PubMed Health⌕ Search

Biomedical subjects

B Trimarco

Publications and source records attributed to B Trimarco.

At least 145 records · Page 8Linked to original sources
PubMed1987

Changes in left ventricular anatomy and systemic hemodynamics induced by antihypertensive therapy with indenolol.

In 20 patients with mild or moderate essential hypertension who responded favorably to indenolol antihypertensive therapy, echocardiography was performed in the basal condition and 6 and 12 months after the beginning of permanent antihypertensive treatment. Indenolol induced a significant decrease in blood pressure, from a basal value of 170 +/- 3/100 +/- 8 mmHg to 142 +/- 4/87 +/- 2 mmHg after 6 months (p less than 0.01) and to 133 +/- 4/84 +/- 2 mmHg after 1 year (p less than 0.01), and in heart rate, from 72 +/- 5 to 61 +/- 3 bpm after 6 months (p less than 0.01) and to 60 +/- 2 bpm after 1 year (p less than 0.01). Simultaneously, there was a significant reduction in cardiac output (from 6.3 +/- .4 to 5.7 +/- .2 liters/min after 6 months, p less than 0.05, and to 5.6 +/- .2 liters/min after 1 year, p less than 0.01), due to a reduction in heart rate, increased stroke volume, and improved left ventricular performance after indenolol. Total peripheral resistance was also reduced, although statistical significance was not attained. However, a significant inverse correlation was found between the initial value of cardiac output and total peripheral resistance and the changes in these parameters induced by indenolol treatment (cardiac output: r = -0.824 and -0.855, total peripheral resistance: r = -0.876 and -0.899 at 6- and 12-month controls, respectively, all p less than 0.001). Finally, there was a parallel decrease in left ventricular wall and septal thickness and estimated left ventricular mass in patients with left ventricular hypertrophy, whereas no change in left ventricular anatomy could be detected in patients with normal left ventricular mass.

Adult↗
PubMed1987

Influence of atrial natriuretic factor on forearm reflex vasoconstriction induced by cardiopulmonary or arterial receptor unloading.

We studied the influence of atrial natriuretic factor (ANF) infusion on the reflex increase in forearm vascular resistance in normotensive subjects. Reflex vasoconstriction was induced by cardiopulmonary receptor unloading [lower body negative pressure (LBNP), -20 mmHg for 15 min] or by carotid baroreceptor deactivation (+60 mmHg increase in external neck pressure by a pneumatic neck-chamber). Atrial natriuretic factor induced a significant increase in the reflex forearm vasoconstriction to LBNP, but did not modify systemic and regional reflex haemodynamic responses to carotid baroreceptor deactivation. These results suggest that ANF has important interactions with the neural control of peripheral circulation. In addition, the study shows that the peptide causes a selective potentiation of the reflex vasoconstrictor response evoked by cardiopulmonary receptor unloading.

Adult↗
PubMed1986

Reversal of left ventricular hypertrophy following treatment with beta-blockers: experience with tertatolol.

Hypertrophy in response to increasing blood pressure in primary hypertension leads to important functional consequences for the left ventricle. In fact, the progression of hypertensive heart disease, from an adaptive left ventricular hypertrophy with compensated ventricular function to severe hypertrophy with left ventricular failure, has been long thought to be related to the severity and duration of hypertension. Antihypertensive treatment seems to prevent or minimize the occurrence of left ventricular hypertrophy, but questions arise as to whether this therapy is also able to restore normal hemodynamic conditions, or at least to minimize the hemodynamic abnormalities. This review aims at summarizing current knowledge on the effects of the antihypertensive treatment with beta-blockers, including tertatolol, on hypertension-induced left ventricular hypertrophy. The pathogenetic mechanisms underlying the cardiovascular changes associated with hypertension are discussed. A decrease in left ventricular wall thickness as well as in left ventricular mass has been reported in most of the studies performed with different types of beta-adrenergic blocking agents. The extent of this reduction seems to be related not only to the fall in systemic blood pressure, but also to a decrease in sympathetic stimulation. With regard to the functional consequences of hypertension, the reversal of left ventricular hypertrophy following antihypertensive treatment with beta-blockers is usually associated with an improvement in left ventricular performance. This phenomenon can hardly be ascribed to the direct effects of beta-blocking agents. It is more likely to be related to the concomitant reduction in the afterload and to the improved left ventricular compliance, associated with a decrease in left ventricular wall thickness.

