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Biomedical subjects

G Grassi

Publications and source records attributed to G Grassi.

At least 37 records · Page 2Linked to original sources
PubMed1990

Cardiogenic reflexes and left ventricular hypertrophy.

Studies performed in both animal and human species have shown that receptors anatomically located in the cardiac walls and in the pulmonary vascular bed exert a powerful influence on sympathetic vasoconstrictor tone and renin release from the kidney. This paper will review recent data collected by our group on the effects on this homeostatic reflex function of two different models of cardiac hypertrophy, i.e. that associated with arterial hypertension and that induced by prolonged physical training. It will also examine whether and to what extent cardiopulmonary reflex control of circulation can be restored after an effective antihypertensive pharmacological treatment has induced a regression of the structural alterations of the heart. The results of these studies suggest that cardiopulmonary reflex control of circulation is markedly impaired in the presence of cardiac hypertrophy, with (severe hypertensive subjects) or without (athletes) high blood pressure values. In hypertensives, furthermore, therapeutic regression of cardiac hypertrophy seems to restore, although not fully normalize, this reflex function. Taken together these findings suggest that cardiac hypertrophy, per se, is a condition characterized by the loss of the reflex functions exerted by cardiac receptors, with adverse consequences on cardiovascular homeostasis.

Adult↗
PubMed1990

Antigenic analysis of the coat protein of beet necrotic yellow vein virus by means of monoclonal antibodies.

By means of monoclonal antibodies (MAbs), five (groups of) epitopes were identified on particles of beet necrotic yellow vein virus (BNYVV). Epitopes 1 and 2, which were located on the opposite extremities of virus particles, are discontinuous (SDS-labile) epitopes which were destroyed when the particles were treated with trypsin. Epitope 3 is a continuous (SDS-stable) epitope located at the same extremity as epitope 2. It was not destroyed when the particles were treated with trypsin and was present on an Escherichia coli-expressed fusion protein containing amino acids (aa) 1 to 103 of the BNYVV coat protein. The continuous epitope 4, which was located along the entire length of the particles, was found to be present on a fusion protein containing aa 104 to 188 of the BNYVV coat protein but not on trypsin-treated virus particles. In Western blots, these treated particles yielded two slightly smaller coat proteins which failed to react with MAbs specific for epitope 4 but did react with polyclonal antisera and MAbs specific for epitope 3. BNYVV coat protein has a trypsin cleavage site on the carboxyl side of arginine in position 182, so it is therefore suggested that epitope 4 is located on the exposed C terminus, which is composed of aa 183 to 188. Epitope 5 was also located along the entire length of the particles but in a more uneven distribution than epitope 4. This may be because it is a discontinuous epitope that is very sensitive to subtle changes in protein conformation.

Antibodies, Monoclonal↗
PubMed1990

Early alterations of the baroreceptor control of heart rate in patients with acute myocardial infarction.

Experimental coronary occlusion is accompanied by an acute impairment of the baroreceptor-heart rate reflex. This study was planned to determine whether this impairment also occurs in humans. In 30 patients admitted to a coronary care unit for an anterior (n = 14) or inferior (n = 16) transmural myocardial infarction (MI), we measured 1) the increase in RR interval induced by stimulating carotid baroreceptors through progressive reductions in neck chamber pressure, 2) the increase in RR interval induced by stimulating arterial baroreceptors through intravenous boluses of phenylephrine, and 3) the reduction in RR interval induced by deactivating arterial baroreceptors through intravenous boluses of nitroglycerin. Measurements were performed 49.5 +/- 2.4 hours (mean +/- SEM) after the MI. The results were compared with those of five age-matched patients admitted to the coronary care unit for chest pain and found free from ischemic heart disease. The sensitivity of the carotid baroreceptor-heart rate reflex (slope of the linear regression of RR interval over neck pressure changes) was markedly less in MI than in control patients (3.8 +/- 0.5 vs. 5.9 +/- 0.6 msec/mm Hg, p less than 0.05), the reduction being similar in patients with anterior and inferior MI. This was the case also for the baroreflex sensitivity measured by the phenylephrine and the nitroglycerin methods (slope of the linear regression of RR interval over systolic blood pressure changes). However, 10.2 +/- 0.3 days later, the baroreflex sensitivity measured by all three methods increased significantly (p less than 0.05 or 0.01) and became similar to that of control subjects, which showed no significant change from the early to the late period after admission into the coronary care unit. Thus, MI is accompanied by an acute marked impairment of the baroreceptor control of the heart in humans, and this is the case both for an anterior and an inferior MI. The impairment is largely transient in nature, however, and a clear-cut recovery of the baroreflex can be seen a few days later.

