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Biomedical subjects

B Trimarco

Publications and source records attributed to B Trimarco.

At least 73 records · Page 4Linked to original sources
PubMed1995

Regulation of aldosterone biosynthesis by adrenal renin is mediated through AT1 receptors in renin transgenic rats.

The transgenic (TG) rat (mREN2)27 is characterized by overexpression of the additional mouse Ren-2d gene in the adrenal cortex with marked suppression of renal renin. We have previously shown that in salt-depleted TG rats enhanced activation of mineralocorticoid biosynthesis is associated with selective stimulation of adrenal renin. To investigate whether the local renin-angiotensin system regulates aldosterone biosynthesis in the adrenal cortex of TG rats, we studied the effects of the AT1-angiotensin subtype receptor antagonist DuP 753 on aldosterone production in 5-week-old TG rats during salt restriction. All the rats (n = 56) were shifted from regular chow to a diet containing only 0.04% NaCl for 1 week. The AT1-receptor antagonist DuP 753 (10 mg/kg per day in drinking water) was administered to 27 of these rats during low-salt diet. Subgroups of rats were killed at 0,4, and 7 days. Low-salt diet increased both adrenal renin activity (from 31 +/- 3 to 77 +/- 4 and 85 +/- 2 ng angiotensin I.h-1.mg protein-1 at 4 and 7 days, respectively; P < .001) and mRNA (by 68.4 +/- 10% and 80 +/- 17% from baseline, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1995

Enhanced detection of viable myocardium by technetium-99m-MIBI imaging after nitrate administration in chronic coronary artery disease.

UNLABELLED: The aim of this study was to assess whether nitrate administration improves the imaging capabilities of 99mTc-MIBI tomography in detecting viable myocardium in coronary artery disease (CAD). METHODS: Thirty-one patients with angiographically proven CAD and chronic LV dysfunction (ejection fraction 39% +/- 9%) underwent two 99mTc-MIBI studies on separate days: one under rest conditions and the other after nitroglycerine (0.005 mg/kg per os) administration. Within 1 wk, all patients also underwent rest-redistribution 201Tl imaging. Eight patients were also studied by echocardiography before and 5 +/- 3 mo after coronary revascularization. RESULTS: On resting 99mTc-MIBI images, 302 segments had normal uptake, 183 segments had moderately reduced uptake and 197 had severely reduced uptake. Of the segments with severely reduced uptake, 54 (27%) had increased uptake after nitroglycerine and were viable on 201Tl images. Of the 143 (73%) segments with severely reduced 99mTc-MIBI uptake and no change after nitroglycerine, 81% were nonviable on 201Tl images. In the eight patients studied before and after revascularization, 87% of segments with reversible 99mTc-MIBI defects and abnormal LV function demonstrated functional recovery after revascularization, whereas 89% of segments with irreversible 99mTc-MIBI defects did not. CONCLUSION: In patients with chronic ischemic LV dysfunction, nitrate administration improved the detection of severely hypoperfused but still viable myocardium on 99mTc-MIBI images.

Coronary Circulation↗
PubMed1995

Myocardial viability index in chronic coronary artery disease: technetium-99m-methoxy isobutyl isonitrile redistribution.

UNLABELLED: The purpose of this study was to evaluate whether an additional redistribution image after a rest 99mTc-MIBI injection enhances detection of viable myocardium and predicts functional recovery after coronary revascularization in patients with chronic coronary artery disease (CAD). METHODS: Thirty-one patients (29 men, mean age 55 +/- 10 yr) with proven CAD and left ventricular (LV) dysfunction (ejection fraction 39% +/- 9%) underwent resting 99mTc-MIBI tomography with initial (1 hr) and delayed (5 hr) images. Within 1 wk of MIBI imaging, all patients underwent rest-distribution 201Tl imaging. Eight patients also underwent two-dimensional echocardiography before and 5 +/- 3 mo after coronary revascularization. RESULTS: On the initial 99mTc-MIBI images, 302 myocardial segments were normal, 183 showed moderate and 197 severe reduction of tracer uptake. Of these 197 segments, 47 (24%) demonstrated increased tracer uptake (> or = 10% versus initial) on delayed images (from 43% +/- 8% to 60% +/- 8%, p < 0.001) and were considered as showing 99mTc-MIBI redistribution. These 47 segments were observed in 20 (65%) patients in whom 201Tl images detected viable myocardium in the same segments. In the eight patients studied before and after revascularization, 83% of segments with 99mTc-MIBI redistribution and abnormal LV function showed functional recovery after revascularization, while 96% of segments without 99mTc-MIBI redistribution did not show functional recovery. CONCLUSION: Resting 99mTc-MIBI redistribution frequently occurs in patients with chronic CAD. Acquisition of 99mTc-MIBI redistribution images enhances detection of viable myocardium and predicts functional recovery after revascularization.

