Haemoconcentration, shear-stress increase and carotid artery diameter regulation after furosemide administration in older hypertensives.

The aim of the present study was to determine whether changes of carotid wall shear stress induced by changes in blood viscosity after diuretic administration cause carotid arterial dilatation in elderly hypertensives, as reported in the cat. Arterial wall shear rate (ultrasound technique, profilmeter FRP III), the systo-diastolic diameter (echotracking technique) and the mean blood flow velocity and volume of the common carotid artery, the blood viscosity (rotational viscometer) and the finger arterial blood pressure (Finapress Ohmeda) were measured in 12 young volunteers (aged 25+/-2 years) and in 12 elderly hypertensives (aged 80+/-4 years) treated with short-acting calcium antagonists up to 24h before the study, both at baseline and after intravenous furosemide infusion (0.5mg/min), when the haematocrit had increased by at least two percentage points. After furosemide administration the mean arterial blood pressure decreased and blood viscosity and carotid systolic shear stress increased in both groups. However, common carotid artery diameter increased only in the young controls but not in the elderly hypertensives. These data show that an increase in carotid shear stress caused by haemoconcentration induces carotid vasodilatation only in young healthy subjects, and not in elderly hypertensives. This effect may be related to impaired endothelium function and/or arterial wall mechanics.

Systemic and regional haemodynamic effects of aortofemoral angiography.

UNLABELLED: The aim was to investigate the regional and systemic haemodynamic consequences of bolus injection of fluids with different physical properties in the course of routine aortography. Iopamidol was compared with an equiosmolar solution of mannitol and with a 0.9 N saline solution. Continuous blood flow and Pulsatility Index (PI), as an index of regional vascular resistance, were measured by Doppler technique. Finger arterial pressure and heart rate were monitored at the time and for 3 min following each intraaortic bolus injections. The patients who underwent routine aortography were grouped according to the site of the flow measurements: common femoral artery, common carotid artery and brachial artery. Flow changes induced by the bolus infusion were evident for all the fluids but only at the femoral artery level. After an immediate (3 +/- 2 s) and brief (2 +/- 2 s) but marked reduction of flow and in-phase increase of PI following the bolus, further haemodynamic changes were observed only in the femoral artery, with a peak at 35 +/- 10 s and returning to baseline values after 70 +/- 15 s, in terms of both increased mean blood velocity and decreased PI. Saline and mannitol induced overall blood velocity alterations of 54% and 80%, respectively, and PI reductions of 44% and 57% compared with those induced by iopamidol. In the other vascular areas there was only a 17 +/- 2% increase of the physiological early diastolic backflow at the brachial artery level. Blood pressure decreased and heart rate increased in phase with the flow changes of the femoral artery. IN CONCLUSION: (1) a dramatic rheodynamic perturbation at the site of injection induces a vasodilating stimulus; (2) the haemodynamic response following injection results in marked vasodilation of only the tributary vascular bed; (3) flow steal may occur from other beds towards the lower limb vascular beds owing to vascular impedance imbalance; (4) a reduction of systemic arterial pressure is induced in phase with the regional vascular events and a reflex increase of the heart rate; and (5) the physical properties of the injected fluids influence the intensity of the perturbation, although the decisive triggering factor is the counterflowing bolus per se.

Baroreceptor-heart rate reflex sensitivity enhancement after urinary bladder distention in essential hypertensives.

Our objective was to determine if urinary bladder distention modifies the sensitivity of the baroreceptor-heart rate reflex in hypertensive and control subjects. The baroreceptor-heart rate reflex sensitivity was measured in 15 male patients (mean age 37+/-8 years) with mild untreated hypertension (mean 163+/-8/ 95+/-12 mmHg) and 17 age- and sex-matched control subjects before and after urinary bladder distention. Bladder filling was performed infusing saline heated to 37 degrees C via a urinary catheter; the volume infused in each patient corresponded to that which caused the urge to void without reaching the pain threshold. The baroreceptor-heart rate reflex sensitivity was determined correlating the variations of the systolic pressure and of the peak blood flow velocity in the common carotid artery with the variations of the ECG RR' interval of the following heart beat, both during spontaneous and phenylephrine-induced fluctuations of the haemodynamic variables. After bladder distention the diastolic pressure of the hypertensive subjects increased significantly (95+/-12 vs. 100+/-12 mmHg: P < 0.02), whereas the heart rate decreased (RR= 873+/-70 vs. 926+/-80 ms; P < 0.005). These parameters were unchanged in the normotensive subjects (84+/-9 vs. 83+/-8 mmHg and 914+/-158 vs. 913+/-140 ms, respectively). The baroreceptor-heart rate reflex sensitivity, measured on the basis of spontaneous pressure and carotid blood flow velocity fluctuations in relationship to RR changes, decreased in the normotensive subjects after bladder distention (10.7+/-4.6 vs. 9.4+/-2.7 ms/mmHg; P < 0.05 and 423+/-99 vs. 356+/-102 ms/kHz; P < 0.01, respectively), whereas it increased in the hypertensive patients (6.9 +/- 3.6 vs. 8.3 +/- 2.8 ms/mmHg; P < 0.03, and 332 +/- 86 vs. 381+/-97 ms/kHz; P < 0.03 respectively). After bladder distention and phenylephrine administration the baroreceptor-heart rate reflex sensitivity, measured by the correlation between systolic pressure and RR interval, increased only in the hypertensive group (10.2+/-5.4 vs. 15.2+/-7.7 ms/mmHg; P < 0.005). In conclusion urinary bladder distention provokes in hypertensives but not normotensive controls a brisk parasympathetic response of the component of the baroreceptor-heart rate reflex which controls heart rate.

