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Biomedical subjects

M Motolese

Publications and source records attributed to M Motolese.

At least 37 records · Page 2Linked to original sources
PubMed1990

Comparative evaluation of cardioselectivity of metoprolol OROS and atenolol: a double-blind, placebo-controlled crossover study.

Cardioselectivity of a single oral dose of metoprolol oral osmotic (OROS) (14/190 mg) and atenolol (100 mg) was compared in 12 patients with reversible obstructive airway disease by assessing the dose-response curve to increasing doses of inhaled salbutamol. The beta-blocking activity of the two drugs, which was determined by measuring heart rate, blood pressure, and derived indexes at peak plasma drug levels, was similar. Both metoprolol and atenolol significantly reduced forced vital capacity and peak expiratory flow, with no difference between drugs. Atenolol but not metoprolol also significantly reduced forced expiratory volume in 1 second and specific airway conductance. Both metoprolol and atenolol shifted the dose-response curve of specific airway conductance to the right. The results indicate that the new OROS delivery system for metoprolol, which produces a relatively constant plasma drug level, provides a cardioselectivity comparable to or greater than that of atenolol at maximum plasma levels.

Adolescent↗
PubMed1990

Transient myocardial ischaemia: a multivariate analysis on clinical, angiographic and ergometric variables.

The availability of ambulatory ECG monitoring allows identification of transient myocardial ischaemia, the clinical relevance of which is currently being investigated. Ninety-four consecutive patients with ischaemic heart disease and a positive exercise test (greater than or equal to 1 mm ST-segment depression) were studied to evaluate the prevalence of transient myocardial ischaemia (either painless or painful) during 24-h dynamic electrocardiogram (ECG) and the clinical, angiographic and ergometric variables predicting its appearance. Two-hundred-and-eighty-one episodes of transient electocardiographic myocardial ischaemia were recorded in 69 patients (73.4% of all patients). Transient myocardial ischaemia was more frequent, although not significantly so, in patients with diabetes, with previous myocardial infarction, or with multivessel disease. When tested by multivariate analysis, neither the clinical variables nor the severity of coronary artery disease allowed prediction of the occurrence of transient myocardial ischaemia during dynamic ECG. The duration of exercise testing up to the ischaemic threshold (ST-segment depression = 1 mm) and the peak heart rate during exercise were more accurate predictors of transient myocardial ischaemia (P = 0.019 and 0.012 respectively). Patients with transient myocardial ischaemia had a lower ischaemic threshold (355 +/- 175 vs 498 +/- 150 s, mean +/- SD, P = 0.001) despite a lower peak heart rate (129 +/- 18 vs 137 +/- 12 beats min-1, P = 0.047) than patients without transient myocardial ischaemia. In conclusion, exercise testing may help select patients for examination by dynamic ECG.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗
PubMed1989

Blunting of atrial natriuretic factor response to volume expansion by benazepril in hypertensive patients.

To verify the hypothesis that the angiotensin converting enzyme (ACE) level may affect the metabolism of circulating atrial natriuretic factor (ANF), the acute and chronic effects of benazepril on plasma ANF levels were studied in hypertensive patients under basal conditions and in response to acute volume expansion. Ten essential hypertensives entered a double-blind crossover study, and were randomly allocated either to placebo or to 10 mg benazepril orally once a day for 2 days; after a placebo washout period of 2 days the groups were crossed over. On the second day of each crossover period, volume expansion was induced by infusing 1 litre saline in 30 min, and blood samples for ANF measurements were drawn at times -5, 0, 5, 15, 30, 35, 40, 50 and 60 min. Oral benazepril at 10 mg/day was then given to all patients for 4 weeks, and the volume expansion with saline was repeated. After the 2-day acute benazepril treatment, blood pressure fell from 166.1 +/- 3.6/105.1 +/- 0.9 to 140.1 +/- 4.6/85.6 +/- 2.1 mmHg (P less than 0.01 for both systolic and diastolic blood pressure), whereas ANF fell from 29.4 +/- 3.6 to 24.1 +/- 3.7 pg/ml (NS) after the acute benazepril treatment and to 17.7 +/- 3.6 pg/ml (P less than 0.01) after the chronic benazepril treatment. The volume expansion itself did not induce significant changes in mean arterial pressure, either during the placebo treatment or during the acute chronic benazepril treatment. The rise in ANF values in response to saline infusion during placebo was prompt, beginning at min 15 and reaching a maximum at min 40.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Regional and systemic hemodynamic and humoral effects of transdermal nitroglycerin in mild hypertension.