Coronary Disease↗
PubMed1995

[Arterial hypertension and atherosclerosis: their epidemiology and physiopathology].

Several epidemiologic studies have demonstrated that hypertensive patients have an increased risk for the development of atherosclerosis. Although the appearance of atherosclerosis only in those parts of vascular system subjected to high blood pressure suggests that the mechanical stress is the principal factor involved in the development of atherosclerosis, the mechanisms underlying the linkage between hypertension and atherosclerosis are not yet completely understood. In fact, the evidence that antihypertensive treatments are not able to abolish the increased incidence of ischemic accidents in hypertensive patients suggests that other cellular and molecular mechanisms are involved in the pathogenesis of atherosclerosis. The pathogenesis of hypertension is a multifactorial process that involves the interaction of genetic and environmental factors which determine the abnormalities of volume regulation, the enhanced vasoconstriction and the remodeling of the arterial wall which is characterized by hypertrophy and proliferation of vascular smooth muscle cells. On the other hand, the increased growth response of vascular smooth muscle cells represents one of the principal characteristics of atherosclerosis. Thus, increased vascular smooth muscle cell growth is a common feature in the pathogenesis of both atherosclerosis and hypertension.

Arteriosclerosis↗
PubMed1995

Rilmenidine in patients with left ventricular hypertrophy: beyond the reduction of left ventricular mass.

It is generally accepted that the development of left ventricular hypertrophy (LVH) represents a multifactorial phenomenon that also involves neurohormonal mechanisms. This finding may account for the ability of angiotensin-converting enzyme inhibitors to induce faster and more complete reversal of LVH than that observed with other antihypertensive treatments. The sympathetic system is also involved in the genesis of hypertension-induced LVH. We assessed the effects of satisfactory long-term treatment with rilmenidine, a new oxazoline with a potent antihypertensive action, on cardiovascular structural abnormalities and cardiac endocrine function in hypertensive patients with left ventricular hypertrophy. Eleven patients underwent M-mode and two-dimensional Doppler echocardiography, peripheral pulsed Doppler flowmetry, determination of plasma atrial natriuretic factor [(ANF) pg/ml] and renin activity, and 24-h urine electrolyte excretion under control conditions, after 4 weeks of blood pressure normalization, after 1 year of satisfactory antihypertensive treatment and, finally, 4 weeks after therapy withdrawal. I.VH (g/m2 body surface area) was reversed after 1-year treatment (from 152 +/- 5 to 131 +/- 4, p < 0.05). One-year treatment induced an improvement in brachial artery compliance (cm4/dyne.10(7)) (from 0.92 +/- 0.06 to 1.16 +/- 0.08, p < 0.05) that persisted after withdrawal of treatment (1.17 +/- 0.06, p < 0.05). Plasma renin activity and urinary electrolyte excretion did not change throughout the study, whereas ANF remained unchanged after blood pressure normalization (48.4 +/- 6.2 versus 44.7 +/- 2.9, NS), fell after reversal of LVH (28.6 +/- 3.4, p < 0.05), and remained significantly lower than under control conditions after therapy withdrawal (27.5 +/- 2.9, p < 0.05). These results demonstrate that a satisfactory long-term antihypertensive treatment with rilmenidine is able to reverse cardiovascular structural changes and to restore cardiac endocrine function.

Antihypertensive Agents↗
PubMed1994

Effects of one-year treatment with rilmenidine on systemic hypertension-induced left ventricular hypertrophy in hypertensive patients.

