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Biomedical subjects

G Bellini

Publications and source records attributed to G Bellini.

At least 55 records · Page 3Linked to original sources
PubMed1986

[Vascular and rhegmatogenous peripheral retinal changes in essential systemic arterial hypertension].

The authors examined the peripheral retina of 106 patients affected by essential hypertension grading from 1st to 3rd, as classified by WHO. Research of peripheral retinal vascular alterations and of theoretically possible resulting degenerative changes (lattice degeneration, while without pressure and snail tract degeneration) was carried out. The study included a control group of 39 healthy subjects. A statistical analysis of the resulting data was performed. This showed that the frequency of retinal peripheral vasculopathy is higher in the hypertensive group and is significantly related to the severity of hypertensive retinal angiopathy. In the same way, the incidence of peripheral retinal degenerative changes proved to be significantly higher among the hypertensive group than in the control group. However, a correlation between the frequency of retinal degenerative processes and the presence of vascular changes could not be assessed. The results obtained are discussed, suggesting that peripheral retinal angiopathy could act as a risk factor leading to degenerative alterations on a formerly predisposed retinal tissue.

Adult↗
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↗
PubMed1981

Body fluid volumes in the spontaneously hypertensive rat.

1. Plasma volume, packed cell volume (PCV), blood pressure, extracellular fluid volume (ECFV) and evans blue disappearance rate were measured in conscious spontaneously hypertensive rats and in weight-matched Wistar normotensive rats. 2. Over the weight range studied (250-350 g), plasma and blood volumes were significantly lower in the spontaneously hypertensive rat. Extracellular fluid volumes were similar in the two groups. PCV and Evans blue disappearance rates were significantly higher in the spontaneously hypertensive rat. 3. Negative correlations were obtained between plasma volume and mean arterial pressure and between the plasma/interstitial fluid volume ratio and mean arterial pressure. 4. The normal extracellular fluid volume and the lack of correlation with mean arterial pressure excludes volume expansion as a pressor mechanism during the established phase of hypertension in the spontaneously hypertensive rat.

Animals↗
PubMed1979

Neurogenic activity--angiotensin II interaction during the development and maintenance of renal hypertension in the rat.

1. Pentolinium tartrate (a ganglionic blocker) was injected in conscious rats during the early and late phases of two-kidney renal hypertension produced by aortic ligation. 2. In the early phase ( 5 days after aortic ligation), ganglionic blockade resulted in a decrease in blood pressure equal to that obtained in normotensive rats. Later, at days 12 and 40, for equally severe hypertension, ganglion blockade resulted in a greater decrease in blood pressure. 3. A 30 min infusion of [Sar1, Ala8]angiotensin II during the pentolinium-induced nadir in blood pressure resulted in a further decrease in blood pressure at day 5. Later, at days 12 and 40, this effect was smaller. 4. A 300 min infusion of [Sar1, Ala8]angiotensin II normalized the blood pressure in hypertensive rats at day 40. This delay response may be secondary to a central effect of the antagonist, reducing neurogenic tone or peripheral antagonism of locally generated angiotensin II in the blood vessel walls. 5. At day 40, removal of the small left kidney resulted in a greater decrease in blood pressure. This suggests the presence of a renal factor other than renin in the chronic phase of this hypertension.

Angiotensin II↗
PubMed1978

[Hemodynamic effects of antihypertensive drugs].

The physiopathology of hypertension is not fully understood, though the haemodynamic pictures accompanying the various arterial forms have been established. Clinical employment of antihypertensive drugs should tend to correct these pictures and the extent to which this is true is examined in the light of the latest evidence with respect to the drugs most commonly used.

Adrenergic beta-Antagonists↗
PubMed1978

Effect of administration of Sar1-Ala8-angiotensin II during the development and maintenance of renal hypertension in the rat.

1. Sar1-Ala8-Angiotensin II (an angiotensin antagonist) was infused in rats during the development and maintenance of renal hypertension produced by aortic ligation between renal arteries. 2. In the early phase (5 and 12 days after ligation), infusion of the antagonist markedly decreased blood pressure although it did not reach normal pressures. Later (day 40) only a modest decrease in blood pressure was noted. 3. Removal of the small left kidney always decreased the blood pressure to normal pressures. 4. It is concluded that the renin-angiotensin system is the major pressor component in the initiation of this hypertension. Later, other factors of renal origin assume a pressor function.

Angiotensin II↗