Venous distensibility, forearm blood flow (FBF, plethysmographic technique), systemic blood pressure (BP), and derived forearm vascular resistances were measured in 11 borderline-mild hypertensive, otherwise healthy male subjects for a 24-h period during either placebo or transdermally delivered nitroglycerin (NTG 10 mg/24 h). The drug caused arteriolar and venular forearm vasodilation and hypotension which, although persisting throughout the 24-h observation period, reached an apparent maximum during the first hours but later tended to wane. Since NTG plasma levels were constant at that time, the data may suggest development of vascular hyporesponsiveness during continuous exposure to NTG. Venous hematocrit (Hct) decreased during transdermal NTG, indicating the plasma volume expanding action of the drug, apparently dissociated from vasodilation per se. Because no significant changes in either plasma norepinephrine (NE) or plasma renin activity occurred in these subjects, counterregulatory sympathetic or angiotensin II (AII)-mediated vasoconstriction was probably not involved in the hemodynamic action of transdermally delivered NTG.

Administration, Cutaneous↗
PubMed1987

Antihypertensive effect of a new formulation of slow release oxprenolol in essential hypertension.

To test whether a new formulation of a slow release oxprenolol (SLOx) can produce a steady 24-h antihypertensive effect, we recorded 24-h intraarterial blood pressure (Oxford technique) in eight ambulant inpatients (age 44.5 +/- 3.0 years, mean +/- SE) with a mild or moderate hypertension who were untreated since three weeks. The study was started seven days after hospitalization and was conducted according to a randomized doubleblind cross-over design. Blood pressure recordings were made after (a) a 7-day administration of SLOx in a single evening dose, and (b) a 7-day administration of placebo. This design allowed to determine the effect of SLOx without interference from nonspecific blood pressure lowering factors. Blood pressure effects of handgrip, submaximal cyclette exercise, and cold pressor test 20-24 h after the administration of SLOx and placebo were also evaluated. The blood pressure tracing was analyzed beat-to-beat by a computer which provided also the analysis of the heart rate data. The 24-h mean systolic and diastolic blood pressure measured during placebo were 144.6 +/- 6.4 and 81.1 +/- 3.9 mm Hg, the corresponding heart rate being 76.9 +/- 3.5 beats/min. SLOx reduced these values by 6.2, 10.6, and 4.8%, respectively, all effects being similarly evident throughout the blood pressure recording. The pressor responses to handgrip, cyclette exercise, and cold pressor test were not affected by SLOx. By contrast, the small tachycardic response to handgrip and the large tachycardic response to submaximal cyclette exercise were significantly reduced by the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Antihypertensive activity of a new vasodilator, cadralazine, administered alone or in combination with a beta-blocker.

The antihypertensive activity of a new arterial dilator, cadralazine, was evaluated in 40 patients with mild-to-moderate arterial hypertension. Cadralazine was given once daily over 6 weeks, and blood pressure and heart rate were recorded 24-26 hours after dosing. Cadralazine dose was 10 mg daily initially, and 15 or 20 mg daily from the 3rd or 5th trial week according to a target diastolic pressure reduction to 95 mmHg or below. Slow-release metoprolol 200 mg once daily was added when heart rate increase exceeded 25% of the pretreatment value. Blood pressure showed a significant and progressive reduction throughout the study period, both in the patients receiving cadralazine as monotherapy (19 patients) and in those who added metoprolol (21 patients). The target diastolic pressure reduction was reached in 2 patients with the 10-mg dose, in 19 of the remaining 38 patients with the 15-mg dose, and in 13 of the other 19 patients with the 20-mg dose. Considering only those patients who did not add metoprolol, the target was reached in the 2 patients with the 10-mg dose, in 10 of the 19 patients with the 15-mg dose and in 7 of the 19 patients with the 20-mg dose. None of the laboratory tests showed clinically relevant changes. Neither LE cells nor antinuclear antibodies were found. In conclusion, cadralazine is a promising long-acting antihypertensive vasodilator. A clinically satisfactory antihypertensive effect is achieved mostly by a 15-mg or a 20-mg dose given once daily.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1984

Plasma norepinephrine and left ventricular hypertrophy in systemic hypertension.