In patients with essential hypertension, left ventricular hypertrophy (LVH) increases the risk for cardiovascular morbidity and mortality. Thus its reversal represents one of the principal end-points of antihypertensive treatment. We assessed the cardiovascular effects of 1-year antihypertensive treatment with rilmenidine (1 or 2 mg/day orally), a new oxazoline with a potent antihypertensive action that acts selectively through imidazoline-preferring receptors. In 11 hypertensive patients (mean age, 49 +/- 2 years) with LVH, we measured systemic hemodynamics, large artery compliance, cardiac anatomy, and endocrine function. Patients underwent M-mode and 2-dimensional echocardiography as well as Doppler and peripheral pulsed Doppler flowmetry, determination of plasma atrial natriuretic factor (ANF) levels and renin activity (PRA), and of 24-hour urinary electrolyte and creatinine excretion in control conditions (systolic/diastolic blood pressure, 148 +/- 3/102 +/- 1 mm Hg), 4 weeks after blood pressure normalization (131 +/- 2/84 +/- 2 mm Hg; p < 0.01), after 1 year of satisfactory antihypertensive treatment (142 +/- 3/90 +/- 1 mm Hg; p < 0.01) and, finally, 1 month after therapy withdrawal (155 +/- 3/106 +/- 2 mm Hg; difference not significant [NS]). One-year of rilmenidine treatment induced an improvement in brachial artery compliance (from 0.92 +/- 0.06 to 1.16 +/- 0.08 cm4/dyne; p < 0.05), which persisted after withdrawal of treatment (1.17 +/- 0.06 cm4/dyne; p < 0.05). LVH was reversed after 1 year of rilmenidine treatment (from 152 +/- 5 to 131 +/- 4 g/m2 body surface area; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗
PubMed1994

Acute noradrenergic activation induces insulin resistance in human skeletal muscle.

We assessed in normal subjects the effects of an acute increase in forearm norepinephrine (NE) release, evoked by -20 mmHg lower body negative pressure (LBNP), on insulin-mediated muscle glucose uptake. Seven normal subjects underwent the following two insulin euglycemic clamps in random sequence: one during application of LBNP and the other without LBNP (control study). In the control study, hyperinsulinemia (approximately 60 microU/ml) produced a significant increment in forearm NE release, measured by using the forearm perfusion technique combined with infusion of tritiated NE (from 4.91 +/- 1 to 7.94 +/- 1.33 ng.l-1.min-1; P < 0.05). Forearm glucose uptake rose from 0.97 +/- 0.13 to 5.2 +/- 0.2 mg.l-1.min-1 in response to insulin infusion. When the insulin clamp was performed during LBNP, forearm NE release rose to significantly higher values than those of the control study (from 4.33 +/- 0.52 to 12.7 +/- 1.46 ng.l-1.min-1; P < 0.01 vs. control). Under these conditions, the stimulatory effect of insulin on forearm glucose uptake was markedly reduced (from 0.78 +/- 0.10 to 3.2 +/- 0.7 mg.l-1.min-1; P < 0.02 vs. control). Forearm blood flow and plasma epinephrine and free fatty acid concentrations were comparable in the two study sessions. These data demonstrate that an acute activation of endogenous NE release antagonizes insulin-mediated glucose uptake in forearm skeletal muscle, probably accounted for by a direct metabolic effect of NE.

Adult↗
PubMed1994

Enhanced adrenal renin and aldosterone biosynthesis during sodium restriction in TGR (mREN2)27.

