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Biomedical subjects

M Volpe

Publications and source records attributed to M Volpe.

At least 163 records · Page 9Linked to original sources
PubMed1985

Clinical and neuropsychological correlates of cerebral ventricular enlargement in schizophrenia.

A comprehensive assessment of computed tomography (CT) with respect to clinical, historical and neuropsychological variables has been carried out in a sample of DSM III schizophrenics fairly heterogeneous with respect to duration and severity of illness and in a normal control group matched for sex, age and educational level. The mean value of ventricular brain ratio (VBR) was significantly higher in schizophrenics than controls. Seven patients (21.2%) who had VBRs exceeding 2 SD of the control mean showed a significantly longer duration of illness than the other schizophrenics with significantly higher scores on the subscales alogia, effective flattening and attentional impairment of SANS, on the scales self-care and behaviour in crises and emergencies of DAS, on the scales rhythm, tactile, visual, reading, arithmetic, memory and left hemisphere of LNNB, and on the subtests arithmetic, digit span, digit symbol and block design of WAIS. These results confirm earlier reports of an enlargement of lateral cerebral ventricles in a subset of schizophrenics, and its association with a higher degree of cognitive and neuropsychological impairment, social maladjustment and defectual symptomatology. Moreover, they suggest that the neuropathological process likely to underlie the increase of cerebral ventricular size progresses during the course of the illness rather than predating its onset.

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

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

Effect of atrial natriuretic factor on renin secretion, plasma renin and aldosterone in dogs with acute unilateral renal artery constriction.

Atrial natriuretic factor (ANF) decreases renin secretion rate (RSR), plasma renin activity (PRA) and plasma aldosterone (PA) in normal dogs. To clarify further the mechanisms responsible for these effects, the left renal artery was constricted in seven anaesthetized dogs prior to ANF administration. Constriction of the left renal artery decreased (P < 0.05) ipsilateral mean renal perfusion pressure (MRPP, 29 +/- 7%), renal plasma flow (RPF, 42 +/- 11%) and glomerular filtration rate (GFR) and filtered sodium load (FLNa, 21 +/- 8.8%). Ipsilateral RSR and peripheral PRA tended to increase, although not significantly. Atrial natriuretic factor infusion did not alter GFR in the clamped kidney and failed to decrease RSR or PRA. Despite this, PA levels decreased significantly (7.8 +/- 2.4 to 5.6 +/- 1.8 ng%). These results suggest that ANF-induced inhibition of renin secretion is largely consequent on its renal haemodynamic actions and that suppression of aldosterone by ANF in vivo is due, in part, to direct effects on the adrenal cortex.

Aldosterone↗
PubMed1985

Atrial natriuretic factor (auriculin): structure and biological effects.

Atrial natriuretic factor (ANF) is a recently discovered peptide present in secretory granules specifically found in atrial muscle cells. Multiple structurally related peptides have been isolated from atrial tissues, all of which are derived from a common 152-amino-acid precursor. ANF induces profound natriuresis and diuresis in experimental animals and also causes relaxation of precontracted vascular smooth muscle. ANF has striking renal hemodynamic actions (most consistently an increased glomerular filtration rate), which probably explain its natriuretic effects. ANF also can inhibit renin secretion in vivo and causes direct inhibition of basal and stimulated aldosterone production. It lowers arterial blood pressure, probably reflecting in part its vasorelaxant actions, and this effect is particularly marked in renin-dependent (and possibly other vasoconstricted) models of hypertension. Although the exact structure and regulation of the presumed circulating form(s) of ANF remain to be clarified, available information suggests that it may be a new, previously unrecognized factor in the regulation of fluid volume and renal and cardiovascular function.

Aldosterone↗
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

QT/QS2 ratio as an index of autonomic tone changes.

