine treatment (180 mg daily, Week 1). It was possible to pursue the same nifedipine daily dosage for 2 months in 10 patients, who were re-evaluated after 8 wk of treatment and after nifedipine withdrawal the following week. At Week 1, mean pulmonary transmural pressure was reduced (32.8 +/- 4.1 versus 27.3 +/- 2.8 mm Hg, mean +/- SE, p less than 0.05) via active pulmonary vasodilation because the pulmonary driving pressure/flow curve was shifted right and downward. Both mean transmural pulmonary pressure lowering effect and active pulmonary vasodilatation regressed during long-term nifedipine treatment. Oxygen reduced pulmonary transmural pressure (32.8 +/- 4.1 versus 28.6 +/- 2.9 mm Hg, p less than 0.05, Week 0); however, this effect always disappeared during nifedipine treatment. We conclude that nifedipine should not be used as long-term treatment for COPD-related pulmonary hypertension and that nifedipine inhibits the oxygen capability to reduce pulmonary pressure.