The aim of the study was to investigate the relationships between tissue renin and the steroid production in the adrenal cortex during dietary sodium restriction in the transgenic rat (TGR) (mREN2)27. Thus the effects of a 1-wk low-sodium intake (0.04% NaCl) were studied in 5-wk-old male TGR (n = 33, systolic blood pressure = 151 +/- 3 mmHg) and in 24 age- and sex-matched outbred normotensive Sprague-Dawley (SD) rats. Measurements of plasma and tissue hormones were obtained at 0, 4, and 7 days of a low-sodium diet. Sodium restriction caused sustained increases of adrenal renin activity (from 28.5 +/- 3.5 to 87.5 +/- 4.5 ng.mg protein-1.h-1 on day 7) and of adrenal renin mRNA (+63 +/- 13 and +43 +/- 7% on days 4 and 7, respectively), whereas plasma renin activity (from 3.3 +/- 0.3 to 4.4 +/- 0.6 ng.ml-1.h-1) and renal renin activity (from 0.85 +/- 0.25 to 0.7 +/- 0.4 microgram.mg protein-1.h-1) did not change. The stimulation of the adrenal renin-angiotensin system was associated with a large increase of the aldosterone synthase cytochrome P-450 mRNA (+165 +/- 35 and +184 +/- 44%, on days 4 and 7) and of plasma aldosterone levels (from 125 +/- 32 to 338 +/- 59 pg/ml, P < 0.01). In SD rats, in spite of a more consistent increase in renal and circulating renin, mineralocorticoid production did not increase significantly. These results demonstrate that the exaggerated biosynthesis of aldosterone in TGR during sodium restriction is associated with an activation of renin in the adrenal cortex but not in the kidney.

Adrenal Glands↗
PubMed1994

Insulin blunts sympathetic vasoconstriction through the alpha 2-adrenergic pathway in humans.

We investigated the mechanisms underlying the insulin-induced attenuation of sympathetic forearm vasoconstriction in healthy humans. In 5 subjects, we applied 20 mm Hg lower body negative pressure for 30 minutes in control conditions and during a 60-minute infusion of insulin (0.05 mU/kg per minute) in the brachial artery and measured forearm norepinephrine kinetics and hemodynamics. In 11 subjects, we applied graded lower body negative pressure at 5, 10, 15, and 20 mm Hg for 5 minutes each in control conditions and during the simultaneous intrabrachial administration of insulin (0.05 mU/kg per minute) (5 subjects) or insulin plus ouabain (3.5 micrograms/min per liter) (6 subjects) to investigate whether insulin acts through a potentiation of the vascular smooth muscle Na+,K(+)-ATPase. To assess a possible effect of insulin on a specific adrenergic receptor pathway, in a further study group we evaluated (1) the forearm vascular response to intrabrachial infusion of the alpha 1-adrenergic receptor agonist phenylephrine (0.5, 1, and 2 micrograms/kg per minute; n = 7) and of the alpha 2-adrenergic receptor agonist BHT-933 (0.5, 1, 2, and 4 micrograms/kg per minute; n = 9), and (2) the effects of intra-arterial infusion of prazosin (0.5 microgram/100 mL per minute) alone or combined with insulin on the forearm vascular response to graded lower body negative pressure (7 subjects). Insulin blunted the peak increase in forearm vascular resistance (from 13 +/- 2 to 6 +/- 2 U, P < .05) but not the rise in forearm norepinephrine spillover induced by 20 mm Hg lower body negative pressure (from 8.3 +/- 1.8 to 11.1 +/- 3.5 pmol/min per liter, P = NS). Ouabain administration did not prevent the insulin-induced attenuation of the forearm vasoconstrictive response to graded lower body negative pressure. Insulin infusion in the brachial artery did not modify the forearm vasoconstriction induced by intra-arterial infusion of phenylephrine but significantly reduced the increase in forearm vascular resistance induced by BHT-933 (F = 6.111, P < .001). Finally, intra-arterial infusion of prazosin significantly attenuated the forearm vasoconstriction induced by graded lower body negative pressure. The residual vasoconstrictive response was abolished by insulin infusion. Taken together, these findings suggest that insulin interacts with the sympathetic nervous system at the vascular level predominantly through the alpha 2-adrenergic vasoconstrictive pathway.

Adrenergic alpha-Agonists↗
PubMed1994

Trandolapril in patients with essential hypertension: effects on vascular and cardiac structural changes.

