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Biomedical subjects

G Mercuro

Publications and source records attributed to G Mercuro.

At least 37 records · Page 2Linked to original sources
PubMed1997

Effects of acute administration of transdermal estrogen on postmenopausal women with systemic hypertension.

We studied 16 postmenopausal women with mild to moderate hypertension according to a randomized, double-blind protocol. They received patches of transdermal estradiol-17beta rated to deliver 100 mg/day of substance or matched placebo. A 24-hour ambulatory blood pressure (BP) monitoring was performed at baseline and after drug administrations. Our data show that estradiol-17beta exerts beneficial effects, both in lowering elevated BP levels and in maintaining a uniform BP control over 24 hours. Estrogen replacement therapy could be considered when significant changes in BP occur during the postmenopausal period.

Administration, Cutaneous↗
PubMed1997

Association between psychiatric disorders and Marfan's syndrome in a large Sardinian family with a high prevalence of cardiac abnormalities.

BACKGROUND: Marfan's syndrome is an inherited disorder of connective tissue associated with characteristic abnormalities of the skeletal, ocular, and cardiovascular systems. Marked clinical variability and age dependency of all manifestations of Marfan's syndrome may render the unequivocal diagnosis difficult in mildly affected, young subjects. HYPOTHESIS: The study and care of a 32-year-old woman with evidence of Marfan's syndrome, several cardiac abnormalities, and paranoid schizophrenia led to an investigation of her consenting relatives to verify the penetrance of Marfan's syndrome and the degree of comorbidity between the disease and psychiatric disorders. METHODS: The patient and 12 subjects belonging to three generations of her family underwent cardiovascular, skeletal, ophthalmologic, and psychiatric examinations. Two-dimensional and Doppler echocardiography were performed. RESULTS: One female index patient and six of her first-degree relatives were found to be affected by Marfan's syndrome. All seven patients were found to have mitral valve prolapse associated with other cardiac abnormalities. Four of these patients were affected by the following psychiatric disorders: generalized anxiety disorder, major depressive disorder, paranoid schizophrenia (two cases). Six more relatives without Marfan's syndrome showed mitral valve prolapse in association with other echocardiographic features. Two of these were found to be affected by a major depressive disorder. CONCLUSIONS: The present data support the hypothesis that a psychiatric condition, associated with a significantly high frequency of cardiac involvement, may be part of the phenotype of Marfan's syndrome.

Adolescent↗
PubMed1993

Extraneuronal noradrenaline in the prefrontal cortex of morphine-dependent rats: tolerance and withdrawal mechanisms.

The changes in extracellular concentrations of noradrenaline (NA) in the prefrontal cortex of morphine-dependent rats were studied by microdialysis following an acute morphine challenge and during naloxone-precipitated withdrawal. Animals were implanted with morphine- or placebo-containing pellets for 5 days. In control rats a challenge dose of morphine (5 mg/kg s.c.) induced a maximum decrease in NA output of about 45% of pre-drug levels. In contrast, morphine challenge had no effect on extraneuronal NA concentrations in morphine-implanted animals. In control animals, naloxone (2 mg/kg i.p.) produced no behavioral effect nor changed NA levels. However, in morphine-dependent animals naloxone suddenly increased extraneuronal NA by 175% of baseline dialysate levels in the first sample after the injection and precipitated a morphine-withdrawal symptomatology that paralleled the changes in NA output. Thus, chronic morphine treatment in rats results in the development of tolerance to the acute inhibitory effect of morphine on extraneuronal NA and is associated with a stimulation of prefrontocortical NA output during naloxone-precipitated withdrawal.

Animals↗
PubMed1992

Biphasic effect of ethanol on noradrenaline release in the frontal cortex of awake rats.

Ethanol elicited a biphasic effects on the extracellular noradrenaline (NA) concentrations in the rat frontal cortex, as assessed by microdialysis in awake animals. A low dose of ethanol (0.2 g/kg i.p.) raised NA output to about 160% of baseline levels. In contrast, a dose of 2 g/kg inhibited NA output to about 70% of pre-drug levels. These results suggest that the decrease in cortical NA output may reflect the sedative-hypnotic properties of ethanol at high doses, whereas the stimulation of extraneuronal NA may represent a biochemical correlate of the arousal and increased alertness elicited by low doses of ethanol.