Adrenergic beta-Antagonists↗
PubMed1986

Impaired responsiveness of the ventricular sensory receptor in hypertensive patients with left ventricular hypertrophy.

We studied the control of forearm vascular resistance (FVR) by cardiopulmonary receptors in seven patients with hypertension and left ventricular hypertrophy (LVH) and in seven normotensive control subjects. Increasing levels of lower body negative pressure (LBNP) (-10 and -40 mm Hg) induced a progressive decrease in central venous pressure (CVP) and an increase in FVR. The changes in these two variables were correlated both in normal subjects and patients with hypertension (slope for normal subjects = -29.9, for patients with hypertension = -40.3, NS). After propranolol, there was a significant reduction in the increase in FVR induced by -40 mm Hg LBNP in normal subjects (+107 +/- 5 vs +129 +/- 15 mm Hg/ml/sec, p less than .05) but not in patients with hypertension. Consequently, the slope of the delta CVP/delta FVR regression was reduced in normal subjects (-20.6, p less than .01) but not in patients with hypertension. In another seven normal subjects and seven patients with hypertension and LVH we assessed the effects of -10 and -40 mm Hg LBNP on left ventricular filling pressure (LVFP). LBNP induced similar changes in CVP, LVFP, and total peripheral resistance both in normal subjects and in patients with hypertension. Propranolol failed to modify the effects of LBNP on CVP and LVFP in both groups and reduced the response of total peripheral resistance to -40 mm Hg LBNP only in normal subjects. Propranolol did not reduce the response of FVR to the cold pressor test and sustained handgrip or the arterial baroreflex response to the injection of phenylephrine and increased neck tissue pressure. Thus, hypertension-induced LVH seems to be associated with a selective impairment of the left ventricular sensory receptors.

Adult↗
PubMed1986

Effects of lower body negative pressure in hypertensive patients with left ventricular hypertrophy.

We studied the response of forearm vascular resistance to lower body negative pressure (LBNP) at -10 and -40 mmHg in seven established hypertensives with left ventricular hypertrophy (LVH) and seven age-matched normotensive controls. To evaluate the specific role of ventricular baroreceptors, we also investigated the effects of propranolol on the reflex response. Under control conditions, graded LBNP induced a progressive decrease in central venous pressure (CVP) and increased forearm vascular resistance. Changes in CVP and forearm vascular resistance were inversely correlated both in controls (r = -0.944) and in hypertensives (r = -0.960), P less than 0.001 for both. No difference was found between the regression slopes obtained for the two groups (normotensives, -30; hypertensives, -40; NS). After propranolol there was a significant reduction in the increase in forearm vascular resistance induced by -40 mmHg LBNP in normotensives but not in hypertensives. Consequently, the slope of the regression delta CVP/delta forearm vascular resistance was reduced in normotensives (-21) but not in hypertensives. In contrast, propranolol did not attenuate the vasoconstrictor response to other stimuli. Left ventricular hypertrophy therefore seems to be associated with changes in the role of the different cardiopulmonary receptor areas during mediation of the haemodynamic response to stimulated orthostatic stress.

Adult↗
PubMed1986

Carotid baroreceptor unloading decreases plasma atrial natriuretic factor in hypertensive patients.

