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Biomedical subjects

P Moruzzi

Publications and source records attributed to P Moruzzi.

At least 37 records · Page 2Linked to original sources
PubMed1989

Neural influences on the human pulmonary circulation as a defence reaction to volume depletion.

The role of the autonomic nervous system in the regulation of pulmonary vasomotility in man is unsettled and great emphasis is usually given to changes in flow as the main regulating mechanism. In order to simulate hypovolemia, which might reduce the mechanical influence of flow and disclose a neural mechanism, we decreased venous return through balloon distention in the inferior vena cava in 12 normal subjects, during right heart catheterization performed for diagnostic purposes. Caval obstruction was graduated to reduce cardiac output, right atrial and pulmonary arterial pressures, without altering systemic arterial pressure and heart rate. The sympathetic nervous system was activated by arithmetic and cold pressor tests. During the former, the increase in cardiac output was more than halved by venous return restraint, as compared to the unrestrained condition, and clear pulmonary vasoconstriction, instead of vasodilatation, was observed. During the cold test, cardiac output remained almost steady, in the absence as in the presence of balloon expansion. In both conditions pulmonary arteriolar resistance rose, but in the latter this increase was more than doubled. This study suggests that the autonomic nervous system is involved in the regulation of pulmonary vasomotility in man, its role being unveiled when the mechanical influence of flow is reduced by mimicking a hypovolemic state.

Adult↗
PubMed1989

Neural influences on the pulmonary vascular bed in man.

1. Impedance to venous return by distention of a balloon in the inferior vena cava (IVCB) was utilized in 10 patients, during diagnostic procedures, to reduce blood flow through the lungs at baseline and to buffer its changes during stimulation of the adrenergic system, which was obtained with mental arithmetic (AT) and cold pressor (CPT) tests. 2. When venous return was unimpeded, cardiac output rose by 2.06 1/min during the AT and remained steady during the CPT, and arteriolar resistance in the pulmonary circuit was significantly reduced and slightly raised, respectively. 3. During IVCB, baseline cardiac output decreased by 710 ml/min, it rose by 925 ml/min during the AT and again remained steady during the CPT; pulmonary arteriolar resistance was unchanged from before obstruction at baseline and was significantly augmented by both tests. In particular, AT became a clear vasoconstrictor stimulus, having originally produced vasodilatation. 4. These observations support the view that lung blood vessels in man are sensitive to adrenergic influences and that vasoconstriction can be elicited in circumstances in which the flow through the lungs is restrained. The physiological importance of the neural regulation of the pulmonary circulation in man remains undefined.

Adult↗
PubMed1989

Pulmonary vasoconstrictor overreactivity in borderline systemic hypertension.

Raised vascular pressure and resistance and vasoconstrictor overreactivity to adrenergic stimulation are hallmarks of the pulmonary circulation in sustained primary hypertension. The aim of this study was to investigate the reasons for these disorders. In 10 males with borderline systemic hypertension, pulmonary haemodynamic variables were similar to those of an age matched group of eight normotensive subjects. In normotension, arithmetic and cold pressor tests (sympathetic activators) caused slight vasodilatation and vasoconstriction, respectively. In hypertension both tests showed an obvious vasoconstrictor effect. Restriction of blood flow through the lungs by distension of a balloon in the inferior vena cava is known to increase pulmonary vasoconstrictor reactivity in normal man. As a result of this manoeuvre, pulmonary pressure fell in the normotensive controls without variation in pulmonary vascular resistance, whereas in the hypertensive group there was an increase in resistance and the pressure did not change. In normotensive subjects with caval balloon, the sympathetic activating stimuli both became constrictor and caused vascular resistance to rise to the levels attained in the hypertensive patients during adrenergic stimulation in the absence of obstruction to venous return. In the hypertensives, these stimuli were not able to enhance the pulmonary vascular resistance further. This shows that in these patients maximal vasoconstriction was already achieved through the simple restraint of blood flow with vena caval obstruction. We suggest that in the early phases of systemic hypertension lung vessels are hypercontractile so that they overreact to hypoperfusion or to sympathetic stimulation, even before there is a stable rise in pressure and resistance.

Adult↗
PubMed1989

Electrophysiologic and haemodynamic correlates in supraventricular tachycardia.

In 16 subjects with paroxysmal supraventricular tachycardia (SVT) we sought a relationship between haemodynamic changes associated with artificially induced arrhythmias and the electrophysiological properties of the related atrioventricular (AV) nodal reentry circuit. In 10 patients (group 1) induced SVT was typical (long AH) and caused a significant fall in cardiac output (-1.720 ml min-1) and arterial systolic pressure (-18 mmHg). In six subjects (group 2), induced SVT was atypical (long HA) and did not significantly alter the output of the heart and systolic pressure, despite the elicitation of similar tachycardia. The opposite AV nodal reciprocation pattern which resulted in a substantial increase in AH/HH in group 1 and in a slight rise of the same variable in group 2, may explain these haemodynamic differences. In fact, atrial and ventricular systoles occurred simultaneously and impeded the ventricular filling in the former group, while a regular subsequence of contraction was maintained in the latter group. In group 2, systolic arterial pressure and cardiac output fell to the same level as in group 1 when right atrial pacing, at a similar rate of SVT, determined an increase of AH/HH similar to that observed during typical tachycardia. Thus, the haemodynamic response to SVT differs significantly between the two types of reciprocating tachycardia, particularly as regards cardiac output and blood pressure, and is mainly influenced by the temporal relationship between atrial and ventricular systole, independent of the rate of contraction. The different conduction velocities of the reciprocating circuit limbs and their interrelation seem to be major determinants of the haemodynamic pattern of SVT.