The effects of changes in sympathetic tone on QT/QS2 ratio were studied in 10 healthy subjects aged 21 to 24 years. The subjects underwent a bicycle ergometer exercise, a tilt test, a decrease in carotid transmural pressure induced by means of pneumatic neck chamber, an i.v. injection of phenylephrine. A phonocardiogram and ECG were simultaneously recorded at a paper speed of 100 mm/s to evaluate QT and QS2 intervals in each test. In basal conditions, the QT/QS2 ratio was less than 1, whereas it increased progressively during the physical exercise and became greater than 1 at peak exercise. Both the upright position and the increase in neck-tissue pressure induced a significant increase in the QT/QS2 ratio as compared with the basal values, whereas i.v. administration of phenylephrine reduced significantly the QT/QS2 ratio. These results demonstrate that those stimuli which induce a rise in adrenergic activity may increase the QT/QS2 ratio. In contrast, the reflex inhibition of the adrenergic activity induced by phenylephrine is accompanied by a reduction in QT/QS2 ratio. Therefore, the QT/QS2 ratio might represent a reliable index of sympathetic cardiac tone.

Adult↗
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↗
PubMed1984

Relationships between left ventricular mass and clinical, biohumoral and hemodynamic parameters in human hypertension.

The relationships between left ventricular mass (LVM), assessed by echocardiography, and several biohumoral and hemodynamic parameters were studied in 63 mild or moderate hypertensive patients and in an age-matched group of 23 normotensive subjects. In hypertensive patients, but not in normotensives, LVM index was significantly correlated with beta-adrenoceptor responsiveness, as evaluated by the chronotropic response to isoproterenol ( CD25 ) (r = 0.525, p less than 0.001) and with the 24-hour catecholamine urinary output (r = 0.485, p less than 0.001). Both CD25 and the catecholamine urinary output were significantly higher in the hypertensives as compared with the normotensive subjects. Moreover, left ventricular wall thickness (septum + posterior wall) was significantly correlated with CD25 and urinary catecholamines only in hypertensive patients. No significant correlation was found between LVM or wall thickness and body surface area, age, blood pressure, heart rate, cardiac output, total peripheral resistance and left ventricular systolic wall stress, whereas CD25 was correlated with urinary catecholamines only in hypertensive patients (r = 0.606, p less than 0.001). These results seem to support the hypothesis that an elevated adrenergic tone may exert a permissive role in the development of left ventricular hypertrophy in human hypertension.

Adolescent↗
PubMed1984

Antihypertensive and aldosterone-lowering effects of synthetic atrial natriuretic factor in renin-dependent renovascular hypertension.

A 24-amino acid residue synthetic atrial natriuretic factor (ANF) antagonizes angiotensin II-induced vascular contractility and aldosterone production in isolated blood vessels and adrenal cells, respectively. To determine the significance of these effects in vivo, the blood pressure and aldosterone responses to synthetic ANF were evaluated in rats with two-kidney, one clip hypertension (n = 5) and in sham-operated controls (n = 4). In the latter, ANF caused a slight fall in mean blood pressure (-7 +/- 3%) and inconsistent changes in plasma renin and aldosterone. In hypertensive rats, ANF decreased blood pressure by 31 +/- 7 mmHg (17 +/- 3%), comparable to the effect of the angiotensin antagonist saralasin (31 +/- 4 mmHg). Plasma renin activity increased from 48 +/- 15 to 79 +/- 23 ng/ml/h. Despite this, ANF caused marked suppression of plasma aldosterone (from 97 +/- 28 to 20 +/- 8.9 ng/100 ml). These results show that ANF can exert potent antihypertensive and aldosterone-lowering effects in vivo, at least when the renin-angiotensin system is stimulated.

Aldosterone↗
PubMed1983

Predictability of antihypertensive efficacy of selective beta 1 blockers.