Elevated arterial pressure levels increase the hemodynamic load on heart and vessels, thus leading to functional and structural abnormalities. Because cardiac and vascular changes increase the risk of cardiovascular disease, their reversal is an important target of antihypertensive therapy, even though the prognostic value of this regression has not been fully established. In patients with untreated mild-to-moderate essential hypertension and left ventricular hypertrophy, trandolapril, a new angiotensin-converting enzyme inhibitor, reduces blood pressure by decreasing total peripheral resistance and improves both systolic and diastolic ventricular function. The latter effect is not only functional in nature because, after long-term antihypertensive treatment, the improvement in diastolic ventricular function is detectable also after 1-month withdrawal of trandolapril. The concurrent reversal of left ventricular hypertrophy may contribute to the improved left ventricular diastolic function. However, plethysmographic studies suggest that long-term antihypertensive treatment with trandolapril is also able to reverse structural vascular changes in the forearm vascular bed, because after 1-month washout forearm peripheral resistance also is lower than in control conditions. Finally, in hypertensive patients, trandolapril induces significant increases in brachial artery compliance and diameter that persist after 1 month of withdrawal from treatment. The latter observation suggests that trandolapril also is able to reverse the structural changes of the large artery wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

[Non-hemodynamic mechanisms of cardiovascular risk in the hypertensive patient: insulin resistance].

Insulin resistance is a condition which is present in many different diseases all characterized by an increased risk of cardiovascular morbidity and mortality. Generally, the contribution of insulin resistance to the development of cardiovascular pathology is considered to be due to its metabolic consequences. However, recent findings suggest alternative mechanisms by which insulin resistance could exert its role of cardiovascular risk factor. In fact, it has been demonstrated that insulin resistant hypertensive patients have a sympathetic response to euglycemic hyperinsulinemia which is three-fold greater than in normal subjects. This phenomenon could represent an important link between sympathetic nervous system and arterial hypertension. Furthermore, in normal subjects it has been demonstrated that hyperinsulinemia modulates the sympathetic induced vascular response and that this effect is lost in insulin resistant hypertensives. This latter phenomenon could further worsen the consequences of sympathetic overactivity.

Cardiovascular Diseases↗
PubMed1994

[Effects of antihypertensive treatment on carotid vascular changes].

The carotid artery is one of the most important sites in the progression of atherosclerotic lesions. Atherosclerosis is known to be determined by a variety of factors, among which arterial hypertension is one of the most important. Blood pressure control by antihypertensive treatment is thus of great benefit in management of atherosclerosis, particularly in view of the direct action of some classes of antihypertensive agents on atheromatous lesions. Today, modern diagnostic technique allow a non-invasive examination of the artery wall (B-mode ultrasound and pulsed-Doppler), so that early detection of structural and functional alterations is possible. In order to evaluate the efficacy of the long term blood pressure reduction in the progression and/or in the regression of cardiovascular structural abnormalities, we studied intima-media thickness and arterial compliance during one-year antihypertensive treatment with a new calcium-antagonist, lacidipine, or a diuretic hydrochlorothiazide. In both groups we observed a comparable blood pressure reduction (lacidipine: from 166 +/- 5/100 +/- 1 to 142 +/- 4/88 +/- 2 mmHg; hydrochlorothiazide: from 154 +/- 5/102 +/- 2 to 140 +/- 4/88 +/- mmHg; both p < 0.01). On the contrary, only in patients treated with lacidipine did we obtain a significant improvement in carotid blood flow (383 +/- 16 vs 411 +/- 16 ml/min p <) and in arterial compliance (0.8 +/- 0.1 vs 1.2 +/- 0.2 cm/dyne p < 0.01). Indeed, we observed a different behaviour of the intima-media thickness in the two groups (lacidipine: 1.11 +/- 1.4 vs 1.13 +/- 1.5 mm n.s.; hydrochlorothiazide: 1.15 +/- 0.15 vs 1.21 +/- 0.17 mm p < 0.06). Our results demonstrate that an effective antihypertensive treatment with calcium antagonists may influence the progression of carotid vascular abnormalities.

Aged↗
PubMed1994

[Carotid vascular structural changes and left ventricular hypertrophy].

