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Biomedical subjects

G Grassi

Publications and source records attributed to G Grassi.

At least 19 recordsLinked to original sources
PubMed1992

Reflex cardiovascular control in congestive heart failure.

This article reviews evidence that the reflex control of the cardiovascular system provided by negative feedback mechanisms is impaired in congestive heart failure (CHF). The impairment involves vagal and sympathetic modulation of the heart exerted by arterial baroreceptors. It also affects baroreceptor control of blood pressure and peripheral vascular resistance, as well as the cardiopulmonary receptor's ability to modulate sympathetic activity. The degree of such impairment is most marked in severe CHF but is also apparent, to a minor degree, in mild heart failure. Reflex impairment is due to a reduction in the receptor signal, but other factor under investigation are probably also involved. Digoxin and other pharmacologic treatments of CHF improve reflex function, thereby facilitating a reduction in the elevated sympathetic activity and a stepping up of the reduced vagal activity typical of CHF. This may be relevant to a patient's prognosis.

Animals↗
PubMed1992

Cardiopulmonary receptor and arterial baroreceptor reflexes after acute myocardial infarction.

The baroreceptor-heart rate reflex in human is impaired 2 days after a myocardial infarction but it improves 10 days after the acute coronary event. This study investigated whether (1) the baroreceptor-heart rate reflex improvement takes the reflex back to normal, and (2) the cardiopulmonary reflex is affected by myocardial infarction. In subjects studied 8 to 11 days after a transmural anterior or inferior myocardial infarction the baroreceptor-heart rate reflex sensitivity (slope of the linear regression between negative neck chamber pressures and lengthenings in RR interval) was similar to that seen in control subjects (-6.2 +/- 0.8 vs -6.0 +/- 0.6 ms/mm Hg, mean +/- SEM) and did not change when reassessed 10 days later. In contrast, the cardiopulmonary reflex sensitivity (changes in forearm vascular resistance induced by changing central venous pressure through nonhypotensive lower body suction and leg raising) was markedly less in subjects studied 8 to 11 days after myocardial infarction than in control subjects; the reduction amounted to 58.1 +/- 8% (p less than 0.01). The cardiopulmonary reflex sensitivity greatly improved when reassessed 28 to 45 days later. Thus, the baroreflex is normal about 10 days after myocardial infarction. This condition markedly impairs the cardiopulmonary reflex, but the impairment is also transient.

Blood Pressure↗
PubMed1992

Effect of detraining on the cardiopulmonary reflex in professional runners and hammer throwers.

In professional athletes with marked cardiac hypertrophy, reflex influences originating from cardiopulmonary receptors are impaired. To determine whether the reflex is restored after termination of physical training and regression of cardiac hypertrophy 8 former athletes (age 31 +/- 6 years, mean +/- SD) who stopped agonistic activity for 5 +/- 1 years were compared with 15 sedentary subjects (27 +/- 7 years) and 19 active professional athletes (22 +/- 7 years). Cardiopulmonary receptor stimulation and deactivation were obtained by increasing and reducing left ventricular end-diastolic diameter (echocardiography) through leg raising and nonhypotensive lower body negative pressure, respectively. Left ventricular mass index (echocardiography) was markedly and significantly (p less than 0.01) greater in athletes (135 +/- 6 g/m2) than in former athletes (105 +/- 4 g/m2) whose value was similar to that of sedentary subjects (98 +/- 4 g/m2). The reduction in forearm vascular resistance and plasma norepinephrine induced by increasing left ventricular end-diastolic diameter was 24 and 23% less in athletes than in former athletes whose responses were similar to those of sedentary subjects. This was the case also for the responses induced by reducing left ventricular end-diastolic diameter. In contrast, the hemodynamic responses to cold pressor test were similar in the 3 groups. It is concluded that the impairment of the cardiopulmonary reflex observed in athletes is largely reversible when physical training is terminated. This may be due to regression of left ventricular hypertrophy.

Adaptation, Physiological↗
PubMed1992

Sympathomoderating influence of benazepril in essential hypertension.

