Acute effects of smoking on blood pressure and cerebral blood flow.

Chronic smoking, particularly in hypertensives, is associated with an increased frequency of cerebral infarction and subarachnoid haemorrhage; cerebral blood flow (CBF) is also decreased in chronic smokers. The acute effects of smoking upon CBF are less clear. The present study in six volunteers investigated the immediate effects of smoking (and inhaling) three cigarettes, each separated by a 2 hr gap, upon heart rate, blood pressure (BP) and CBF assessed by xenon inhalation and flow velocities in the middle cerebral artery by transcranial Doppler ultrasound. Smoking caused significant increases in heart rate, BP and middle cerebral artery flow velocities, and a significant fall in CBF (individual falls in hemispherical flow could be as great as 40%). These haemodynamic effects are probably caused by nicotine-induced changes in catecholamine release. The possible clinical significance of the BP and CBF changes induced by acute smoking in high-risk groups is discussed.

First-dose effects of enalapril and atenolol upon blood pressure and cerebral blood flow in patients with mild hypertension on diuretic therapy.

The present single-blind, randomised, cross-over, placebo-controlled study was set up to compare the first-dose effects upon blood pressure (BP) and cerebral blood flow (CBF, measured by Xenon inhalation) of a single oral dose of atenolol 50 mg and enalapril 5 mg in ten hypertensive patients receiving a thiazide diuretic. It was found that a) the timing and degree of fall in BP after the first dose of atenolol and enalapril on a diuretic background were similar and generally not associated with symptoms or a fall in CBF, and b) dizziness, which is sometimes associated with the first-dose effect of ACE inhibitors in hypertensives on diuretics, can occasionally occur accompanied by a substantial fall (43%) in CBF in the absence of marked falls in systolic blood pressure. It is suggested that the latter event may be linked to a disturbance of cerebral autoregulation in part dependent on localised renin-angiotensin systems.

Efficacy of nitrendipine in the treatment of elderly hypertensive subjects, and its effect on cerebral blood flow.

The ability of nitrendipine to control blood pressure (BP) over a 12- or 24-h period was assessed in patients greater than 65 years of age who had a systolic BP (SBP) greater than 170 mm Hg and a diastolic BP (DBP) greater than 100-130 mm Hg. Thirty patients were randomized equally into two groups: Group 1 received the drug once daily and Group 2 received it twice daily after a 2-week run-in on placebo. The study was double blind. BP was recorded 24 h (Group 1) or 12 h (Group 2) postnitrendipine. The study design permitted one dose titration if BP exceeded 170/100 mm Hg after 3 weeks of active therapy when the dose was doubled. Patients received 6 weeks of therapy at the preferred dosage. Patients underwent measurements of cerebral blood flow (CBF) initially and on three further occasions: after the final dose of placebo, and after the first and last doses of nitrendipine. With active therapy, mean SBP and DBP fell in both groups when subjects were in the sitting and standing postures, except that in Group 1 at Week 5 only, standing SBP and DBP were not significantly reduced on the 10 mg once daily regimen. At the preferred dose, eight of the 15 patients in Group 1 and 13 of the 15 patients in Group 2 responded with a reduction of standing DBP of 10 mm Hg or greater, 24 and 12 h, respectively, after the last dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of nitrous oxide on cerebral blood flow in normal humans.

We have studied the effect of nitrous oxide on cerebral haemodynamics in 24 healthy male volunteers. Hemispherical cerebral blood flow (CBF) was measured using the xenon-133 inhalation technique, blood flow velocities in the right middle cerebral artery were calculated using transcranial Doppler ultrasound and the pulsatility index (PI)--the inverse of which is theoretically proportional to flow in the vessel under investigation--was derived from analysis of the spectrally analysed velocity pulse wave form obtained from the middle cerebral artery. Each variable was measured with the subject inhaling 100% oxygen (1st baseline), 30% nitrous oxide in oxygen, 100% oxygen (2nd baseline) and 60% nitrous oxide in oxygen. CBF was significantly greater with 30% (0.01 > P > 0.001) and 60% nitrous oxide (P < 0.001) compared with baseline, although the difference between 30% and 60% nitrous oxide was not significant. Changes in 1/PI correlated closely with those in hemispherical CBF. Blood flow velocities increased significantly with 30% (P < 0.001) and 60% nitrous oxide (0.005 > P > 0.001), the difference between 30% and 60% nitrous oxide also being significant (0.005 > P > 0.001). We observed a plateau in the change in CBF caused by nitrous oxide and suggest that this may be explained by activation of intact autoregulative mechanisms in healthy human brain.

Mitral valve prolapse, aortic compliance, and skin collagen in joint hypermobility syndrome.

Mitral valve prolapse was sought clinically and with phonocardiography and M mode and sector echocardiography in 15 women aged 22-57 years with joint hypermobility syndrome. The type III:III + I collagen ratio was measured in skin biopsy specimens and was found to be raised in seven of 10 patients sampled. Thirteen patients had increased aortic wall compliance measured by the continuous wave Doppler ultrasound technique. Ten (67%) patients had mitral valve prolapse shown by auscultatory signs or echocardiography or both--a prevalence at least three times greater than that in the general adult population. It is concluded that if the abnormality of collagen biosynthesis found in skin biopsy samples in these patients is also present in their mitral valve tissue this may predispose them to prolapse of the valve.