Adult↗
PubMed1988

Combined hemodynamic overload of the left and right ventricles as a possible cause of interventricular septum preponderance in high blood pressure.

We tested whether overload of the two ventricles may be associated with a preponderance of interventricular septum in patients with high blood pressure. The rationale is that the septum is shared by the greater and lesser circulation and that in hypertension the latter shows the same qualitative hemodynamic alterations as the former. Among 65 hypertensive patients, 40 (group 1) showed (echo) posterior wall thickness within the mean +/- 1 SD of 62 normal subjects, and 25 (group 2) had a posterior wall thickness exceeding the mean + 1 SD of the normal population. Both groups were subdivided into subgroups A and B, which included patients whose ventricular septum was similar to (within the mean + 1 SD) and thicker than (exceeding the mean + 1 SD) the posterior wall thickness in the corresponding group, respectively. Resting differences in systemic and pulmonary pressure and vascular resistance among subgroups 1A, 1B, and 2A were not significant; however, in subgroup 2B these variables exceeded those in the other subgroups to a significant extent. During cold pressor testing (CPT) the levels reached and the changes in pressure and resistance from baseline values in both circuits were much greater in subgroups B than in subgroups A. The baseline plasma norepinephrine value showed a trend toward an increase from subgroup 1A to 1B and from subgroup 2A and 2B; during CPT norepinephrine invariably changed and in subgroups B it rose significantly more than in subgroups A. It was not determined whether this caused the hemodynamic overload in subgroups B.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Pulmonary vasomotor responses to neural activation in man.

Passive adaptation to changes in flow is an established mechanism of regulation of pulmonary vasomotility. The role of the autonomic nervous system is not well defined in man. To separate the neural from the mechanical component (variation in flow) the venous return and the lung blood flow of six normal men (while undergoing haemodynamic diagnostic procedures) were impeded by a balloon tipped catheter placed in the inferior vena cava. Mental arithmetic and cold pressor tests were used as sympathetic activators. When the venous return was impeded cardiac output was reduced by a mean of 540 ml compared with baseline. During the arithmetic test the rise in cardiac output fell from 2140 ml when venous return was unimpeded to 890 ml when venous return was impeded. This stimulus changed from being a slight pulmonary vasodilator to being an unequivocal vasoconstrictor. Cold stimulation had little effect on cardiac output and caused an increase in pulmonary arteriolar resistance. This effect was more than doubled when flow through the lungs was impeded. These observations suggest that a neural regulation of the pulmonary circulation exists in man, which is disclosed (arithmetic test) or potentiated (cold pressor test) when the influence of mechanical factors is prevented or reduced.

Adult↗
PubMed1988

[Neural influences on pulmonary vasomotility in man].

In man, the extent, the physiological role and even the existence of neural influences on the pulmonary vasomotility are not defined. A major obstacle to these evaluations is passive adaptation of the lung vessels to changes in flow, making it hard to separate the active from the passive component of vasomotion during adrenergic activation. In this study, which was carried out in 8 patients during diagnostic procedures, the inflation of a balloon in the inferior vena cava was utilized to reduce blood flows through the lungs and to buffer its changes consequent to stimulation of the adrenergic system. Neural activation was obtained with the mental arithmetic and the cold pressor tests. When venous return was unimpeded, cardiac output rose by 2,060 ml during the former and remained stable during the latter test, and arteriolar resistance in the pulmonary circuit was significantly reduced and slightly increased, respectively. Under vena cava obstruction, cardiac output decreased in the baseline by 600 ml; it rose by 925 ml during the arithmetic test and again remained stable during the cold test; pulmonary arteriolar resistance was unchanged since before obstruction in the baseline and was significantly augmented by both test. These observations support the view that lung blood vessels in man are sensitive to adrenergic influences and the vasoconstrictor component of these becomes effective in circumstances in which the flow through the lungs reduced. The physiological importance of these influences remains unclear.

Adolescent↗
PubMed1987

The lesser circulation in patients with systemic hypertension.

