Search PubMed⌕ Search

Biomedical subjects

M Maccario

Publications and source records attributed to M Maccario.

At least 109 records · Page 6Linked to original sources
PubMed1994

Interaction of salbutamol with pyridostigmine and arginine on both basal and GHRH-stimulated GH secretion in humans.

OBJECTIVE: It is well known that acetylcholine and arginine stimulate GH secretion while activation of beta-adrenergic receptors inhibits GH secretion in man. We aimed therefore to ascertain whether or not the inhibitory influence of beta-adrenergic receptors on GH secretion would over-ride the stimulatory one of acetylcholine and arginine. DESIGN: We studied the interaction of salbutamol, a beta 2-adrenergic agonist (SAL, 0.08 mg/kg orally) with pyridostigmine, a cholinesterase inhibitor (PD, 120 mg orally), or arginine (0.5 g/kg i.v.) on both basal and GHRH (1 microgram/kg i.v.)-stimulated GH secretion. SUBJECTS: Fourteen healthy male volunteers, aged 20-35 years, were studied. MEASUREMENTS: Serum GH was measured in duplicate by immunoradiometric assay. RESULTS: In study A, SAL inhibited the GH response both to GHRH (P < 0.01) and ARG (P < 0.002). ARG enhanced the GHRH-induced GH rise (P < 0.01) but its effect was abolished (P < 0.02) by SAL pretreatment. In study B, SAL inhibited the GH response both to GHRH (P < 0.01) and PD (P < 0.02). PD enhanced the GH response to GHRH (P < 0.001) but its effect was abolished (P < 0.05) by SAL pretreatment. In both studies, the GH response to GHRH alone was similar to that to the neurohormone when combined with ARG + SAL or PD + SAL. CONCLUSION: Our results show that beta 2-adrenergic activation by salbutamol is able to inhibit not only the GH rise induced by GHRH, arginine and pyridostigmine, but even the potentiating effect of both arginine and pyridostigmine on the GH response to GHRH. They indicate that catecholamines, acetylcholine and arginine play a major role in GH secretion having opposite influences aimed to balance the function of the hypothalamus-GH-IGF-I axis in man.

Adult↗
PubMed1994

[Comparison between low and high doses of aprotinin in heart surgery].

High dose aprotinin has been used in cardiac surgery (Royston 1987) to reduce post operative bleeding. A low dose aprotinin ie 2000000 KIU in the oxygenator prime, has been also proposed. OBJECTIVE. To evaluate postoperative losses and holomogous blood transfusions, in patients undergoing cardiac surgery treated with low and high dose aprotinin. METHODS AND MATERIALS. Ninety-nine patients, between January and May 1993, have randomized in 3 groups: A, high dose aprotinin; B, low dose aprotinin; C, control. All patients were treated with additional blood saving techniques routinely used in our center. Statistical analysis was performed by means of ANOVA and Tukey Kramer test. MAIN RESULTS. Five patients (3 in group A, 1 each in groups B and C) have been excluded during the trial. The groups resulted omogeneus and comparable. Total blood losses were 372 +/- 159 ml in group A, 401 +/- 178 ml in group B (difference are not significative); the 621 +/- 255 m1 in group C are highly significative. Patients transfused were 18.7% in group C, 10.34% in group A and 6.20% in group B. CONCLUSIONS. Effects of low dose aprotinin are comparable to high dose. Further advantages with low dose are reduction of collateral effects and intolerance phenomena and a better cost benefits ratio.

Aged↗
PubMed1994

[Predictive value of the shunt-to-infarct size ratio as a surgical risk factor in patients with decompensated post-ischemic interventricular septal rupture].

Postischemic septal rupture has always been evaluated, in respect of surgical indication, as regards the time lapse between infarct and rupture, interval between rupture and operation, extension of myocardial damage and general risk factors such as age, sex and associated pathologies. But in fact the surgeon is dealing with a two sided problem, the MI and the rupture, and thus surgical results depend upon both the residual ventricular function after MI and the consequences of volume overload on a damaged muscle. Surgical indication could not be based on a single criterion only. Extension of the MI alone is not fully predictive of operative mortality because, aside the reperfusion injury, the repair further jeopardizes viable myocardium and alters ventricular geometry; although the shunt appears unrelated to mortality it certainly interferes with operative outcome at least because of the time elapsed between rupture and repair. So far an index which could correlate the extension of myocardial damage and the entity of the shunt with each other was not available. Patients with septal rupture follow an emergency protocol and are often insufficiently investigated but every patients has a least one echo-Doppler evaluation or even a ventriculography while one or more ECGs are always available. With the presumption that the Qp/Qs is roughly indicative of the right ventricular volume overload and that ecg signs of myocardial infarct are always reliable, we have reviewed among our 24 patients with septal rupture those where a full ecg tracing and a quantitative Echo or angiographic evaluation of the shunt were available.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Initial experience of mitral valve replacement with total preservation of both valve leaflets.