Atrial natriuretic factor (ANF) release is known to be regulated by distension of the atrial wall; other factors affecting ANF secretion have not yet been defined. In order to evaluate the effects of the reflex activation of the sympathetic nervous system on ANF plasma levels, in 11 patients with essential hypertension progressive deactivation of carotid baroreceptors was induced by 4-min graded increases in external neck tissue pressure. Carotid sinus hypotension induced progressive increases in blood pressure (BP), heart rate (HR) and forearm vascular resistance (FVR), while plasma renin activity and catecholamine concentrations did not change significantly. Despite the lack of changes in right atrial pressure during this manoeuvre, plasma ANF levels showed a progressive and significant reduction, which was correlated with the increase in FVR. Although a contribution by other factors cannot be ruled out, our data suggest that the reflex activation of sympathetic nervous system is associated with reduced ANF release, independent of changes in atrial pressure.

Adult↗
PubMed1986

Effects of prostaglandin synthesis inhibition on sympathetic-and parasympathetic-mediated coronary hemodynamic responses.

In chloralose-anesthetized dogs with the left circumflex coronary artery perfused at constant flow, the effects of indomethacin or naproxen on coronary and systemic responses to sympathetic and parasympathetic stimulation were evaluated. Sympathetic stimulation was evoked either by 1-min carotid artery occlusion or by epinephrine (5 micrograms) or norepinephrine (5 micrograms) intracoronary administration. Reflex or direct parasympathetic stimulation was produced by ouabain (40 micrograms) or acetylcholine (2.5 micrograms) injection, respectively, in the perfused coronary artery. The administration of indomethacin or naproxen reduced the integrated areas of coronary vasodilatation induced by epinephrine and norepinephrine. The extent of this reduction was dose-dependent with both indomethacin (epinephrine: r = 0.774, n = 35, P less than .001; norepinephrine: r = 0.766, n = 35, P less than .001; norepinephrine: r = 0.799, n = 35, P less than .001) up to 1.5 and 7 mg/kg, respectively. Further increase in dosage of both prostaglandin synthesis inhibitors failed to induce further reduction of integrated areas of coronary vasodilatation. In contrast, the maximum fall in coronary perfusion pressure, induced by both catecholamines, remained unmodified after inhibition of prostaglandin synthesis, whereas a faster return of the perfusion pressure to base line was observed. The extent of cyclooxygenase activity inhibition induced by indomethacin or naproxen, assessed through the radioimmunoassay of thromboxane B2, showed a consistent dose-dependent increase until complete inhibition was attained with 1.5 mg/kg of indomethacin and 7 mg/kg of naproxen. No significant change in the coronary and systemic hemodynamic response induced by carotid occlusion and by ouabain or acetylcholine intracoronary administration was observed. Furthermore, complete cyclooxygenase inhibition, induced by either indomethacin or naproxen, was able to reduce the coronary vasodilatation induced by isoproterenol (5 micrograms) intracoronary injection but failed to modify the coronary vasoconstriction elicited by both epinephrine and norepinephrine in propranolol-treated dogs. These data indicate that the prostaglandin system is involved in the coronary vasodilatation induced by humoral sympathetic stimulation, whereas coronary hemodynamic responses to both neural sympathetic or parasympathetic stimulation are not influenced by the administration of prostaglandin synthesis inhibitors.

Acetylcholine↗
PubMed1985

Role of prostaglandins in the renal handling of a salt load in essential hypertension.