The possibility that hemodynamic and biohumoral factors may help predict the antihypertensive effectiveness of selective beta 1 blockers was investigated. The effects of 3 wk of treatment with two selective beta 1 blockers, metoprolol and atenolol, were observed in 54 patients with mild or moderate essential hypertension. No significant difference between the hemodynamic effects of the two drugs was found. The percent fall in systolic blood pressure induced by the two correlated strongly with the pretreatment values of the chronotropic response to isoproterenol and with the pretreatment values of cardiac output, heart rate, and plasma renin activity (PRA). There was no correlation between the decrease in systolic blood pressure induced and initial 24-hr urinary catecholamine output, total peripheral resistance, and plasma aldosterone. Percent fall in diastolic blood pressure correlated only with the pretreatment levels of PRA. Our results support the view that the hypotensive effect of beta 1 blockers are predictable on the basis of the pretreatment values of chronotropic response to isoproterenol, PRA, heart rate, and cardiac output.

Adult↗
PubMed1983

Haemodynamic and clinical effects of long-term treatment of essential hypertension with captopril.

Captopril, an orally active inhibitor of angiotensin converting enzyme, was administered for 12 months to 20 patients with mild or moderate essential hypertension who initially responded favourably to this pharmacological treatment. Captopril induced a significant reduction in blood pressure which remained unmodified throughout the study. This fall in blood pressure was mainly due to a significant decrease in total peripheral vascular resistance, since no change in cardiac output was observed. Simultaneously, there was no significant change in left ventricular anatomy and performance evaluated by echocardiographic technique.

Adult↗
PubMed1983

Increased cardiac output and lowered peripheral resistance during metoprolol treatment.

Echocardiography was performed at every six months in hypertensives well controlled on metoprolol, 100 mg twice a day. After six months' treatment blood pressure was reduced from 177/110 mm Hg to 147/88 (p less than 0.02). LV wall thickness (septum + posterior wall) was unchanged 2.10 cm (2.14), and a significant drop in cardiac output (CO) to 5.0 l/min (6.1, p less than 0.02) was recorded (pretreatment values in brackets). After 24 months' treatment LV wall thickness was reduced to 1.94 cm (p less than 0.02), total peripheral resistance (TPR) to 17.3 mm Hg/l/min (23.4, p less than 0.02) and CO increased to 6.7 l/min (6.1, n.s.). After six months' treatment, there was thus a drop in BP with a significant drop in CO and unchanged TPR. After 24 months' treatment, however, CO was back to the pretreatment level and the drop in BP was entirely caused by a drop in TPR which was probably secondary to a reduction in the wall thickness of the arterial resistance vessels as judged by the relationship between the reduction in wall thickness in the LV and the reduction in TPR during the treatment.

Adult↗
PubMed1983

Valsalva maneuver in the assessment of baroreflex responsiveness in borderline hypertensives.

Baroreceptor function was assessed by (1) the reflex response during Valsalva maneuver, (2) phenylephrine injection, and (3) increase in neck tissue pressure by a neck-chamber in 15 borderline hypertensives (B) and in 15 age-matched normotensives (N). B responded to the fall in blood pressure, occurring in phase II of Valsalva maneuver, with an increase in blood pressure and a decrease in the R-R interval of comparable extent to those observed in normals. On the contrary, in phase IV B showed a depressed heart rate reflex response whether evaluated by the slope of the regression line obtained by plotting the R-R interval versus the systolic blood pressure (slope: B = 6.1 +/- 3.3; N = 35.6 +/- 7, p less than 0.005) or by the change in R-R interval (delta R-R interval: B = 67.5 +/- 37 ms; N = 319 +/- 55 ms, p less than 0.005). On the other hand, both phenylephrine injection and neck-chamber procedure showed an impaired baroreflex responsiveness in B. A linear positive correlation was found between the individual values of the slopes obtained during phase IV of Valsalva maneuver and after phenylephrine injection both in N (r = 0.944, p less than 0.001) and in B (r = 0.84, p less than 0.001). Finally, a linear positive correlation was found between the individual values of the slopes obtained by the phenylephrine technique and the corresponding maximum percent change in R-R interval during phase IV of the Valsalva maneuver both in normals and in hypertensives. In conclusion, overshoot bradycardia during Valsalva maneuver seems to show enough specificity in the evaluation of baroreflex responsiveness to be employed in epidemiological studies in this area.

Adolescent↗