Carotid Sinus↗
PubMed1990

Cardiopulmonary receptor reflexes in normotensive athletes with cardiac hypertrophy.

Cardiopulmonary receptor control of the circulation is impaired in a variety of diseases having cardiac hypertrophy as a common feature. Whether this also occurs in the so-called "physiological" cardiac hypertrophy of the athlete, however, is unknown. We studied nine sedentary healthy subjects and 19 age-matched professional runners or hammer throwers who had trained at least 2 hours per day, 5 days per week for 7 years. The left ventricular mass index (echocardiography) was 99 +/- 7.4 and 135 +/- 5.9 g/m2 in the two groups, respectively. Cardiopulmonary receptor stimulation and deactivation were obtained by increasing and reducing left ventricular end-diastolic diameter for 5 minutes by leg raising and lower body negative pressure, keeping both stimuli at a level not affecting blood pressure and heart rate. In the sedentary healthy subjects, forearm vascular resistance (the ratio between mean arterial pressure and forearm blood flow) and plasma norepinephrine fell during leg raising (forearm vascular resistance, -7 +/- 1.7 units; norepinephrine, -57.4 +/- 1.4 pg/ml) and increased during lower, body negative pressure (forearm vascular resistance, 20 +/- 5.3 units; norepinephrine, 97.7 +/- 21.5 pg/ml). For similar or greater alterations in left ventricular end-diastolic diameter, the correspondent changes observed in the professional runners or hammer throwers were -5.3 +/- 1.3 units (forearm vascular resistance), -35.4 +/- 9.6 pg/ml (norepinephrine), 9.1 +/- 1.4 units (forearm vascular resistance), and 30.9 +/- 6.9 pg/ml (norepinephrine). This represented an attenuation of 25%, 38%, 55%, and 68%, respectively (p less than 0.01), of the control response.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

[Male transsexualism and hormonal therapy: radiologic pictures of the breast].

Often the male transsexual takes hormonal drugs, sometimes under medical prescription but most frequently by his personal choice. They wish to obtain a development of mammary gland and the disappearance of hair from facial skin. Prolonged hormonal and incorrect treatments, mainly for too high dosage and absence of association with progesterone, assumption of oestrogens, can cause the growth of mammary tumours. The Authors present the results of a clinical and radiological study on 15 patients, 12 in treated with hormonal drugs for two years and 3 without any therapy.

Adult↗
PubMed1989

Effects of dilevalol on forearm circulation in essential hypertension.

In 6 patients with untreated hypertension of mild or moderate degree, dilevalol was infused in the brachial artery. Doses were calculated to produce plasma levels approximating those achieved after oral dosing (0.03, 0.07, 0.1, 0.3 micrograms.kg-1.min-1) and also to produce plasma levels exceeding oral dosing (0.5, 1.0, 2.0 micrograms.kg-1.min-1) without causing any blood pressure or heart rate changes. The effects of the infusion on forearm blood flow were assessed by venous occlusion plethysmography. Dilevalol caused a progressive increase in flow in all subjects up to the intermediate dose given, with the effect being attenuated when the dose was increased further. Simultaneous propranolol infusion reduced the increase in flow induced by dilevalol, shifting the dilevalol-induced vasodilation dose response curve to the right. Isoproterenol infusion caused a marked, dose-related increase in flow that was equally well reduced by simultaneous infusion of dilevalol or propranolol. These results indicate that dilevalol effectively blocks peripheral vascular beta receptors in humans. The drug also acts as a partial beta 2-receptor agonist, causing vasodilation which can be reduced by co-administration of propranolol.

Adrenergic beta-Agonists↗
PubMed1989

Investigation of reflexes from volume and baroreceptors during converting-enzyme inhibition in humans.