OBJECTIVE: In essential hypertension, captopril attenuates forearm vasoconstriction reflexly induced by deactivation of cardiopulmonary and arterial baroreceptors, thus exerting a sympathomoderating effect. We investigated whether this is a common effect of angiotensin converting enzyme (ACE) inhibitors. METHODS AND DESIGN: Cardiopulmonary and arterial baroreceptors were deactivated by progressively reducing central venous pressure (CVP) through progressively greater lower body negative pressures in eight untreated mild essential hypertensives on a moderately low-sodium diet (50 mmol/l per day). This deactivation was performed after oral administration of the non-sulphidrylic ACE inhibitor benazepril (10 mg) and placebo according to a double-blind randomized crossover experimental design. RESULTS: After placebo, the reduction in CVP increased forearm vascular resistance (FVR; mean arterial pressure: plethysmographic forearm blood flow ratio). After benazepril, baseline blood pressure (beat-to-beat finger pressure) and FVR were significantly reduced whilst plasma angiotensin II was suppressed and PRA increased (both measured by radioimmunoassay). The FVR increases induced by progressive CVP reduction were less than after placebo administration, and the overall difference was statistically significant. Benazepril did not affect the reflex FVR reduction observed by increasing CVP through leg raising, nor the reflex changes in plasma norepinephrine measured by high-performance liquid chromatography accompanying the changes in FVR. CONCLUSIONS: Benazepril attenuates sympathetic vasoconstriction as does captopril. This effect (which is mainly operative during an increased sympathetic drive and exerted through a reduction of adrenoceptor responsiveness) is thus likely to be a class- rather than a compound-related feature.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Effect of oral dilevalol on forearm circulation in essential hypertension.

In 7 patients with untreated mild essential hypertension, a single 200-mg dilevalol dose was administered orally. Blood pressure (BP, left brachial artery catheter), heart rate (HR), and left and right forearm blood flows were measured and left and right forearm vascular resistances were calculated before and for approximately 3 h after drug administration. Dilevalol administration was followed by a sustained reduction in BP, little change in HR, and a similar pronounced and sustained increase in left and right forearm blood flows and reduction in left and right forearm vascular resistances. At the end of the observation period, the changes in left forearm circulation were unaffected by left brachial artery infusion of saline but markedly reduced by left brachial artery infusion of propranolol at doses that had no effect on BP, HR, and contralateral forearm vasodilatation. Thus, at an oral dose exerting an antihypertensive effect, dilevalol induces a marked and persistent vasodilation due largely to the beta-adrenoceptor agonism of the drug.

Administration, Oral↗
PubMed1992

Alpha 1-blocking properties of carvedilol during acute and chronic administration.

Carvedilol is a beta-adrenergic-blocking drug with vasodilating properties. This vasodilation has been ascribed to alpha 1-adrenergic blockade, but it has never been shown in the clinical setting. We addressed this issue by studying eight patients with mild essential hypertension who were given prazosin, 2 mg or carvedilol, 25 mg p.o. following a 2-week washout from previous treatment, according to a randomized double-blind, crossover experimental design. Before and 2 h after the administration of either prazosin or carvedilol, the patients were infused i.v. with increasing doses of phenylephrine (0.2-1.2 microgram/kg/min) and isoproterenol (0.01-0.05 microgram/kg/min). The patients were thereafter maintained on carvedilol 25 mg daily for 3 weeks, and the i.v. phenylephrine and isoproterenol infusions were repeated 2 h after the last tablet administration. The results showed that the single dose of carvedilol and prazosin lowered blood pressure (beat-to-beat finger pressure measurement) to a similar extent, but that heart rate was unaffected by prazosin and reduced by carvedilol. The tachycardic response to isoproterenol was abolished by carvedilol and unaffected by prazosin, whereas the pressor response to phenylephrine was reduced by carvedilol and virtually abolished by prazosin. The antihypertensive, beta-blocking and alpha 1-adrenergic-blocking effects of carvedilol were unchanged following prolonged administration of the drug. Thus, at a clinically effective dose, carvedilol not only has beta- but also sizeable alpha 1-blocking effects. These effects are preserved during prolonged administration of the drug. For a comparable antihypertensive action, however, the alpha 1-blocking effect is less pronounced than that of an alpha 1-blocker such as prazosin.

Adrenergic alpha-Antagonists↗
PubMed1992

Epitope mapping on fragments of beet necrotic yellow vein virus coat protein.