In the literature there are few studies evaluating carotid vascular atherosclerotic involvement in patients with essential arterial hypertension. Nowadays with new non-invasive methodological methods, such as Doppler-echotomography, it is possible to evaluate accurately structural vascular and cardiac changes. In this study we evaluated the relationship between carotid vascular structural changes and cardiac left ventricular mass index in 15 normotensive subjects and in 15 patients with essential hypertension. We performed a B-mode echotomography (7.5 MHz) of a common carotid in order to measure the diameter of the vessel and intima-media wall thickness. In the same subjects we determined echocardiographic left ventricular mass index and we measured arterial pressure by sphygmomanometric method. There was no statistical significant difference in the two groups except that in systolic, diastolic and mean arterial pressure (96 +/- 2 vs 123 +/- 2 mmHg, p < 0.01), left ventricular mass index (102 +/- 3 vs 118 +/- 3 g/m2, p < 0.01) and in the common carotid intima media wall thickness (0.91 +/- 0.01 vs 2.23 +/- 0.02 mm). In the normotensive subject mean arterial pressure correlated significantly with age (r = 0.699) and with common carotid arterial diameter (r = 0.523) (both p < 0.05). In hypertensive patients, on the contrary, mean arterial pressure correlated with left ventricular mass index (r = 0.523), carotid arterial diameter (r = 0.627) and common carotid intima media wall thickness (r = 0.847). These results demonstrate that in hypertensive patients cardiac abnormalities accompanied vascular structural changes.

Carotid Arteries↗
PubMed1994

[The effects of plasma cholesterol reduction on vasoconstriction due to sympathetic activation in patients with moderate primary hypercholesterolemia].

Recent studies have demonstrated that hypercholesterolemia is one of the major factor involved in the progression of coronary heart disease and that the reduction in plasma cholesterol reduces mortality for cardiovascular events. Indeed, recent experimental studies have demonstrated alterations in vascular reactivity in atherosclerosis. The aim of this study was to evaluate in patients with primary hypercholesterolemia the consequences of an effective of chronic treatment with inhibitor of HMG-CoA reductase on vascular responsiveness to cold pressure test. We observed a significant reduction in total plasma cholesterol during the study that was accompanied by a significant decrease in the response of peripheral vascular resistances to cold pressure test (55 +/- 4% vs 73 +/- 5% p < 0.01). There was also a significant relationship between the reduction of total cholesterol and the response of vascular resistance to the cold pressure test (r = 0.853, p < 0.05). Our results demonstrate that the reduction in total plasma cholesterol may influence the haemodynamic response induced by the activation of the sympathetic system.

Adult↗
PubMed1994

Enhanced thallium-201 uptake after reinjection: relation to regional ventricular function, myocardial perfusion and coronary anatomy.

The aim of this study was to clarify the significance of enhanced thallium-201 (201Tl) uptake after reinjection following 4-hour redistribution imaging. Thirty-four patients with coronary artery disease (CAD) and left ventricular (LV) dysfunction (ejection fraction 32 +/- 10%) underwent exercise-redistribution (ER) 201Tl scintigraphy with rest injection, resting technetium-99m methoxy isobutyl isonitrile (MIBI) imaging, 2D-echocardiography, and coronary angiography. Wall motion (WM) was graded on echocardiographic images. A total of 510 myocardial segments were quantitatively analyzed. A total of 267 (52%) segments had normal (N) 201Tl uptake, 53 (10%) reversible (RD), and 190 (37%) irreversible (ID) 201Tl defects on ER images. Of these 190 ID, 84 (44%) showed enhanced 201Tl uptake after reinjection (Re+) and 106 (56%) remained unchanged after reinjection (Re-). MIBI uptake was significantly higher in RD compared to Re+ and Re- (both p < 0.01), and in Re+ compared to Re- (p < 0.01). The WM score was significantly lower in RD and Re+ compared to Re- (p < 0.01), while no difference was observed between RD and Re+. The severity of coronary artery stenosis was significantly lower in RD compared to Re+ and Re- (both p < 0.01), but no difference was observed between Re+ and Re-. The occurrence of collaterals was significantly higher (p < 0.01) in Re+ (69%) compared to Re- (38%). In conclusion, in patients with CAD and impaired LV function, enhanced 201Tl uptake after reinjection in myocardial segments with ID on ER images was associated with less severe WM abnormalities, higher MIBI uptake and the presence of collaterals.(ABSTRACT TRUNCATED AT 250 WORDS)

Collateral Circulation↗