This article emphasizes the importance of testing baroreceptor and cardiopulmonary receptor control of circulation during angiotensin-converting enzyme (ACE) inhibitor treatment in hypertensives, because removal of angiotensin II-dependent stimulation of the sympathetic nervous system could impair reflex blood pressure homeostasis. In essential hypertensive subjects, the sympathetic vasoconstriction that occurs in skeletal muscle after deactivation of cardiopulmonary receptors was reduced after short-term or prolonged administration of the ACE inhibitor, captopril. However, another sympathetic target of the cardiopulmonary reflex, that is, renin release, was unaltered by both short-term and prolonged administration of captopril. Furthermore, the blood pressure and heart rate influences of arterial baroreceptors were preserved or even enhanced after administration of captopril. Thus important reflex mechanisms for cardiovascular homeostasis are not adversely affected by ACE inhibition, which preserves blood pressure levels during gravity challenges or exercise. Preliminary data suggest that this may be even more evident for benazepril.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Bactericidal activity of meropenem and interactions with other antibiotics.

MICs of meropenem for selected clinical isolates of bacteria were determined. Killing curves were performed on strains of methicillin-sensitive Staphylococcus aureus, methicillin-resistant Staph. aureus (MRSA), methicillin-resistant Staph, epidermidis, Escherichia coli, Klebsiella spp., Enterobacter cloacae, Pseudomonas aeruginosa, Citrobacter freundii and Acinetobacter spp. A reduction of greater than or equal to 3 x log10 in viable cells was observed at 4 and 6 h of exposure to 4 and 8 x MIC, and this was usually maintained at 24 h (with a few exceptions for methicillin-resistant Staph, epidermidis and Ent. cloacae). At the MIC and twice the MIC regrowth tended to occur at 24 h although this varied from strain to strain. The interaction with other antibiotics was determined by the chequerboard technique. Usually an additive or synergistic effect was observed when meropenem or imipenem was used in combination with an aminoglycoside against Gram-negative species, while in a few cases antagonism occurred in combination with beta-lactams. Against Staph, aureus, MRSA and Staph, epidermidis synergism was usually obtained with combinations with teicoplanin or vancomycin and either synergism or addition with combinations with rifampicin, co-trimoxazole or ciprofloxacin.

Anti-Bacterial Agents↗
PubMed1989

Cardiac hypertrophy impairs cardiac receptor control of circulation in man.

The cardiopulmonary reflex control of circulation (which, in man, depends largely on cardiac receptors) is impaired in hypertensive subjects who have left ventricular hypertrophy. To determine whether hypertension or cardiac hypertrophy per se is responsible for this, we studied nine sedentary normotensive subjects aged 23 +/- 1 years and nine age-matched normotensive weight-lifters with echocardiographic signs of left ventricular hypertrophy (left ventricular mass index for the weight-lifters: 134 +/- 7; for the sedentary subjects: 99 +/- 7 g/m2; P less than 0.01). Cardiac receptors were manipulated by increasing and decreasing the left ventricular end-diastolic diameter (LVEDD) by raising the leg and by reducing the lower-body negative pressure, respectively, and the reflex responses were assessed from the changes in forearm vascular resistance and plasma noradrenaline (high performance liquid chromatography assay). Forearm vascular resistance and the noradrenaline concentration were reduced by increasing the LVEDD, and were increased when the LVEDD was reduced. For a given change in the LVEDD, the responses were markedly less in the weight-lifters than in the non-athletes. In contrast, the haemodynamic effects of a cold pressor test were similar in both groups. Thus, the cardiopulmonary reflex is impaired in normotensive subjects in whom intense physiological training has led to an increase in left ventricular hypertrophy. This suggests that structural alteration of the heart per se is responsible for the phenomenon.

Adult↗
PubMed1989

Effect of angiotensin converting enzyme inhibition on cardiovascular regulation during reflex sympathetic activation in sodium-replete patients with essential hypertension.