We compared a series of 7 consecutive patients who underwent mitral valve replacement with preservation of both leaflets to a control group of 97 patients who underwent standard mitral valve replacement at our institution during the same period. Use of inotropic drugs and duration of postoperative intensive care were compared and shown to be markedly reduced in the study group; however, statistical analysis was not applied due to the small number of patients. Comparison of the available pre- and postoperative echocardiographic values showed a decrease in left ventricular end-diastolic and end-systolic diameters in patients with preserved leaflets, particularly in those with mitral regurgitation of degenerative origin.

Aged↗
PubMed1993

Repetitive GHRH administration fails to increase the response to GHRH in obese subjects. Evidence for a somatotrope defect in obesity?

Spontaneous GH secretion as well as GH response to several stimuli including GHRH have been shown to be reduced in obesity. To clarify the pathogenesis underlying these alterations, in six obese patients (3 males and 3 females, age 20-44 yrs, BMI = 42.1 +/- 2.2) on unrestricted diet we studied the effect of 8 day GHRH pretreatment (1 micrograms/kg iv each day) on the acute somatotropic response to the neurohormone administered both alone and combined with arginine (ARG, 0.5 g/kg iv infused from 0 to 30 min) which likely inhibits the release of hypothalamic somatostatin. Before treatment the GH response to GHRH (AUC: 231.9 +/- 106.4 micrograms/l/h) was potentiated (p < 0.001) by ARG (932.6 +/- 166.2 micrograms/l/h). However, the GH responses to the neurohormone both alone and combined with ARG were lower (p < 0.02 and 0.002, respectively) than in normals (712.4 +/- 111.6 and 2608.3 +/- 453.2 micrograms/l/h, respectively). After repetitive GHRH administration, in obese subjects baseline GH and IGF-I levels were unchanged. Also the GH responses to GHRH both alone (217.3 +/- 68.1 micrograms/l/h) and combined with ARG (756.3 +/- 202.9 micrograms/l/h) were not modified. In conclusion, our data demonstrate the failure of GHRH pretreatment to improve the somatotrope hyporesponsiveness to GHRH both alone and combined with ARG suggesting the existence of a somatotropic defect in obesity.

Adult↗
PubMed1993

Comparison of the potentiating effect of pyridostigmine, arginine and propranolol on the GHRH-induced GH release in short children.

The effect of pyridostigmine (60 mg orally), arginine (0.5 g/kg iv) and propranolol (PROP, 40 mg orally) on GHRH (1 microgram/kg iv)-induced GH release was studied in seven short children. Pyridostigmine and arginine induced a similar potentiating effect on GHRH-induced GH rise (Peak, mean +/- SEM: 56.9 +/- 12.8 and 48.6 +/- 8.5 micrograms/L, respectively vs 12.3 +/- 1.6 micrograms/L; p < 0.05). Combination of GHRH with propranolol induced an increase of GH that was significant only with regard to peak (28.9 +/- 8.4 micrograms/L) but not to AUC. However, GH rises observed after GHRH combined with PD or ARG did not significantly differ from that recorded after coadministration of GHRH and PROP both for peak and AUC. Our results confirm that pyridostigmine and arginine have a striking potentiating effect on the GHRH-induced GH rise in children and show that the tests with GHRH + PD and GH + H + ARG are ore reliable than that with GHRH + PROP to explore the secretory capacity of somatotroph cells.

Adolescent↗
PubMed1992

Interactions of galanin and arginine on growth hormone, prolactin, and insulin secretion in man.

Galanin (GAL), a 29 amino acid neuropeptide, is known to increase both basal and growth hormone-releasing hormone (GHRH)-induced growth hormone (GH) secretion while not significantly increasing prolactin (PRL) secretion in man. GAL is also endowed with an inhibiting effect on glucose-stimulated insulin release in animals, but not in man. We studied the effect of GAL (80 pmol/kg/min infused over 60 minutes) on the arginine- (ARG, 30 g infused over 30 minutes) stimulated GH, PRL, insulin, and C-peptide secretion in eight healthy volunteers (age, 20 to 30 years). GAL induced an increase of GH (GAL v saline, area under curve [AUC], mean +/- SEM: 316.5 +/- 73.9 v 93.2 +/- 20.9 micrograms/L/h, P less than .05), but failed to modify both PRL and insulin secretion. GAL enhanced the ARG-induced stimulation of both GH (1,634.1 +/- 293.1 v 566.9 +/- 144.0 micrograms/L/h, P less than .02) and PRL secretion (1,541.9 +/- 248.8 v 1,023.8 +/- 158.7 micrograms/L/h, P less than .02). On the contrary, GAL blunted the ARG-stimulated insulin (816.3 +/- 87.7 v 1,322.7 +/- 240.9 mU/L/h, P less than .05), as well as C-peptide secretion (105.1 +/- 9.8 v 132.8 +/- 17.3 micrograms/L/h, P less than .02). ARG administration induced a transient increase of glucose levels (P less than .01 v baseline) followed by a significant decrease (P less than .05 v baseline). This latter effect was prevented by the coadministration of GAL. In conclusion, these results show that in man GAL potentiates the GH response to ARG, suggesting that these drugs act at the hypothalamic level, at least in part, via different mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Arginine potentiates but does not restore the blunted growth hormone response to growth hormone-releasing hormone in obesity.