Animals↗
PubMed1992

[Nicardipine attenuates the sympathetic reflex of orthostatism: do dihydropyridine-sensitive calcium channels regulate noradrenaline release?].

Twelve hypertensive subjects were treated for 2 weeks with the dihydropyridine calcium channel antagonist nicardipine (40 mg daily) according to a double-blind, placebo-controlled study protocol. Nicardipine treatment significantly decreased systolic and diastolic blood pressure and increased plasma noradrenaline levels measured at supine rest. However, the treatment significantly inhibited the physiological increase of circulating neurotransmitter following sympathetic stimulation induced by orthostatism. These results suggest that dihydropyridine-sensitive calcium channels may modulate the noradrenaline release from nerve terminals of the peripheral sympathetic nervous system.

Adult↗
PubMed1991

[The vascular and metabolic mechanisms of the development of the atherosclerotic plaque].

Atherosclerosis is a degenerative disease responsible for the majority of deaths in the western populations. According to the idea of the reaction to injury the endothelial cells lining the vascular wall are exposed to repeated insults to their integrity. The injury results in a loss of functional attributes of endothelium and leads to a sequence of events including platelet adherence and aggregation, release of platelet granular components, migration and proliferation of medial smooth muscle cells into the intima. Examples of types of injury include chemical injury, as in hyperlipidemia, or mechanical stress associated with critical changes in vascular flow. Atherosclerosis has been considered a disease primarily concerned with lipid metabolism by regarding the intramural caseous material of atheromatous arteries as the sine qua non of the disease. The limitation of the lipid theory is that the conventional cholesterol-fed animal does not exactly reproduces the pathology of atherosclerosis. An alternative theory suggests that atherosclerosis is induced by mechanical fatigue which produces the progressive change in structure and mechanical properties of the vessel wall. In this view the lipid accumulation is a secondary phenomenon, the consequence of concomitant biochemical alterations of mural constituents. The hypothesis of reaction to injury provides a plausible explanation for the lesion formation and the different theories of atherogenesis are not mutually exclusive.

Animals↗
PubMed1990

Inhibitory effects of catecholamines in the paravertebral sympathetic ganglia of the anesthetized dog.

alpha-Adrenoceptor agonists decreased mean arterial pressure when injected into the arterial blood supply of the paraspinal sympathetic ganglia of pentobarbital-anesthetized open-chest dogs. The hypotensive response occurred concomitantly with selective decreases of vascular resistance in the vessels innervated by neurons arising from these ganglia, and both of these responses were blocked by the ganglionic blocking agent, hexamethonium. The hypotensive response to phenylephrine was selectively blocked by terazosin; alpha 1 selective agonist, and antagonist, respectively, while the hypotension produced by intra-arterial clonidine was blocked by rauwolscine; alpha 2 selective agonist and antagonist, respectively. Either terazosin or rauwolscine reduced the hypotension produced by noradrenaline or dopamine. These results demonstrated the presence of both alpha 1- and alpha 2-adrenoceptors in the paraspinal sympathetic ganglia. Activation of either alpha-adrenoceptor subtype inhibited ganglionic transmission.

Adrenergic alpha-Agonists↗
PubMed1990

Different patterns of left ventricular filling in arterial hypertension.