Renal function and systemic hemodynamics were assessed in 10 hypertensive patients and in 10 age-matched normotensive subjects during control conditions (80 mEq of sodium/day) and after a salt load, either alone (480 mEq/day) or combined with indomethacin or sulindac. Indomethacin was used to induce ubiquitous inhibition of prostaglandin synthesis and sulindac to inhibit prostaglandin synthesis in all tissues except the kidney. Under control conditions there was no significant difference between the 2 groups in any measurement except blood pressure and total peripheral resistance. Also, the changes induced by salt load in the 2 groups were comparable. However, after indomethacin administration, only hypertensive patients showed a significant reduction in the 24-hour sodium excretion (from 417 +/- 61 to 317 +/- 49 mEq, p less than 0.05), so that the difference between this value and the corresponding value of normotensive subjects (453 +/- 79 mEq) became significant (p less than 0.05). The changes in sodium excretion in hypertensive patients were significantly correlated with the changes in renal plasma flow (r = 0.803, p less than 0.01). However, cardiac output and renal blood flow showed a similar pattern in normal and hypertensive persons. Finally, after the addition of sulindac to salt load, the differences in the 24-hour sodium excretion vanished. These results were also confirmed in an ancillary study performed, using the same protocol, in 10 other hypertensive patients using ibuprofen rather than indomethacin. Our data suggest that renal prostaglandins participate in renal disposal of chronic salt load in hypertensive patients but not in normal persons.

Adolescent↗
PubMed1985

Carotid sinus reflex control of coronary blood flow in human subjects.

Systemic and coronary hemodynamics were assessed before and during a reduction in carotid transmural pressure. This reduction was induced by means of a pneumatic neck chamber in 15 normal subjects and 15 hypertensive patients with a normal coronary arteriogram. A reduced baroreflex responsiveness was demonstrated in hypertensive patients as compared with normal subjects by evaluating both the reflex bradycardia evoked by intravenous administration of phenylephrine and the reflex increase in blood pressure during carotid sinus hypotension. In normal subjects, the reduction in carotid transmural pressure induced a significant increase in mean blood pressure, total peripheral resistance, cardiac output, heart rate, coronary vascular resistance, coronary blood flow assessed by the continuous thermodilution method and myocardial oxygen consumption. In hypertensive patients, the same stimulus significantly increased mean blood pressure, cardiac output, heart rate and coronary blood flow while no significant change was detected in coronary vascular resistance and myocardial oxygen consumption. The increase in mean blood pressure, total peripheral resistance and cardiac output was significantly higher in normal subjects than in hypertensive patients. These results suggest that in normal subjects carotid sinus hypotension evokes reflex coronary vasoconstriction, whereas this response is blunted in hypertensive patients with reduced baroreflex sensitivity.

Adult↗
PubMed1985

Late phase of nitroglycerin-induced coronary vasodilatation blunted by inhibition of prostaglandin synthesis.

In chloralose-anesthetized dogs with the left circumflex coronary artery perfused at constant flow, the effects of increasing doses of indomethacin or naproxen on the coronary and systemic hemodynamic responses to a 5 microgram intracoronary injection of nitroglycerin (NTG) were evaluated. The integrated areas of NTG-induced coronary vasodilatation were reduced after administration of indomethacin or naproxen. The extent of this reduction was increased progressively by augmenting the dose of indomethacin and naproxen up to 1.5 and 7 mg/kg, respectively. We also assessed the extent of cyclooxygenase inhibition induced by indomethacin or naproxen through the radioimmunoassay of thromboxane B2, which reflects thrombin-induced activation of platelet thromboxane A2 production during whole blood clotting. The level of inhibition progressively increased and complete inhibition was attained with 1.5 mg/kg indomethacin and 7 mg/kg naproxen. Further increase in dosage failed to induce further reduction of integrated areas of coronary vasodilatation, and a correlation was found between the extent of the reduction of the integrated areas of coronary vasodilatation and the dose of indomethacin (r = .828, n = 35, p less than .001) or naproxen (r = .729, n = 35, p less than .001). Finally, the NTG-induced maximum fall in coronary perfusion pressure remained unmodified after inhibition of prostaglandin synthesis, but there was a faster return of the perfusion pressure to the basal value.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Participation of endogenous catecholamines in the regulation of left ventricular mass in progeny of hypertensive parents.