The location of five SDS-stable epitopes on the coat protein (CP) of beet necrotic yellow vein virus was determined by reacting Escherichia coli-expressed free CP, as well as fusion proteins (FP) containing fragments of the CP, with polyclonal and monoclonal antibodies on Western blots. Epitope 1, which has previously been found to be exposed on only one extremity of the virus particle, was located in the region between amino acids (aa) 1 and 7, i.e. on the N terminus of the CP. It was blocked when the N terminus of the CP was linked to a portion of the beta-galactosidase sequence in an FP. Epitope 3, which has previously been found to be exposed on the opposite extremity of the particle, was located in the region between aa 37 and 59. Epitope 4, which is exposed along the entire length of the particle, occurs on the C terminus of CP (aa 183 to 188). Two previously unknown epitopes were identified in the regions between aa 115 and 125 and 125 and 140, respectively. The former was located on the same extremity of the particle as epitope 3, the latter became accessible only after denaturation of the particle. Nothing is known about the probably non-adjacent aa sequences that participate in the formation of the two SDS-labile epitopes (epitopes 2 and 5) which are found on one extremity and along the entire length of the particle, respectively.

Blotting, Western↗
PubMed1992

Physical exercise in essential hypertension.

Although several studies have shown that physical training lowers blood pressure values both in normotensives and in hypertensives, the mechanisms accounted for this effect are not clearly elucidated. It has been reported that the decrease in blood pressure and heart rate that accompanies physical training is associated not only with an increase in vagal tone but also with a reduction in plasma norepinephrine levels. Whether this reduction really means a decrease in sympathetic neural discharge is unknown, however. To clarify this issue, we have performed in 7 normotensives direct recording of postganglionic muscle sympathetic nerve activity from the peroneal nerve by microneurography before and after 10 weeks of an endurance training which increased oxygen consumption by 10%. It was shown that the blood pressure lowering effect of the training program was accompanied by a marked reduction in resting sympathetic nerve activity. These data provide the first direct evidence that in man, the blood pressure reduction induced by physical training is mediated by the neural sympathetic mechanisms.

Blood Pressure↗
PubMed1992

Cigarette smoking and the adrenergic nervous system.

The acute increase in blood pressure and heart rate that accompanies cigarette smoking is associated with a rise in plasma catecholamines and it is thus believed to result from stimulation of the adrenergic nervous system. We have employed direct recording of efferent post-ganglionic sympathetic nerve activity by the microneurographic technique from the peroneal nerve to determine whether this stimulation occurs centrally or peripherally. It was shown that during cigarette smoking blood pressure, heart rate, plasma norepinephrine and epinephrine do increase markedly. Sympathetic nerve activity, however, shows a concomitant specular reduction. Thus peripheral (adrenal gland stimulation, reduction in norepinephrine reuptake, reduction in catecholamine clearance, etc.) rather than central mechanisms explain the adrenergic involvement in the acute hemodynamic effect of smoking, the central sympathetic drive being inhibited rather than excited probably as a result of arterial baroreceptor stimulation.

Blood Pressure↗
PubMed1992

Changes in arterial compliance induced by physical training in hammer-throwers.

OBJECTIVE: Physical training induces multiple changes in the cardiovascular system which allow an increased performance along with increased oxygen consumption. The present study was designed to investigate whether the changes include an increase in arterial compliance. METHODS AND DESIGN: In six normotensive right-handed hammer-throwers (aged 21.3 +/- 1.8 years, mean +/- SE) we measured radial artery diameter continuously via a new non-invasive echo-tracking device, and beat-to-beat blood pressure. Arterial compliance was calculated by an arctangent model. In each subject measurements were made from both the left and the right arm. The data were compared with those obtained in six age-matched normotensive controls. RESULTS: Compared to the controls, the hammer-throwers had similar blood pressure, a lower heart rate and plasma norepinephrine and a higher left ventricular mass index and radial artery diameter. In the athletes, right radial artery compliance was significantly greater than either right or left radial artery compliance in the sedentary subjects (+61 and 63%, P < 0.05). It was also significantly greater than contralateral radial artery compliance (+53 +/- 8%, P < 0.05). CONCLUSIONS: Physical training is accompanied by an increase in arterial compliance. In our hammer-throwers this increase was mainly evident in the more highly trained arm, suggesting that local mechanisms are involved in this phenomenon.

Adult↗
PubMed1992

[Meteoropathy: a syndrome continuously on the increase].

The authors describe the different kinds of meteoropathies, pointing out how these disorders are becoming ever more frequent in countries belonging to the consumer and welfare society due to the progressive lowering of body resistance and immunologic responses. These "unfavourable meteosyndromes", as meteoropathies should be called, develop when wave disturbances arrive, and are more manifest and persistent in subjects with neurologic disturbances, i.e. in the presence of anxiety, stress, hypertension, coronary artery disease, arthropathy, hyperthyroidism, etc. The different moments in which meteoropathies are more frequent and the possible therapies are also discussed.

Climate↗
PubMed1991

Vascular eicosanoids and platelet-aortic wall interactions in spontaneously hypertensive rats.

