Search PubMed⌕ Search

Biomedical subjects

G C Maggi

Publications and source records attributed to G C Maggi.

At least 37 records · Page 2Linked to original sources
PubMed1983

Prostacyclin effect on heart rate in the pig.

The purpose of this study was to assess the hemodynamic response after prostacyclin infusion into the venous system and into the carotid artery in the pig. During the study the following circulatory variables were studied: mean systemic arterial pressure, mean pulmonary arterial pressure, wedge pressure, heart rate, cardiac output, systolic and diastolic left ventricular pressure, stroke volume, total systemic resistance, total pulmonary resistance, left ventricular stroke work. Our results confirm that prostacyclin is a powerful hypotensive agent. The hypotensive effect seems to be due to a peripheral vasodilatation of arterial and venous vessels. Venous infusion caused only 19% tachycardia, as opposed to 36% caused by arterial infusion for the same percentage of blood pressure reduction. This suggests that prostacyclin probably stimulates cardiopulmonary vagal receptors. The effect of prostacyclin on heart rate, therefore, may be twofold and in opposite directions: one action causing tachycardia secondary to hypotension, and the other inviting bradycardia through direct vagal stimulation.

Animals↗
PubMed1982

[Arrhythmias in the mitral valve prolapse syndrome].

Possible connections have been investigated between PVc (premature ventricular contractions) and echocardiographic patterns in 23 patients affected by MVPS. Pansystolic prolapse has been found in 12 cases and mid-systolic prolapse in 11. A correlation has been found between significant ventricular arrhythmias (50 PVc/24 h) and mid-systolic prolapse. These findings suggest the mechanical origin of cardiac rhythm disorders.

Adolescent↗
PubMed1982

Effect of ibopamine on heart rate and spontaneous premature ventricular beats in patients with angina pectoris.

Seven male patients suffering from angina pectoris with spontaneous premature ventricular beats were given oral ibopamine 50 mg t.i.d. for 5 consecutive days, after at least 6 days of observation under basal conditions. A number of clinical parameters were explored during the basal and treatment periods, including repeated 24-hour Holter recordings in each case. The heart rate, expressed as mean hourly rate, minimum and maximum values per observation period, and nocturnal value, showed no clinically or statistically significant change with treatment. There was no worsening of pre-existing arrhythmias or chest pain. All other test parameters remained unchanged. This confirms the excellent tolerance of ibopamine in patients with ischaemic heart disease.

Aged↗
PubMed1981

Prostacyclin effect on cardiovascular system in man evaluated by echocardiography.

This was an echocardiographic study of the cardiovascular effects of prostacyclin (PGI2) infused intravenously to human volunteers at the rate of 20 ng . kg-1 . min-1 for 10 minutes. The following parameters were recorded in the steady state, at one-minute intervals throughout infusion and the ensuing recovery period: systolic, diastolic, and mean blood pressure (SBP, DBP, MBP); heart rate (HR); left ventricle end-diastolic (EDD) and end-systolic diameter (ESD); stroke volume index (SVI); cardiac index (CI); peripheral vascular resistance (PVR); left ventricle fractional shortening (FS) and ejection fraction (EF). We detected a progressive reduction of MBP without any HR modification. MBP reduction was associated with a reduction of PVR and a parallel rise of CI and SVI. There was also an increase of FS and EF reflecting a reduced ESD. We conclude that PGI2 infused in man at the rate stated above causes hypotension reflecting an arterial vasodilating effect; a lack of heart rate reflex response to afterload reduction (probably a nerve-mediated effect of PGI2); and no venous vasodilation, judging from the absence of any change in end-diastolic diameter.

Adult↗
PubMed1980

Role of hypotension induced by PGI2 on the control of depth and frequency of breathing.

We studied the respiratory response to infusion of prostacyclin (PGI2) in 7 anaesthetized pigs in an attempt to understand whether the changes in pattern of breathing were due to a direct action of the substance or to the concomitant hypotensive effect. The depth and frequency of breathing were analyzed in terms of the threshold-inhibition curve for termination of inspiration (VT/TI relationship) and of bulbo-pontine rhythm, estimated from inspiratory and expiratory time during occlusion of the airways at the end expiratory level (TE/TI relationship). This provide the central respiratory rhythm when the phasic lung volume receives no input from pulmonary stretch receptors. The hypotension induced by PGI2 increased pulmonary ventilation mainly through a change in VT and caused a slight rightward displacement of VT/TI relationship without modifying the slope of the curve. This effect seems to be vagally mediated. PGI2 also changed the bulbo-pontine rhythm. Our results show that PGI2 modifies the vagal discharge and bulbo-pontine rhythm by two opposite mechanisms: hypotension and an apparent direct action on carotid and aortic baroreceptors.

Animals↗
PubMed1980

Analysis of hemodynamic and respiratory effects of PGI2 in the pig.

Cardiovascular and pulmonary effects of prostacyclin (PGI2) were investigated in the anaesthetized pig before and after vagosympathectomy at 1',2',3',4',5',10',15' and 20' after the beginning of the infusion. The animals were perfused with PGI2,2ug/kg/min for 4 min. We measured the following parameters : mean arterial pressure, heart rate, cardiac output, stroke volume, mean pulmonary arterial pressure, mean wedge pressure, left stroke work, total systemic resistance, total pulmonary resistance, tidal volume, respiratory frequency, minute volume, lung resistance and compliance, end-tidal CO2, transpulmonary pressure. Our findings suggest that the hypotension observed is due to a reduction in total peripheral resistance by a direct effect of PGI2 on the vascular bed without inhibition of the sympathetic nervous system. Prostacyclin does not directly modify cardiac function and produces a decrease in preload by venous dilation. The changes in pattern of breathing are related to the hypotensive effect of PGI2.

Animals↗
PubMed1979

[Respiratory effects of PGI-2 in the pig].

In anaesthetised pig the intravenous perfusion of 2 micrograms/Kg/min/4 min of PGI2 induces within 30'' respiratory changes that spontaneously disappear after perfusion. The PGI2 induces a decrease of respiratory frequency while total pulmonary resistance increases significantly. This changes of pattern of breathing are correlated to tonus of vagus nerve and after vagosimpathectomy are not present. The relationship of tidal volume/frequency has been evaluated according to the blood pressure variation.

Animals↗
PubMed1979

[Hemodynamics in swine treated with PGI 2].

The hemodynamic response of pig perfused by PGI2 (2 micrograms/kg/mm/4 min) has been studied before and after vagosympathectomy. Prostacyclin produces hypotension, which depends to an reduction of total peripheral resistances, without cardiac involvement. A venous dilatation is also present with reduction of preload and of systolic volume. The authors conclude assessing that prostaciclyn act by peripheral mechanism.

Animals↗