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Biomedical subjects

B F Robinson

Publications and source records attributed to B F Robinson.

At least 55 records · Page 3Linked to original sources
PubMed1980

Effects of nifedipine on resistance vessels, arteries and veins in man.

1 The effect of nifedipine on peripheral blood vessels has been studied in man. 2 Nifedipine induced dilatation of the forearm resistance vessels when given either by local intra-arterial infusion or sublingually (10 mg). 3 Local infusion of the drug did not relax hand veins preconstricted by infusion of noradrenaline and neither local infusion nor sublingual administration prevented constriction mediated by the sympathetic nervous system. Nifedipine was, however, a potent inhibitor of hand vein contractions induced by high concentrations of potassium provided that the noradrenergic component of the response was suppressed by simultaneous infusion of phentolamine. 4 Sublingual nifedipine (10 mg) did not dilate the elbow collateral arteries. 5 The effects of nifedipine on peripheral blood vessels are similar, but not identical, to those of verapamil. The pattern of action, with dilatation of resistance vessels but not capacitance, resembles that of hydralazine rather than glyceryl trinitrate and this suggest that nifedipine may prove useful in the treatment of hypertension.

Adult↗
PubMed1979

Comparative dilator effect of verapamil and sodium nitroprusside in forearm arterial bed and dorsal hand veins in man: functional differences between vascular smooth muscle in arterioles and veins.

Verapamil and sodium nitroprusside induce a dose dependent dilatation in the forearm arterial bed and preconstricted dorsal hand vein in man. Verapamil is about twenty times more effective in dilating arterioles than veins; sodium nitroprusside is about ten times more effective in veins than arterioles. These differences can be related to functional differences between the two types of vessel.

Adult↗
PubMed1976

Mechanism of action of beta-blocking drugs in angina pectoris: a review.

The effect of beta-blockers in improving exercise tolerance in angina pectoris can be accounted for by the reduction in heart rate and arterial pressure than they produce. The failure of a few patients to respond despite reduction in heart rate and the failure of those who do respond to obtain the full expected benefit suggests that beta-blockade has some action that offsets in while or in part the advantage gained from reduction in heart rate and pressure. This action might include an increase in left ventricular size with consequent increase in work, or an increase in left ventricular diastolic pressure with resultant impairment of blood flow to the inner layers of the myocardium.

Adrenergic beta-Antagonists↗
PubMed1975

Plasma renin activity during and after dynamic and static exercise.

The effect of dynamic and static exercise on plasma renin activity was investigated in three normal males. Near maximal supine exercise for 10 min on a bicycle ergometer caused a small increase in plasma renin activity during exertion with a much larger increase during recovery which reached a peak between 10-20 min. Supine exercise at half this level and static exercise (hand-grip) had no detectable effect on plasma renin activity.

Heart Rate↗
PubMed1972

Clinical investigation of an antagonist at alpha- and beta-adrenoceptors-AH5158A.

1. The alpha- and beta-adrenoceptor blocking action of AH 5158A was investigated in man using the veins of the hand, the arterial bed of the forearm, and certain responses of the circulation as a whole.2. In the veins, locally infused AH 5158A resulted in specific and competitive antagonism of the constrictor response to locally infused noradrenaline and of the dilator response to isoprenaline.3. Brachial artery infusions of AH 5158A resulted in competitive antagonism of the arterial blood flow changes produced by local infusions of noradrenaline and isoprenaline.4. Systemic infusion of AH 5158A (0.5-0.9 mg/kg) produced clear blockade of the heart rate response to systemic infusion of isoprenaline. It also attenuated the response to exercise at 80 watts for 4 min; mean arterial pressure during exercise was reduced by 16% and heart rate by 18%. Blockade lasted at least 1 hour.5. AH 5158A caused small changes in arterial pressure and heart rate at rest supine, but had no effect on the response of pressure and rate to tilting.

Adrenergic alpha-Antagonists↗
PubMed1972

Comparison of blockade at alpha-adrenoceptors by thymoxamine and phentolamine in peripheral arteries and veins of man.

1. The antagonism at alpha-adrenoceptors by thymoxamine and phentolamine of the response to noradrenaline was investigated in the limb veins and arteries of man.2. Brachial artery infusions of thymoxamine (40 mug/min) produced rises in resting arterial flow of up to 100%. When infused mixed with noradrenaline, thymoxamine (40 mug/min) attenuated the blood flow response to noradrenaline. Blockade was of a similar degree to that which occurred following a 10 min infusion of phentolamine (40 mug/min).3. Local intravenous infusion of thymoxamine (400-2,000 ng/min) mixed with noradrenaline attenuated the venoconstrictor response to noradrenaline. The degree of attenuation was similar to that seen after a 10 min infusion of phentolamine (500 ng/min). Blockade after thymoxamine did not last longer than 16 minutes. Neither thymoxamine nor phentolamine altered resting venous compliance.4. Local intravenous infusions of thymoxamine (500 ng/min) and phentolamine (500 ng/min) abolished the sympathetically mediated venoconstriction produced by overbreathing.5. Systemic injection of thymoxamine (0.1 mg/kg) did not block the reduction in forearm arterial flow produced by locally infused noradrenaline. In two out of three experiments, however, it produced some antagonism of noradrenaline induced venoconstriction. Systemic phentolamine (5 mg) blocked the effect of noradrenaline in the arterial bed, but antagonized its actions in the veins in only one out of three experiments.

Adrenergic alpha-Antagonists↗
PubMed1970

Effect of ergotamine and ergometrine on forearm venous compliance in man.

The effect of ergotamine and ergometrine on the venous compliance of the forearm has been studied in normal persons. Ergotamine tartrate (0.25 mg. intravenously) led to a fall in venous compliance amounting to 49% on average, while ergometrine maleate (0.25 mg. intravenously) caused a reduction of 41%; these changes were statistically significant. The potent veno-constrictor action of these ergot alkaloids appears to be a major component of the circulatory response to small doses and may be important in provoking the harmfull cardiovascular side-effects (such as angina and pulmonary oedema) that are sometimes observed in patients with pre-existing heart disease.

Angina Pectoris↗