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Biomedical subjects

B Fabris

Publications and source records attributed to B Fabris.

At least 55 records · Page 3Linked to original sources
PubMed1988

Acute effects of intravenous infusions of alcohol on baroreceptor sensitivity in essential hypertension.

To assess the acute effects of alcohol on baroreceptor reflex in moderate and heavy drinkers with essential hypertension and in healthy subjects who drank moderately, four groups of age and sex matched subjects were studied. Group 1 consisted of 10 healthy subjects (age range 21-50 (mean 37.4(10.5) years), who usually drank less than 200 g of alcohol per week; group 2 patients (age range 21-50 (mean 37.4(10.3) years) with mild or moderate essential hypertension and whose weekly alcohol consumption was less than 200 g; and groups 3 and 4 patients with mild or moderate hypertension (age range 21-50 (mean 37.2(10.2) years and 21-52 (mean 38.1(10.4) years respectively), who usually drank greater than 700 g of alcohol per week. In groups 1-3 an infusion of alcohol (7 mg.kg-1.min-1) in 500 ml of 5% glucose was administered for 1 h to keep blood concentrations constant (6-7 g.litre-1), whereas in group 4 the dose was doubled (blood concentration 10-11 g.litre-1). Baroreceptor sensitivity was measured by the phenylephrine method before and after alcohol infusion and one or two days later before and after infusion of 500 ml of 5% glucose. In healthy subjects and in moderate drinkers with hypertension the alcohol reduced baroreflex sensitivity significantly (from 17.5(9.5) to 13.8(8.4); p less than 0.01 and from 15(10) to 10.5(6.7) ms.mmHg-1, p less than 0.01 respectively), whereas in the heavy drinkers with hypertension it was significantly reduced only at the highest dose of alcohol (from 12.5(6) to 7.9(3.5) ms.mmHg-1; p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Inhibition of angiotensin converting enzyme (ACE) in plasma and tissues: studies ex vivo after administration of ACE inhibitors.

Two methods of radio-inhibitor binding to tissue membrane homogenates and in vitro autoradiography have been used for ex vivo studies on the inhibition of tissue angiotensin converting enzyme (ACE) following acute and chronic administration of ACE inhibitors. Tissue ACE is differentially inhibited in time and degree in different tissues of the rat. Plasma and kidney ACE are inhibited completely at low doses whereas lung and aorta are only inhibited by 60-70%, even after very high does of ACE inhibitors. In the brain only those structures outside the blood-brain barrier are inhibited at low doses but at high doses perindopril appears able to cross the blood-brain barrier. Similarly, testicular ACE is not inhibited and appears to be protected by a blood-testis barrier. Preliminary results suggest that after chronic administration there is also a variable pattern of induction and inhibition of ACE in different tissues. By relating the degree of tissue inhibition to physiological responses it may be possible to determine the role of local renin-angiotensin systems in regional haemodynamics and in the hypotensive action of ACE inhibitors. Further, the techniques of radioligand inhibitor binding and in vitro autoradiography can be extended to other important cardiovascular enzymes (renin and kallikrein) when suitable high affinity specific inhibitors become available.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Arterial compliance and baroreceptor sensitivity after chronic treatment with indapamide.

Arterial compliance, assessed by the ratio of stroke volume to pulse pressure, and baroreceptor sensitivity (Oxford method), were determined in ten patients with essential hypertension, treated with placebo or indapamide (2.5 mg/day), in a cross-over, single blind study. After three months of therapy, mean arterial pressure was significantly reduced from 127 +/- 10 to 118 +/- 9 mmHg, (P less than 0.001), as was total peripheral vascular resistance (from 3017 +/- 561 to 2457 +/- 614 dyne/sec/cm-5/m2, P less than 0.001). Significant increases occurred in cardiac index (3.47 +/- 0.55 to 4.03 +/- 0.86 l/min/m2, P less than 0.01), baroreceptor sensitivity assessed with phenylephrine (from 11.69 +/- 7.9 to 15.0 +/- 9.1 msec/mmHg, P less than 0.01) or with nitroglycerine (from 4.77 +/- 1.6 to 7.11 +/- 2.7 msec/mmHg, P less than 0.01) and arterial compliance (from 1.27 +/- 0.42 to 1.55 +/- 0.57, P less than 0.01). A significant direct correlation was found between arterial compliance and baroreceptor sensitivity assessed during induced increase and reduction of BP, both during placebo (r = 0.88, P less than 0.001 and r = 0.77, P less than 0.01, respectively) and during active therapy (r = 0.94, P less than 0.001 and r = 0.92, P less than 0.001, respectively). These results support the conclusion that chronic treatment with indapamide enhances arterial compliances and reduces the heart load and blood vessel stress. The same effect could explain the enhancement of baroreceptor sensitivity promoted by the drug.

Adult↗
PubMed1986

Antihypertensive activity of arylidenaminoguanidine derivatives.

The synthesis of new benzylidenaminoguanidine compounds is described. Some of these compounds were tested for antihypertensive activity in conscious unrestrained spontaneously hypertensive rats. The compounds examined possess a significant antihypertensive activity, qualitatively different from that of clonidine. For the tested compounds, the absence of the transient rise in blood pressure, which appears immediately after administration of clonidine-like drugs, is noteworthy.

Animals↗
PubMed1983

Effect of indapamide on the baroreceptor reflex in essential hypertension.

The effect of chronic treatment with indapamide on blood pressure (BP), baroreceptor sensitivity (BRS) and vascular reactivity (VR) were investigated in 10 patients with essential hypertension. After 3 months of therapy with indapamide 2.5 mg/d the mean arterial pressure (MAP) had decreased from 135 +/- 6 to 112 +/- 2 mmHg (p less than 0.001); the heart rate (HR) had not changed, VR had decreased from 6.1 +/- 1.2 to 4.8 +/- 1.8 (pg . min . kg)-1 (p less than 0.05), and BRS had increased from 8.3 +/- 3.7 to 12.2 +/- 5.3 ms/mmHg (p less than 0.005), with a leftshift of the relationship between BP and heart period. An inverse correlation was found between the pre-treatment systolic blood pressure and the change in baroreceptor sensitivity after indapamide (r = 0.59; p less than 0.05). In conclusion, chronic treatment with indapamide enhances BRS and resets the reflex. The resetting may account for the lack of tachycardia at rest observed after treatment with indapamide. The mechanism by which indapamide interferes with the baroreceptor reflex requires further investigations.

Adult↗
PubMed1983

Baroreflex function after therapy withdrawal in patients with essential hypertension.

1. Baroreceptor sensitivity and vascular reactivity to noradrenaline were assessed in patients with essential hypertension chronically treated with diuretics during treatment and 6-8 weeks after its withdrawal. 2. Stopping diuretics was followed by an increase in mean arterial blood pressure and vascular reactivity, while baroreceptor sensitivity decreased. 3. Baroreceptor sensitivity during treatment correlated directly with the time during which patients remained normotensive after stopping diuretics. 4. An inverse correlation was found between vascular reactivity and baroreceptor sensitivity after diuretic withdrawal and between the patients' age and baroreceptor sensitivity during diuretic therapy. 5. We conclude that the impairment of baroreceptor sensitivity after stopping diuretic therapy could result in an enhanced vascular response to noradrenaline, and a sensitive baroreflex could contribute to the control of blood pressure during diuretic treatment and buffers the return of high blood pressure when diuretics are stopped.

Adult↗