In order to investigate whether angiotensin II (Ang II) may contribute to cardiovascular regulation through facilitation of the adrenergic function, we examined the haemodynamic and humoral effects of the application of lower-body negative pressure (LBNP) in sodium-replete patients with essential hypertension before and after acute and chronic angiotensin converting enzyme (ACE) inhibition. We measured the changes in blood pressure, heart rate, central venous pressure, forearm blood flow, plasma noradrenaline, renin activity and Ang II induced by LBNP of two different magnitudes: a milder one deactivating predominantly the cardiopulmonary receptors (mild LBNP), and a greater one deactivating both the cardiopulmonary and the arterial baroreceptors (strong LBNP). We found that during mild LBNP systemic blood pressure was maintained after acute and chronic ACE inhibition, as in control studies; however, the decrements in forearm blood flow and the increments in forearm vascular resistance caused by LBNP were diminished after ACE inhibition (the latter by 69 and 67%, respectively, in acute and chronic studies), in spite of the fact that the falls in central venous pressure and the increases in noradrenaline (NA) were similar to those observed in control conditions. During strong LBNP, the fall in systemic blood pressure was greater after acute and chronic ACE inhibition than in control conditions and was associated with a reduction in the response of forearm vascular resistance similar to that observed during mild LBNP, while the increments in NA were again superimposable to those seen before ACE inhibition. These alterations in the haemodynamic responses to LBNP induced by ACE inhibition were associated with significant increments in basal plasma renin activity and with marked reductions in Ang II. These findings suggest that even in the sodium-replete state, Ang II exerts a facilitatory action on adrenergic function that is physiologically relevant for the regulation of forearm blood flow and the maintenance of blood pressure during the application of gravitational stresses.

Adult↗
PubMed1989

Bone marrow purging for multiple myeloma by avidin-biotin immunoadsorption.

Avidin-biotin immunoadsorption, a technique based on the high affinity between the protein avidin and the vitamin biotin, has been used to remove neoplastic plasma cells from the bone marrow of patients with multiple myeloma. Buffy coat cells obtained from 25 patients were first incubated with monoclonal antibodies (MoAb) capable of recognizing plasma cell-associated antigens (i.e., 8A, 8F6, 62B1, and cocktails of 8A plus 8F6 or 62B1), then with biotinylated goat antimouse immunoglobulin, and passed over a column containing avidin conjugated to Sepharose GMB. Both non-linked and linked cells were analyzed by immunofluorescence and morphological staining. The results showed that over 98% of plasma cells were removed by using 8A or 8F6 alone, while 99.5% +/- 0.4 SD of plasma cell purging was achieved with 2 associated MoAb. In addition, the overall recovery of committed granulocyte-macrophage (CFU-GM),* erythroid (BFU-e), and multilineage (CFU-GEMM) progenitors after column treatment ranged from 39% +/- 15 SD to 50% +/- 6 SD, from 15% +/- 2 SD to 39% +/- 7 SD, and from 16 +/- 4 SD to 64% +/- 10 SD, according to the MoAb employed. On this basis avidin-biotin immunoadsorption appears to be a suitable technique for ex-vivo manipulation of bone marrow infiltrated by neoplastic plasma cells.

Antibodies, Monoclonal↗
PubMed1989

Clinical evaluation of VDD pacing with a unipolar single-pass lead.

Twenty patients with advanced AV block and normal sinus node function underwent pacemaker implantation, randomly receiving a CPI 910 ULTRA II model VDD pacemaker. The first 13 patients received the implantation of a single lead with a screw-in positive ventricular fixation tip and a unipolar ring floating atrial electrode spaced 13 cm from the tip. A subsequent group of seven patients received a conventional porous tinned-tip lead with a pair of unipolar ring floating electrodes. The second solution was adopted because the best atrial signal was not always in the high or mid-high atrium portion, but sometimes in the middle or mid-low position. With the modified double-electrode lead, the floating atrial electrode that detects the best signal can be selected, cutting out the pin of the one not used. The comparisons between minimal atrial slew rate and maximal ventricular slew rate, as well as those between minimal P wave amplitude and maximal R wave amplitude, show a highly significant range difference, as large as P less than 0.01. Surface electrocardiograms, stress tests, and 24-hour Holter monitoring showed the correct functioning of the system with an average sensing failure from 0.05 to 1%. In conclusion, VDD stimulation is feasible with a single unipolar lead and a floating atrial electrode in conjunction with a pacemaker generator (CPI 910 ULTRA II) originally designed for permanent twin-lead implantation.