The elevated blood pressure and vascular resistance in patients with systemic hypertension are paralleled by a proportional rise in pressure and resistance in the lesser circulation. We evaluated the hypothesis that the increased systemic reaction to adrenergic stimulation is shared by the pulmonary vessels. For this purpose we investigated nine normotensive subjects and 24 patients with moderate primary hypertension during mental arithmetic and the cold pressor test. Both groups responded to both stimuli, with a pressure reaction that during arithmetic was mediated through an increase of cardiac output, and a reaction during the cold pressor test mediated through a predominant rise in systemic vascular resistance. The pressure changes were emphasized in the hypertensive population. Pressure in the pulmonary artery in normotensive subjects was not affected by cold and was slightly raised (systolic) during arithmetic. In hypertensive patients, on the other hand, systolic and diastolic pressures were consistently augmented by both tests, and pulmonary arteriolar resistance rose by 42% and 29% of control during the cold pressor test and arithmetic, respectively. Changes in resistance reflected neurally mediated vasoconstriction and not variations in the passive relationship between pressure and flow, since during arithmetic, for a similar rise in flow the driving pressure across the lungs was steady in normotensive subjects and rose significantly in hypertensive patients. In these same patients pressure was augmented by cold in the absence of substantial changes in flow. At baseline and during tests pulmonary wedge pressure, pleural pressure, arterial blood gases, and pH were similar in the two populations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Amygdaloid influences on brain-stem neurones in the rabbit.

1. Electrical stimulation of the central nucleus of the amygdala in the urethane or alpha-chloralose anaesthetized rabbit evokes a bradycardia with a rapid onset and a concomitant fall in arterial blood pressure. 2. Extracellular neuronal activity was recorded in the ipsilateral nucleus tractus solitarius and dorsal vagal nucleus whilst stimulating the ipsilateral central nucleus of the amygdala, the aortic and vagus nerves. 3. A total of 213 neurones were activated by stimulation of at least one of these inputs. 93 of these neurones received a marked excitatory input from the central nucleus with a wide range of latencies (2-100 ms). 50 of these cells also received inputs from either the aortic or vagus nerves, or both. 4. The activity of 42 vagal preganglionic neurones was recorded in the dorsal vagal nucleus of which 22 had properties typical of cardioinhibitory neurones. 9 of these vagal motoneurones received inputs from the central nucleus with latencies between 2 and 100 ms. Of these, 5 had physiological properties indicating they were cardio-inhibitory neurones. 5. We conclude that neurones in the nucleus tractus solitarius and dorsal vagal nucleus can be influenced by descending inputs arising from the central nucleus of the amygdala. Some of these neurones are also likely to be influenced by afferents innervating the thoracic viscera and arterial baroreceptors. The implications of these observations on the role of forebrain-brain-stem interactions in cardiovascular control are discussed.

Action Potentials↗
PubMed1986

Calcium channel blockade with nifedipine reduces the systemic and the pulmonary vascular reactivity to adrenergic activation in hypertension.

In hypertension the systemic and the pulmonary circulation show exaggerated vascular tone and responsiveness to adrenergic stimuli. In 22 hypertensive men we tested whether the regulation of the two vascular beds is improved by calcium entry blockade with nifedipine. Mental arithmetic raised epinephrine plasma concentration (by 80%), cardiac output (CO) and blood pressure in both circuits, and caused systemic vasodilatation and pulmonary vasoconstriction. After the drug the epinephrine reaction was diminished (+20%), variations in CO and systemic blood pressure were almost unchanged and pulmonary vasoconstriction was abolished. A cold pressor test increased norepinephrine plasma concentration (by 24%), systemic and pulmonary pressure and resistance and did not alter CO. The norepinephrine response to cold was enhanced (+35%) by nifedipine, while systemic and pulmonary resistance rises were importantly attenuated (from +24% to +7% and from +41% to +1%, respectively), and greatly diminished the pressure reactivity. A sympatho-adrenal modulation by calcium blockade, per se, might have restrained the vasomotion during arithmetic. The impressive attenuation of the constrictor responses to cold, which was possibly associated with a potentiated sympathetic drive, prospects that the two circuits share a vascular contractile disorder in which calcium ions are involved.

Adult↗
PubMed1982

Circulatory response to prenalterol in normal subjects and in patients with primary congestive cardiomyopathy.

Experimental pharmacology indicates that prenalterol is a selective beta 1-adrenoceptor activator. In 5 normal individuals, 15 minutes after the drug (infused at a dose of 15 micrograms/kg over 5 min) the following circulatory changes were seen: a) increase of cardiac index (+31%), heart rate, stroke index, systolic aortic pressure, left and right ventricular mean rate of ejection and mean rate of the pressure rise in either ventricle during the pre-ejection phase; b) reduction of systemic vascular resistance (-18%), appearance, built-up and disappearance times in the left ventricular dye dilution curves. Pulmonary systolic, diastolic and wedge pressures and vascular resistance did not vary consistently. The circulatory effects persisted almost unchanged 30 minutes after the infusion. In a group of 5 patients with heart failure due to primary congestive cardiomyopathy, refractory to conventional therapy, the haemodynamic response to prenalterol (infused at a dose of 30 micrograms/kg over 5 min) was qualitatively similar to that of normal subjects in 3 cases. In 2 other patients cardiac performance deteriorated. The reasons for this paradoxical effect were not identified. These preliminary results suggest that prenalterol is a potent selective inotropic agent in man, that may assist in the therapeutic management of refractory heart failure due to congestive cardiomyopathy. However, careful haemodynamic monitoring is advisable for its use in this dysfunction until broader clinical experience can be accumulated.

Adrenergic beta-Agonists↗