1 The P-adrenoceptor blocking properties and cardioselectivity of ICI 141, 292 were investigated in healthy male subjects. 2 Seven subjects received in random order oral doses of ICI 141,29220,50,100,200 and 400 mg, atenolol 50 and 100 mg and placebo. ICI 14292 had no effect on supine heart rate which was reduced by atenolol 100 mg. ICI 141,292 50, 100 and 200 mg had no effect on standing heart rate which was reduced by 400 mg at 2 h. Both doses of atenolol caused greater reductions. 3 The maximum percent reduction of an exercise tachycardia after ICI 141,292 200 mg (23.9 ± 3.7%) and 400 mg (24.3 + 5.2%) were similar to atenolol 50 mg (27.3 + 4.7%) but less than atenodol 100 mg (30.8 + 2.9%) (P < 0.02). 4 Six subjects received in random order single oral doses of ICI 141,292 100, 200 and 400 mg, atenolol 50 mg, propranolol 40 mg and placebo. Following each dose each subject received graded infusions of isoprenaline sulphate until heart rate increased by 40 beats min-'. Dose-response curves were constructed for the changes in heart rate, finger tremor, blood pressure and forearm blood flow produced by each infusion. 5 At the 4 ,ug min-' dose of isoprenaline, ICI 141,292 200 mg caused more attenuation than atenolol 50 mg but less than propranolol 40 mg in the changes of heart rate, diastolic blood pressure and finger tremor (P < 0.02). ICI 141,292400 mg caused more attenuation of the changes of all parameters than atenolol 50 mg but less attenuation of the changes in diastolic blood pressure and finger tremor than propranolol 40 mg (P < 0.02). 6 These results indicate that ICI 141,292 is a cardioselective ,-adrenoceptor antagonist with partial agonist activity.
suMMARY The week-to-week, inter-and intraobserver variation in left ventricular echocardiographic measurements has been studied in 10 normal male volunteers and in five patients with stable valvular disease. A two-way analysis of variance showed no statistically significant variation either from week to week or between observers. Furthermore the within observer variation was minimal. Calculation of the coefficient of variation allowed confidence limits to be applied to each of the six ventricular measurements, thus providing ranges of variation in follow-up studies using M-mode echocardiography.The development of M-mode echocardiography has allowed much useful information to be obtained about left ventricular structure and function both in health and disease. One application of echocardiography in this regard is in sequential studies to assess the progression or regression of a disease process or the effect of pharmacological intervention. It is therefore important to establish the degree of variation among echocardiographers in their analysis of data. Recently, clear guidelines were suggested for echocardiographic measurements,' and, using these guidelines, we have looked at the variations in left ventricular dimensions from week to week for four weeks in 10 normal volunteers and five patients with stable valvular heart disease.We have also assessed the inter-and intraobserver error of three physicians in measuring these echocardiograms.
Subjects and methodsFourteen normal volunteers and six patients with stable valvular heart disease (on no medication and not showing evidence of cardiac decompensation)
We have studied the contribution of beta 1- and beta 2-adrenoceptors to the isoprenaline-induced changes in heart rate, blood pressure, forearm blood flow, peripheral vascular resistance, and finger tremor. This was achieved by a comparison of the effects of atenolol 50 mg, ICI 118551 25 mg, propranolol 80 mg, atenolol 50 mg combined with ICI 118551 25 mg, propranolol 80 mg combined with ICI 118551 25 mg, and placebo. Atenolol 50 mg and ICI 118551 25 mg caused similar attenuations in the isoprenaline-induced changes in heart rate and diastolic blood pressure, but the responses after the combination of atenolol and ICI 118551 were similar to those after propranolol 80 mg. There was no difference in the forearm blood flow responses to isoprenaline after atenolol 50 mg and ICI 118551, but atenolol 50 mg did not reduce peripheral vascular resistance compared with placebo. Both responses after treatment with atenolol combined with ICI 118551 were similar to those after propranolol 80 mg. Finger tremor responses to isoprenaline were antagonized by ICI 118551 alone and in combination with propranolol and atenolol but not by atenolol alone, suggesting that the response is beta 2-adrenoceptor-mediated. We conclude that the cardiovascular responses to isoprenaline are mediated by both beta 1- and beta 2-adrenoceptors, whereas the finger tremor response is mediated by beta 2-adrenoceptors.
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