Aged↗
PubMed1989

Decreased cardiopulmonary reflexes with aging in normotensive humans.

Arterial baroreflex is impaired in the normotensive elderly. However, no information is available on the effects of aging on another major reflex mechanism of cardiovascular control, i.e., cardiopulmonary reflex. Three groups of normotensive subjects divided according to age were evaluated during leg raising, which increased central venous pressure, and during lower body negative pressures, which reduced central venous pressure without altering blood pressure and heart rate. These maneuvers stimulated and deactivated cardiopulmonary receptors with only little involvement of arterial baroreceptors. During lower body negative pressures, central venous pressure decreased similarly in three groups, but reflex increases in forearm vascular resistance, plasma norepinephrine, and plasma renin activity were smaller in elderly than in middle-aged and young subjects. Furthermore, during leg raising, comparable increases in central venous pressure caused reflex vascular and humoral responses that were smaller in elderly than in middle-aged and young subjects. Elderly subjects had smaller changes in left ventricular diameter in response to changes in central venous pressure. Blood pressure and vascular responses to cold pressor test were similar in the three groups, excluding a hyporeactivity of older subjects to neural stimuli. Thus aging is associated with an impairment of the cardiopulmonary reflex. This may originate from an impaired ability of cardiac receptors to sense alterations in central blood volume because of an age-dependent reduction in cardiac compliance.

Adult↗
PubMed1988

Cardiopulmonary receptor regulation of renin release.

Cardiopulmonary receptors have been shown to modulate renin release in animals. However, their involvement in reflex control of renin in humans has never been unequivocally established. This report reviews data on the effects on plasma renin activity of maneuvers (lower body negative pressure and passive leg raising) that reduce and increase central venous pressure and cardiac diameter without affecting blood pressure and heart rate, thereby deactivating and stimulating cardiopulmonary receptors with little or no involvement of the arterial baroreceptors. In normotensive subjects, reduction in central venous pressure was accompanied by an increase in plasma renin activity that was similar to the increase observed during tilt that reduced central venous pressure to a similar extent. Conversely, an increase in central venous pressure was accompanied by a reduction in plasma renin activity. The increase in plasma renin activity that followed the reduction in central venous pressure was drastically attenuated in four patients who had undergone cardiac transplantation, along with other reflex effects (changes in forearm vascular resistance and plasma norepinephrine) of cardiopulmonary receptor manipulations. There was a modest reduction in the overall reflex changes in plasma renin activity in patients with mild to moderate essential hypertension compared with normotensive subjects. However, patients with essential hypertension and cardiac hypertrophy showed marked attenuation of all reflex influences of the cardiopulmonary receptors. In five subjects, therapeutic regression of this structural alteration was associated with a clear improvement in the cardiopulmonary reflex. Thus, in humans, cardiopulmonary receptors exert an important reflex control of renin release. This control (which is due in part to receptors located in the cardiac walls) is moderately affected by a mild to moderate blood pressure elevation but is markedly impaired when the elevation produces structural alterations in the heart. Preliminary evidence, however, suggests that the cardiopulmonary reflex may be improved by a reduction in cardiac hypertrophy.

Animals↗
PubMed1988

Cardiopulmonary receptor reflex in hypertension.

Several studies have described the modifications of the arterial baroreceptor reflex in hypertension. Whether this condition alters the other major cardiovascular reflex (ie, that originating from receptors in the cardiopulmonary region) is less well known, however. Herein we describe the importance of the inhibitory control of sympathetic vasomotor and renin influences exerted by the cardiopulmonary reflex in normotensive humans as assessed by deactivating and stimulating heart and lung receptors through reductions and increases in central venous pressure respectively obtained via lower-body negative pressure and passive leg raising. Observations on this reflex obtained in experimental animal models are summarized. Finally, we report recent evidence showing that the cardiopulmonary reflex is only slightly affected by mild or moderate essential hypertension but impaired in hypertension with left ventricular hypertrophy in a fashion positively related to the degree of this cardiac structural alteration. This may further worsen the severity of hypertension. However, the impairment of the cardiopulmonary reflex is reversible with regression of hypertrophy obtained by antihypertensive treatment which is thus beneficial for cardiovascular homeostasis.

Humans↗