To investigate whether adrenergic activity is a determinant of left ventricular hypertrophy in human hypertension, in each of 10 normotensive subjects with two hypertensive parents we have examined the relationship between changes in echocardiographic parameters of left ventricular anatomy and those in circulating catecholamine levels induced by three, 3 week periods of different sodium and potassium intakes. A high sodium-normal potassium regimen induced a significant reduction in upright plasma norepinephrine (from 599 +/- 89 to 379 +/- 45 pg/ml, p less than .01) and in posterior wall (PWT) and interventricular septal (IVST) thickness, as well as in the left ventricular mass index (LVMi). Changes in upright plasma norepinephrine concentrations correlated with those in IVST (r = .822, p less than .01) and in LVMi (r = .833, p less than .01). A low sodium-normal potassium diet resulted in increases in supine and upright plasma norepinephrine levels (from 356 +/- 44 to 488 +/- 89 pg/ml, p less than .001; and from 565 +/- 42 to 744 +/- 33 pg/ml, p less than .01) as well as increases in IVST and LVMi (from 97 +/- 7 to 107 +/- 7 g/m2, p less than .001). The changes in norepinephrine levels in supine and upright subjects correlated with changes in IVST (r = .836, p less than .01 and r = .796, p less than .01) and in LVMi (r = .931, p less than .001 and r = .947, p less than .001). No significant change in plasma catecholamine concentrations or in PWT, IVST, or LVMi was detected after a low sodium-high potassium regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Transient enhancement of sympathetic nervous system activity by long-term restriction of sodium intake.

To further investigate the relationship between salt intake and sympathetic nervous system activity, the short- and long-term effects of a low-salt diet (40 meq/day) were assessed in 10 normal subjects. Measurements of hemodynamic, hormonal, and other parameters were obtained on the day preceding institution of the low-salt diet (day 0) and on days 4, 7, 30, and 60 of the diet. Urinary sodium excretion was 178 +/- 10 meq/24 hr on day 0 and 31 +/- 4, 38 +/- 4, 45 +/- 6, and 47 +/- 7 meq/24 hr on days 4, 7, 30, and 60, respectively (all p less than .001 compared with day 0). Blood pressure, urinary potassium, serum electrolytes, and cardiac function (as assessed by echocardiography) were not modified by the 2 month low-salt diet. Plasma renin activity and plasma aldosterone were significantly elevated above control values throughout the entire period of the low-salt diet. In contrast, plasma norepinephrine concentration increased significantly only on days 4 and 7 (from 253 +/- 20 pg/ml on day 0 to 495 +/- 32 pg/ml, p less than .001, and 347 +/- 22 pg/ml, p less than .05, respectively), returning to baseline at days 30 (280 +/- 18 pg/ml) and 60 (262 +/- 18 pg/ml). Changes in plasma epinephrine paralleled those observed for norepinephrine. Similarly, resting heart rate and the blood pressure response to isometric exercise were significantly increased only on days 4 and 7 of the low-salt diet. These results suggest that sympathetic nervous system activity is enhanced only transiently during a sustained reduction in sodium intake.

Adult↗
PubMed1985

Efficacy of a new antihypertensive agent (indenolol) assessed by ambulatory blood pressure monitoring.

The effects of two-week treatment periods with indenolol (I) and metoprolol (M) were examined by 24-hour mean blood pressure (BP) monitoring in control conditions and during exercise stress test in 7 patients with essential hypertension, using the Oxford method. Both drugs induced a significant reduction in mean BP and heart rate (HR) as compared to pretreatment values (mean BP: from 117 +/- 3 mmHg to 106 +/- 4 after I, p less than 0.05 and to 102 +/- 3 after M, p less than 0.01; HR: from 78 +/- 2 bpm to 66 +/- 2 after I, p less than 0.01 and to 67 +/- 2 after M, p less than 0.01). I and M induced a significant reduction in systolic and diastolic BP throughout the day and most of the night. During bicycle ergometer the basal and peak values of systolic and diastolic BP were significantly lower after both treatments as compared to the pretreatment values (both p less than 0.01). Our data suggest that I once a day possesses a substantial and consistent antihypertensive action, effective over most of the 24 hours.