Relationship between mechanical properties of the carotid artery wall and baroreflex function in acutely treated hypertensive patients.

OBJECTIVE: To evaluate the relationship between the mechanical properties of the carotid artery wall and baroreflex function after acute reduction of blood pressure with lacidipine in essential hypertension. DESIGN: After 15 days of placebo washout, the hypertensive patients underwent a single-blind haemodynamic study before and 90 min after administration of 4 mg lacidipine (a dihydropyridine calcium antagonist). METHODS: Brachial intra-arterial blood pressure was recorded in eight mild-to-moderate essential hypertensive patients aged 40-53 years (mean +/- SEM 46.8 +/- 4.7 years). The carotid pulse diameter was recorded simultaneously by an echo-tracking technique. The mechanical properties of the carotid artery wall were evaluated by calculating Peterson's incremental elastic modulus (Ep) both as an averaged value of 10 heart cycles with stable blood pressure and was the dynamic correlation, on a beat-to-beat basis, of Ep and the systolic blood pressure during a 20 mmHg increase in blood pressure following a bolus injection of phenylephrine. The elastic properties of the carotid artery were investigated further by determining the correlation between the systolic pressure and systolic diameter, beat by beat, during a ramped increase of blood pressure after phenylephrine administration. The baroreceptor reflex sensitivity was measured simultaneously by the Oxford method and by correlating Ep and the electrocardiographic R-R' interval on a beat-to-beat basis during phenylephrine injections. RESULTS: After lacidipine administration Peterson's elastic modulus, measured under resting steady-state conditions, was reduced (18.7 +/- 7.4 versus 16.4 +/- 6 x 10(5) dyne/cm2), whereas the baroreflex sensitivity was unchanged (6.6 +/- 3.3 versus 6.3 +/- 0.2 ms/mmHg) and resetting of the baroreflex had occurred. At the same time, the correlations between the systolic blood pressure and Ep and between the systolic blood pressure and carotid systolic diameter over a 20 mmHg increase in blood pressure were unchanged. Moreover, the correlations between the systolic blood pressure and the R-R' interval and between Ep and R-R' interval during the phenylephrine-induced blood pressure increase did not differ statistically. CONCLUSIONS: The results suggest that the resetting of the baroreflex after the acute reduction in blood pressure caused by lacidipine is dissociated from mechanical changes in the carotid artery wall.

Effects of central alpha 2-adrenergic agonists on systemic haemodynamics and on baroreceptor reflex sensitivity in spontaneously hypertensive rats.

Clonidine, an imidazoline derivative, is a widely used antihypertensive agent which acts by stimulating the alpha 2-adrenergic receptors at the central nervous system. Clonidine also seems to exert beneficial effects on baroreceptor reflex sensitivity which is usually altered by arterial systemic hypertension and arteriosclerosis. Aim of the study was to compare acute and chronic hypotensive response and the effects on baroreflex sensitivity of a newly synthesized central alpha 2-adrenergic agonist, guanfacine, with those induced by clonidine. The effects of acute and chronic treatment were studied by evaluating blood pressure modifications through intraarterial or sphygmomanometric detection. Baroreflex sensitivity was studied before and after acute treatment with the two drugs. Our results show that guanfacine and clonidine may induce comparable effects, both reducing arterial blood pressure levels and heart rate with an order of potency for guanfacine 10 times lower than clonidine. After chronic treatment the effect of guanfacine on blood pressure was more pronounced than that observed after clonidine administration. Both drugs may enhance baroreflex sensitivity, with a more evident effect of guanfacine than clonidine in response to a sudden decrease of blood pressure. This suggests that guanfacine could afford a more effective cardiovascular adaptation during acute hypotension (i.e. during orthostatic hypotension), particularly in the elderly hypertensive patients.

A new ultrasonographic instrument for measuring vessel wall shear stress.

A new ultrasonographic machine (FRP II) has been developed to measure vessel wall shear stress. A multigate ultrasound probe sends an ultrasound beam simultaneously focused in subsequent points 0.2 mm from each other along the transverse axis of a blood vessel. Blood velocity is measured by cross-correlation technique, which allows a rapid and economical analysis. Thus, the instantaneous (every 5 msec) blood velocity profile is reconstructed for the duration of the entire cardiac cycle. In order to verify the precision and sensitivity of the FRP II in measuring shear stress, 36 measurements were performed on the common carotid artery in 9 hypertensive subjects in different hemodynamic conditions. The FRP II-measured shear stress (the product of the shear rate and blood viscosity) was compared to that calculated by the Womersley's mathematical model (Y = 2K.Vcl/D, where Y = shear rate, Vcl = vessel center line blood velocity, D = vessel diameter). A good correlation (r = 0.77, p < 0.0001) was found between the peak systolic shear stresses measured by FRP II and that calculated by the Womersley's mathematical model, although an underestimation for higher values was observed with the latter method. In conclusion, we propose a new ultrasonographic instrument to measure "in vivo" the vessel wall shear stress.