The relations between some pressure and humoral factors, and some echocardiographic indexes of left ventricular (LV) hypertrophy were studied in 64 patients with essential hypertension. Fifty-seven percent of these patients showed echocardiographic evidence of LV hypertrophy (LV mass greater than 215 g). Multivariate stepwise regression analysis showed that only mean blood pressure (BP) and circulating norepinephrine (NE) levels were significantly related to LV mass index in the group of patients with LV hypertrophy. However, mean BP was the only factor related to LV mass index in the subgroup of patients with LV hypertrophy and plasma NE within the normal laboratory range, whereas NE was the sole factor related to LV mass index in the subgroup with LV hypertrophy and abnormally elevated NE levels (greater than mean + 2 standard deviations of the normal laboratory range). Correlation of LV mass index vs NE was -0.35 (not significant) in the former group of patients and 0.89 (p less than 0.01) in the latter group. NE showed no relation with the echocardiographic variables in the hypertensive patients without LV hypertrophy; in this group, diastolic BP was the only factor related to LV mass index. Circulating NE levels were slightly higher in patients with LV hypertrophy (213 +/- 68 ng/liter) than in those without LV hypertrophy (187 +/- 46 ng/liter), but differences were not significant when adjusting NE for age. Plasma renin activity was not dissimilar in the absence or presence of hypertrophy. In conclusion, our findings suggest that NE might be associated with pressure factors in regulating LV hypertrophy development only in a subgroup of hypertensive patients characterized by echocardiographic LV hypertrophy and abnormally elevated circulating NE levels.

Adult↗
PubMed1984

Noninvasive assessment of chronotropic and inotropic response to preferential beta-1 and beta-2 adrenoceptor stimulation.

The relative chronotropic and inotropic activity of preferential beta 1- and beta 2-adrenoceptor stimulation was investigated in seven healthy male subjects in a randomized within-subject, single-blind study. Two doses of beta 1-selective agonist prenalterol (1 mg/hr or 2 mg/hr) and of beta 2-selective agonist salbutamol (300 micrograms/hr or 600 micrograms/hr) were infused intravenously in four separate sessions, with intervals of at least 48 hr between sessions. At each session cuff blood pressure and heart rate (HR) were measured and some hemodynamic information on the inotropic state were derived by echocardiography. Both prenalterol and salbutamol induced increases in HR, but tachycardia was greater after salbutamol, whereas the positive inotropic response to beta-stimulation was greater after prenalterol. At comparable HR rises (prenalterol, from 66.0 +/- 5.5 to 72.2 +/- 4 bpm; salbutamol, from 64.6 +/- 6 to 70.0 +/- 7 bpm), inotropic response seemed to be greater after prenalterol than after salbutamol (systolic blood pressure [SBP]: 133.5 +/- 8 and 120.7 +/- 8 mm Hg; mean velocity of circumferential fiber shortening [Vcf]: 1.54 +/- 0.13 and 1.31 +/- 0.12 c/s; ejection fraction [EF]: 72.4% +/- 5% and 69.5% +/- 4%; stroke index: 47.4 +/- 4 and 41.7 +/- 3 ml/m2). In presence of a chronotropic effect (HR from 64.6 +/- 6 to 70.0 +/- 7 bpm), the low salbutamol dose did not induce any changes in the indices of inotropism (SBP: from 119.2 +/- 6 to 120.7 +/- 8 mm Hg; mean Vcf: from 1.28 +/- 0.11 to 1.31 +/- 0.12 c/s; EF: from 68.1% +/- 5% to 69.5% +/- 4%; stroke index: from 40.2 +/- 3 to 41.7 +/- 3 ml/m2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1984

Ventilatory effects of selective beta 1-(prenalterol) or beta 2-(salbutamol) adrenoceptor agonism in man.

We compared the ventilatory effects of prenalterol (beta 1-selective adrenoceptor agonist) with those of salbutamol (beta 2-selective adrenoceptor agonist) in 6 healthy volunteers. Two intravenous doses of prenalterol (1 mg/60 min, 2 mg/60 min) and of salbutamol (300 micrograms/60 min, 600 micrograms/60 min) were given in random order in 4 separate sessions of 60 minutes each. Pulmonary ventilation per minute (V'E) increased only on the high dose of salbutamol. Mouth occlusion pressure (P0.1) did not vary either on prenalterol or on salbutamol. Only the high dose of salbutamol induced (1) an increase in tidal volume (VT) without changes in respiratory rate (RR), (2) an increase in mean inspiratory flow (VT/Ti) without changes in the fraction of inspiratory time to total cycle duration (Ti/Ttot). During forced expiration, salbutamol elicited a small bronchodilating effect at the level of both large (FEV1, FEF25-75, FEF50) and small (FEV3, FEF75-85, FEF75) airways. Prenalterol induced a very small dilatation of the large airways, and a somewhat more pronounced effect at the level of the small airways. Neither the indexes of ventilatory pattern nor those of bronchial tone showed any statistical or biological differences between values on prenalterol and values on salbutamol. However, both the former and the latter indexes showed a trend to be higher on salbutamol than on prenalterol. Results suggest that salbutamol-induced increase in pulmonary ventilation per minute in subjects without bronchial obstruction is likely the result of a reduced bronchomotor tone at rest, leading to an increase in tidal volume because of the rise in the VT/Ti ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1984

Left ventricular hypertrophy regression in hypertensive patients treated with metoprolol.