We studied the aggregation of collagen and ADP-stimulated platelet-rich plasma (PRP) and the formation of thromboxane B2 (TxB2) by collagen-stimulated PRP in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto control rats (WKY). In addition, we evaluated the inhibition of the aggregation of PRP following homologous or heterologous perfusions through isolated aortas, the release of 6-keto-prostaglandin (PG)F1 alpha from these arteries perfused with PRP, and the sensitivity of PRP to the antiaggregatory activity of the stable PGI2 analogue, iloprost, in both SHR and WKY. The lower activities (aggregation induced by ADP and collagen, collagen-stimulated TxB2 production) of SHR platelets, were not accompanied by morphological differences from WKY platelets. These changes were associated with a greater release of arterial 6-keto-PGF1 alpha, with greater platelet antiaggregatory activity of the arterial wall and with higher sensitivity of platelets to iloprost. The lower reactivity of platelets to aggregating agents, and the greater sensitivity to prostacyclin, associated with a greater production of arterial prostacyclin were the major changes observed in SHR animals. These alterations in the SHR vs. normotensive WKY may lead to an enhanced risk of hemorrhage in the hypertensive state.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Assessment of sympathetic cardiovascular influences in man: haemodynamic and humoral markers versus microneurography.

Evaluation of sympathetic cardiovascular influences has important physiological, pathophysiological and clinical implications. This paper reviews some of the methods employed to measure these influences in man, along with their advantages and disadvantages. The most useful methods appear to be the measurement of plasma noradrenaline (particularly when modified to calculate spillover rate of noradrenaline) and direct recording of sympathetic nerve traffic. With the former, despite the technological advances in measurement, certain methodological problems remain, such as the separation of noradrenaline secretion from clearance. With the latter technique peripheral muscle and skin sympathetic activity can be measured separately but the question of regional vascular variability has still to be resolved. A combination of these two methods may represent the ideal approach. This review considers the complex problems associated with attempts to precisely quantify sympathetic cardiovascular influences in man.

Animals↗
PubMed1991

Left ventricular hypertrophy and the 'cardiogenic reflex' in man.

In man, cardiac receptors exert a continuous restraint on sympathetic activity. Reflexes originating from the heart also restrain renin and vasopressin secretion, thereby being involved both in blood pressure and in blood volume homeostasis. We have shown that these reflexes are markedly depressed in subjects with left ventricular hypertrophy (LVH) due to hypertension and that this is also the case when, in normotensive subjects, LVH is caused by prolonged physical training. In both instances, the cardiogenic reflex impairment is associated with derangement of blood pressure homeostasis. Either spontaneous regression of LVH by physical training cessation or antihypertensive treatment is followed by a marked improvement of the cardiogenic reflex. Thus, LVH also affects the 'afferent' function of the heart. 'Physiological', as well as pathological, hypertrophy has a similar adverse effect. This effect is reversible, however, and the reflex function can be restored by regression of hypertrophy.

Autonomic Nervous System↗
PubMed1991

Implantable pharmacological defibrillator (AIPhD): preliminary investigations in animals.

The treatment of ventricular fibrillation (VF) by means of automatic implantable cardioverter defibrillators (AICD) poses many severe problems and limitations at the present time. In order to overcome these problems, we propose a totally new way to terminate VF or ventricular sustained tachycardia (VST). Our proposal consists of replacing the electric shock, which is dangerous, delayed, and sometimes ineffective, with a "chemical" shock: i.e., a chemical bolus retroperfused in the coronary sinus (CS) immediately after VF arises. The possible device is hypothesized and preliminary investigations in animals, performed to verify the theoretical assumption, are presented. In rabbits, and in larger animals (sheep and swine). Drugs were perfused in the coronary bed: lidocaine was used in 86% and bretylium tosylate in 14% of the animals. The results were: lidocaine immediately terminated VF in 100% and sinus rhythm was restored in rabbits; lidocaine terminated VF in VST in sheep; and in swine, bretylium immediately produced sinus rhythm in one case; in another one, only delayed sinus rhythm was achieved but lasted a short time; in the last case ventricular tachycardia at 128 beats/min appeared. Because new drugs, which are really "defibrillating" drugs, are available (bretylium tosylate, bethanidine, clofilium, tricyclic antidepressants, phenotiazine derivatives), we plan to investigate these defibrillating drugs in isolated hearts, found in suitable animals like dogs (sheep and swine are difficult to defibrillate) and in humans during routine electropharmacological studies.

Animals↗