To determine whether left ventricular (LV) filling dynamics may be influenced by the type of LV morphological adaptation to arterial hypertension, pulsed Doppler mitral flow velocity recordings were performed in 30 hypertensive patients and in 18 normotensive subjects matched for age, body surface and heart rate. Peak early (E) and late (A) mitral flow velocity, A/E ratio (A/E), time to peak E (TP), acceleration (AHT) and deceleration half-time (DHT) of early mitral flow and isovolumic relaxation time (IRT) were measured. Compared with the control group, hypertensive patients showed prolonged IRT and DHT, increased A and A/E, whereas TP, AHT and E were unchanged. Hypertensive patients were classified into two subgroups on the basis of h/r ratio (h/r). Subgroup 1: 16 patients with normal h/r, less than 0.42, (five patients with increased LV mass index, greater than 129.2 g m-2, and 11 patients with normal LV mass index, less than 129.2 g m-2). Subgroup 2: 14 patients with increased h/r, greater than 0.42, (nine patients with increased LV mass index, greater than 129.2 g m-2 and five patients with normal LV mass index, less than 129.2 g m-2). In Subgroup 1 the cardiac output (CO) was increased and the total peripheral resistance (TPR) was unchanged in comparison with the control group. In Subgroup 2 the opposite haemodynamic profile was detected: normal CO and increased TPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Catecholamine injections in canine paravertebral ganglia produce hypotension by neurogenic vasodilatation.

In the present study the alpha 1 selective agonist phenylephrine (PE), the alpha 2 selective agonist clonidine (CLO) and the non-selective endogenous catecholamine norepinephrine (NE) and dopamine (DA) were injected directly into the blood supply of the paravertebral sympathetic ganglia (PSG) of anesthetized open-chest dogs. Intra-arterial injection of all agonists produced dose-dependent decreases in mean arterial pressure (MAP) and femoral vascular resistance (FVR) but had no effect on heart rate. Their potency order was CLO greater than NE greater than PE greater than DA. Intravenous injections of the medium dose for NE and PE produced significant increases in MAP, while the medium dose of CLO injected iv produced a small decrease in MAP. The ganglionic blocking agent, hexamethonium (10 mg/kg iv) completely eliminated the hypotensive response to all agonists. Intra-arterial administration of the alpha 1 selective antagonist terazosin (0.5 mg) significantly reduced the decrease in MAP produced by the ganglionic actions of PE, but had no significant effect on the response to CLO. In contrast, the alpha 2 selective antagonist rauwolscine (100 micrograms) significantly reduced the decreases in MAP produced by ia CLO, but not that produced by ia PE. However, both antagonists inhibited the hypotensive effect of NE and DA. These findings suggest that both subtypes of alpha-adrenoceptors, alpha 1 and alpha 2, are present in the PSG and that both subtypes are inhibitory since their activation results in reduced transmission of impulses through the ganglia.

Animals↗
PubMed1987

Peripheral dopamine receptors in the antihypertensive action of dihydroergotoxine in humans.

The effect of the intravenous administration of dihydroergotoxine (6 micrograms/kg) on arterial blood pressure, heart rate, and plasma concentrations of norepinephrine and 3,4-dihydroxyphenylacetic acid (the deaminated dopamine metabolite) was studied in 20 subjects with essential hypertension (8 men and 12 women aged 32-68 years old, World Health Organization Class I-II). In supine resting subjects, dihydroergotoxine significantly decreased systolic blood pressure (from 175 +/- 5 to 156 +/- 4 mm Hg; p less than 0.001), diastolic blood pressure (from 109 +/- 4 to 95 +/- 3 mm Hg; p less than 0.001), and heart rate (from 71 +/- 2 to 63 +/- 2 beats/min; p less than 0.001) as compared with the results of placebo treatment. Moreover, dihydroergotoxine reduced plasma levels of norepinephrine (from 368 +/- 39 to 238 +/- 33 pg/ml; p less than 0.001) and 3,4-dihydroxyphenylacetic acid (from 1.57 +/- 0.21 to 1.22 +/- 0.13 ng/ml; p less than 0.01). The time course of the blood pressure decrease paralleled that of plasma norepinephrine concentration. Dihydroergotoxine did not suppress the cardiovascular and plasma norepinephrine concentration. Dihydroergotoxine did not suppress the cardiovascular and plasma norepinephrine response to standing. The effect of domperidone, a peripheral presynaptic dopamine receptor antagonist, on dihydroergotoxine response was studied in six of the 20 subjects (3 men and 3 women 48-64 years old). The intravenous administration of domperidone (0.3 mg/kg) prevented the dihydroergotoxine-induced reduction in blood pressure and heart rate and the fall in plasma norepinephrine and 3,4-dihydroxyphenylacetic acid levels. Domperidone administered alone failed to significantly modify any measured variables.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