The long-term effects of metoprolol monotherapy, 100 mg b.i.d., for 16-18 months, were investigated in 8 previously untreated essentially hypertensive patients (resting blood pressure greater than 155/95 mmHg) and echocardiographic evidence of left ventricular hypertrophy (LVH) (left ventricular mass by Penn Cube formula greater than 215 g). Echocardiographic studies, according to the American Society of Echocardiography recording techniques and measurements criteria, were performed before starting treatment and at the end of follow-up. Metoprolol induced a decrease in systolic and diastolic blood pressure and heart rate, accompanied by a reduction of interventricular septum and posterior wall thickness (from 1.21 cm to 1.10 cm, and from 1.15 cm to 1.06 cm, respectively), left ventricular mass index and mean wall stress. All these changes were significant (p less than 0.01). Cardiac index decreased from 3017 ml/m2 to 2632 ml/m2 (p less than 0.01), mostly because of the reduction in the heart rate. In fact, stroke index, ejection fraction and fractional shortening all slightly increased during treatment in respect to pre-treatment values. Plasma renin activity fell from 1.45 ng/ml/h to 0.81 ng/ml/h (p less than 0.01), whereas both plasma noradrenaline and adrenaline concentration at rest did not change. Results indicate that in essentially hypertensive patients who have already developed LVH as a consequence of the hypertension, a long-term metoprolol therapy can successfully induce a reversal of LVH together with an effective blood pressure control, without noticeable adverse effects of changes in cardiac performance.

Adult↗
PubMed1984

Hemodynamic effects of once a day administration of combined chlorthalidone and metoprolol slow-release in essential hypertension.

The effects of a fixed combination of chlorthalidone (25 mg) and metoprolol slow-release (200 mg) (CM) on 24 hour blood pressure (BP) and heart rate (HR) values and their variabilities were evaluated in 6 ambulant hypertensives by the Oxford method, to obtain continuous intra-arterial recording and by computer to have a beat-to-beat analysis of the data. Compared to pre-treatment values, average 24 hour HR and mean BP recorded after 7-10 days of once daily CM orally administration were reduced by 18.4 +/- 3.1 and 14.7 +/- 3.0%, respectively. The effects of CM were also evident during isometric and dynamic exercise, whose pressor and tachycardic responses were left unimpaired (BP) or were only slightly reduced (HR) by CM. The long- and short-term BP and HR variabilities (calculated as variation coefficients among and within half hours, and within minutes) were also left unaffected by CM. These findings indicate that once a day administration of CM effectively reduces BP and HR over the 24 hours, without interfering with cardiovascular homeostasis. The effective and persistent reduction in both these variables (as well as their occurrence during exercise) suggests that the antihypertensive action of this treatment is accompanied by a clear-cut reduction in cardiac work.

Administration, Oral↗
PubMed1984

[Continuous 24-hour registration of intra-arterial pressure in basal states and during therapy with a fixed slow-release oxprenolol-chlorthalidone combination, administered once a day].

Intra-arterial 24 hour blood pressure (BP) recording (OXFORD MEDILOG) was carried out in 10 patients with essential hypertension, 6 males and 4 females, aged between 41 and 58 years, 3 at WHO stage 1 and 7 at stage 2, in basal conditions and after 6 weeks of treatment with a fixed combination of 160 mg of slow-release oxprenolol and 20 mg of chlorthalidone per tablet (tb). The fixed combination was given once daily, in the morning, at the dosage of 1 tb, which was increased to 2 tbs o.d. after the first 2 weeks in 6 patients. Computer calculated mean BP and heart rate (HR) values from each consecutive hour of the day were obtained in all patients. Hourly trend of BP and HR were plotted and circadian variations were thus determined. Treatment with fixed combination o.d. significantly reduced systolic and diastolic BP, compared to pretreatment values, throughout of the 24 hours (p less than 0.01; p less than 0.001), without altering the circadian rhythm. Before and after 6 weeks of treatment, a bicycle exercise test was performed in 8 patients, who reached 85% of the maximal predicted HR. Pretreatment resting mean BP (+/- SD) was 190 +/- 31/108 +/- 10 mmHg (HR: 68 +/- 9 b/min) and those during the last minute of exercise 242 +/- 29/125 +/- 5 mmHg (HR: 147 +/- 13 b/min); posttreatment resting BP was 161 +/- 20/88 +/- 7 mmHg (HR: 58 +/- 7 b/min) and at peak exercise, 212 +/- 16/106 +/- 7 mmHg (p less than 0.025 for the systolic pressure; p less than 0.001 for the diastolic pressure).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