Adrenergic beta-Antagonists↗
PubMed1985

Regulation of left ventricular mass by endogenous catecholamines in hypertensive progeny.

In 10 normotensives with both parents hypertensive, the relationship between changes in echocardiographic parameters of left ventricular anatomy and those in circulating catecholamine levels induced by three 3-week periods of different sodium and potassium intakes were examined. A high-sodium normal-potassium regimen reduced upright plasma norepinephrine (P less than 0.01), posterior wall thickness (PWT) and interventricular septal thickness (IVST) as well as the left ventricular mass index (LVMi). Changes in upright plasma noreprinephrine correlated with those in IVST (r = 0.822, P less than 0.01) and in LVMi (r = 0.833, P less than 0.01). A low-sodium normal-potassium diet increased supine (P less than 0.001) and upright (P less than 0.01) plasma norepinephrine as well as the IVST and LVMi. The changes in supine and upright norepinephrine levels correlated with changes in IVST (r = 0.836 and r = 0.796 respectively, both P less than 0.01) and in LVMi (r = 0.931 and r = 0.947 respectively, both P less than 0.001). No significant change in any of the above parameters was detected after a low-sodium high-potassium regimen. These findings indicate that in hypertensive progeny catecholamines may play a role in the physiological regulation of left ventricular mass (LVM).

Adult↗
PubMed1984

Effect of acebutolol on left ventricular hemodynamics and anatomy in systemic hypertension.

In 18 patients with mild or moderate essential hypertension who responded favorably to acebutolol antihypertensive therapy, echocardiography (echo) was performed in the basal condition and after 6 and 12 months of follow-up. Acebutolol induced a significant decrease in blood pressure (BP), from a basal value of 167 +/- 3/105 +/- 2 mm Hg to 138 +/- 5/90 +/- 2 mm Hg after 6 months (p less than 0.01) and to 134 +/- 3/91 +/- 3 mm Hg after 1 year (p less than 0.01), and in heart rate, from 75 +/- 3 to 63 +/- 2 beats/min after 6 months (p less than 0.01) and to 63 +/- 2 beats/min after 1 year (p less than 0.01). The decrease in BP was achieved through a decrease in cardiac output from 6.3 +/- 0.28 to 5.3 +/- 0.25 liters/min after 6 months (p less than 0.05) and to 5.32 +/- 0.2 liters/min after 1 year (p less than 0.05), which resulted from a reduction in heart rate; stroke volume did not show significant change during the treatment and left ventricular (LV) performance was improved. There was a parallel decrease in LV posterior wall and ventricular septal thicknesses and estimated LV mass. In patients with LV hypertrophy, the change in mass was significantly correlated with the change in heart rate both after 6 and 12 months of therapy (r = 0.6234, p less than 0.05 and r = 0.7121, p less than 0.05 after 6 and 12 months, respectively).

Acebutolol↗
PubMed1984

Ouabain-induced reflex coronary vasodilatation mediated by cardiac receptors.

Experiments were performed to determine the effects of digitalis-induced stimulation of cardiac receptors on the coronary circulation. In chloralose-anesthetized dogs, left circumflex coronary artery was perfused at constant flow, and heart rate was maintained constant by electric pacing. Ouabain injection in the perfused coronary artery produced a significant decrease in coronary perfusion pressure. Epicardial application of lidocaine completely blocked the reflex response. Vagotomy also prevented this reflex response. Sympathetic blockade with intravenous guanethidine or intracoronary phentolamine partially reduced the reflex coronary vasodilatation. Intracoronary atropine also partially reduced the coronary vasodilator response to ouabain. The combined administration of guanethidine and atropine completely abolished the coronary reflex response. These data demonstrate that ouabain can evoke reflex coronary vasodilation by stimulating cardiac receptors. This reflex response is mediated by activating cholinergic vasodilator fibers and inhibiting sympathetic vasoconstrictor fibers.

Animals↗