In a double-blind, cross-over study for 8 weeks, including 10 non-hospitalized elderly hypertensives (average age 73.2 years), WHO stage I-II, the antihypertensive effect of nifedipine slow-release tablets, 20 mg twice daily, was compared with placebo. Nifedipine reduced supine and standing blood pressure values significantly, and no signs of orthostatic hypotension were noted. An initial increment in heart rate was found after 1 week with a subsequent fall towards control values after 8 weeks of nifedipine administration. Heart rate pressure product in the supine position was reduced, and this reduction became statistically significant at the 8th week. Cardiac output measured non-invasively in 8 patients after 6-8 weeks' nifedipine therapy, using an Irex echocardiograph, was on an average 34% higher than in the placebo period (p less than 0.05). Serum electrolytes, cholesterol, HDL cholesterol, blood glucose and renal function were not affected by the drug. Side-effects were few and mild. It is concluded that nifedipine is a potent antihypertensive agent which may represent an attractive first choice alternative in the treatment of elderly hypertensive patients.

Aged↗

PubMed1984

Leg work.

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Adult↗

PubMed1984

Effects of a selective thromboxane synthetase inhibitor, dazoxiben, and of acetylsalicylic acid on myocardial ischemia in patients with coronary artery disease.

Thromboxane A2 (TxA2) may aggravate myocardial ischemia by inducing vasoconstriction and platelet aggregation in small coronary vessels, whereas prostacyclin (PGI2) counteracts these effects. Acetylsalicylic acid (ASA) inhibits the formation of TxA2 as well as PGI2, whereas dazoxiben, a thromboxane synthetase inhibitor, reduces TxA2 formation selectively. In 25 patients with coronary artery disease, 2 identical atrial pacing stress tests were performed: before and after the administration of dazoxiben (200 mg) in 15 patients and before and after ASA (250 mg) in 10. The ischemic response, quantified by coronary sinus and aortic lactate levels and by ST depression, was significantly reduced after administration of dazoxiben (p less than 0.02) but not after ASA. Heart rate at rest, myocardial extraction of free fatty acids and the arteriovenous oxygen difference was unaffected by medication. Both drugs reduced TxB2 levels to the same extent, whereas collagen-induced aggregation was more reduced after ASA than after dazoxiben. The effect of dazoxiben on ischemia was probably a result of inhibited TxA2 and preserved PGI2 production, which increased blood flow to ischemic regions.

Aspirin↗

PubMed1984

Effects of timolol on platelets in coronary sinus blood and on myocardial ischemia during pacing-induced angina.

The effect of timolol on blood platelet function was studied in coronary sinus and caval vein blood at rest and during pacing-induced angina in 20 patients with coronary heart disease. During pacing-induced angina, lactate measurements confirmed that coronary sinus blood was sampled from ischemic regions in 13 men. The ischemia did not influence platelet function. In blood from non-ischemic myocardium, platelet activation was found during pacing: the ADP-induced aggregation, platelet retention and plasma beta-thromboglobulin levels increased moderately but significantly. Timolol administration prevented this platelet activation, possibly by inhibiting catecholamine release from the myocardium, and reduced the ischemic response during pacing as judged from lactate measurements and ST depressions. It is concluded that timolol reduced platelet activation induced in non-ischemic regions of the heart during tachycardia stress as well as myocardial ischemia.

Adult↗

PubMed1984

Determination of cardiac output by Doppler echocardiography.

Cardiac output determined by Doppler echocardiography was compared with that determined by thermodilution at rest and during dobutamine infusion in 10 patients (group A) and by the Fick method at rest in 11 patients (group B). All patients had angina pectoris without valvular heart disease. Maximum spatial blood velocity and cross sectional aortic area were estimated by the Doppler technique and echocardiography. Cardiac output was calculated by multiplying blood velocity by aortic area at various levels in the ascending aorta. The best correlation of cardiac output between the invasive and non-invasive methods was obtained when maximum velocity in the aortic root and the aortic orifice area were used in the calculations. Cardiac output was considerably overestimated when area measurements in the aortic root were used.

Adult↗

PubMed1983

The effect of a thromboxane synthetase inhibitor, dazoxiben, and acetylsalicylic acid on platelet function and prostaglandin metabolism.

Twenty-four men received either placebo, 0.1 g of the thromboxane synthetase inhibitor dazoxiben, 0.25 or 1.0 g of acetylsalicylic acid (ASA). Dazoxiben reduced the maximal rate of collagen-induced platelet aggregation, but less than did ASA. ASA abolished secondary, ADP-induced aggregation, dazoxiben not. Both drugs prolonged the bleeding-time. Plasma thromboxane B2 (TxB2) levels did not change significantly after dazoxiben, whereas the prostacyclin metabolite 6-keto-PGF1 alpha rose. The larger dose of ASA reduced both TxB2 and 6-keto-PGF1 alpha in plasma. Whole blood was allowed to clot in order to estimate prostaglandin metabolism. Both drugs prevented thromboxane production effectively. Formation of 6-keto-PGF1 alpha decreased by 95 per cent after ASA but was more than doubled after dazoxiben. Dazoxiben is a selective and effective thromboxane synthetase inhibitor, but has a weaker effect on platelet reactivity than ASA, possibly because endoperoxide formation is not prevented.

6-Ketoprostaglandin F1 alpha↗

PubMed1983

The effects of nifedipine, a calcium antagonist, on platelet function.

Platelet function was studied before and 1 hour after ingestion of 20 mg nifedipine, a new calcium antagonist, in 20 patients with coronary heart disease. Platelet counts remained unchanged. Platelet adhesiveness, measured as retention in glass bead columns with Hellem's method for native blood, did not drop significantly eigher when 0.9 or 3.6 ml of blood was used. Platelet aggregation, which is dependent on extracellular calcium, was induced in citrated platelet-rich plasma. The mean maximal rate of primary aggregation, initiated with three different concentrations of adenosine diphosphate, was reduced by 20% to 26%. The rate of irreversible collagen-induced aggregation was on average 23% lower after nifedipine. The mean bleeding time was 36 seconds, or 12%, longer after ingestion of the drug. The moderate, but significant reduction of platelet aggregation and prolongation of the bleeding time by nifedipine may be mediated through inhibition of calcium transport across the platelet membrane.

Adenosine Diphosphate↗

PubMed1983

The effect of mother-child separation on the behavior of children experiencing a diagnostic medical procedure.

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Blood Specimen Collection↗

PubMed1983

The influence of open-heart surgery during extreme hemodilution on the hemostatic mechanism in the dog.

12 Labrador retriever dogs had mitral disc valves implanted during cardiopulmonary bypass (CPB) with extreme hemodilution, obtained with preoperative blood withdrawal, the use of blood-free priming fluid during perfusion, and retransfusion of autologous blood. Before operation, platelet adhesiveness as well as the reactivity of the intrinsic and extrinsic coagulation systems were markedly higher than in man. During CPB, the number of functioning platelets was very low, but increased after retransfusion, and were after 4 h twice as high as in 7 human patients who received aortic disc valves during CPB with extreme dilution. The extrinsic coagulation system also reacted much faster during and after CPB in the dogs, and heparin activity was rapidly neutralized and intrinsic coagulation normalized in them. Intravascular coagulation did not occur, and more hemolysis was induced in the dogs than in the patients. 3 of the dogs died from valve thrombosis within 24 h. The high reactivity of platelets and coagulation systems in the dog makes the canine model a very difficult one for experimental open-heart surgery because of a strong tendency to thrombosis.

Animals↗