A blunted growth hormone (GH) response to several stimuli, including growth hormone-releasing hormone (GHRH), has been shown in obesity. Arginine (ARG) has been demonstrated to potentiate the GHRH-induced GH increase in normal subjects, likely acting via inhibition of hypothalamic somatostatin release. To shed further light onto the mechanisms underlying the blunted GH secretion in obesity, we studied the effect of ARG (0.5 g/kg infused intravenously [IV] over 30 minutes) on both basal and GHRH (1 micron/kg IV)-stimulated GH secretion. Eight obese subjects (aged 26.4 +/- 3.9 years; body mass index, 39.0 +/- 1.9 kg/m2) and eight normal control volunteers (aged 27.0 +/- 1.7 years; body mass index, 22.3 +/- 0.5 kg/m2) were studied. In obese subjects, the GH response to both GHRH and ARG was lower (P less than .01 and P less than .002, respectively) than in controls. ARG potentiated the GH response to GHRH in obese patients (P less than .0003). However, in these patients, the GH secretion elicited by GHRH, even when coadministered with ARG, persisted at reduced levels (P less than .005) when compared with controls. Basal insulin-like growth factor-1 (IGF-1) levels did not significantly differ in obese subjects and in normal subjects (161.1 +/- 37.0 v 181.0 +/- 12.8 micrograms/L). In conclusion, ARG enhances the blunted GHRH-induced GH increase in obese patients, but the GH responses to ARG alone and to ARG + GHRH persist at lower levels than in normals. Thus, our results suggest the existence of a reduced pituitary GH pool in obesity.

Adolescent↗
PubMed1992

Inhibition by salbutamol of GHRH-induced GH release in type 1 diabetes mellitus.

Patients with type 1 diabetes mellitus (IDDM) show augmented GH secretion, which is implicated in the pathogenesis of microvascular complications. On the other hand, it is well known that beta-adrenergic receptors have inhibitory influence on GH secretion, likely via stimulation of hypothalamic somatostatin. Since the possibility of pharmacological suppression of GH secretion would be of value in IDDM, we investigated the effect of salbutamol (SAL, 4 mg orally at -60 min) on the GH response to GHRH (1 micrograms/kg iv at 0 min) in 6 well-controlled (mean HbA1c +/- SEM: 7.3 +/- 0.5%) patients with IDDM. Salbutamol was able to inhibit basal GH levels (p < 0.05) as well as to abolish the GHRH-induced GH rise. After SAL administration, a significant (p < 0.05) reduction of glucagon levels was also found. Our data show that the enhancement of beta 2 adrenergic activity by oral therapeutical doses of SAL inhibits basal and GHRH-stimulated GH secretion in patients with IDDM.

Adult↗
PubMed1992

Superior sagittal sinus thrombosis and pulmonary embolism: a syndrome rediscovered.

Pulmonary emboli as a fatal complication of superior sagittal sinus thrombosis was once well recognized in the literature but appears to have been forgotten. The sagittal sinus appeared to be the source of pulmonary emboli in previously reported cases. Even in patients with no evidence of systemic thrombosis, but who have sagittal sinus thrombosis, the possibility of dislodging pulmonary emboli should be strongly considered. We report a case of nontraumatic sagittal sinus thrombosis complicated by multiple pulmonary emboli and a fatal saddle embolism, likely originating from the thrombosed sinus. Our review of the literature between 1942 and 1990 yielded 203 cases of intracranial venous thrombosis. The overall mortality rate was 49.3%. In 23 cases (11.3%), the venous sinus thrombosis was associated with pulmonary emboli and in these the overall mortality rate was 95.6%. In the 203 cases in our review, those patients who received anticoagulation therapy also had a statistically significant better outcome. Therefore, the presence of pulmonary emboli in association with sagittal sinus thrombosis mandates a sober assessment of the need of anticoagulation therapy in the absence of obvious contraindication.

Adult↗
PubMed1992

Ten years of surgery of aortic dissections and aneurysms. Clinical experience and original contributions.

From January '82 to April '91, 117 patients with aortic disease were operated upon at our University Hospital in Genoa, Italy. Thirty-seven had arch dissections or aneurysms; 66 had acute aortic dissection type A and 14 had aortic dissections or aneurysms type B, acute and chronic. Patients with arch or type B aortic pathology but without surgical indication and cases of post-traumatic aortic transections are not included. There were 84 male and 33 female patients with a mean age of 52 (6 min and 74 max). In the acute patients, the mean interval between clinical onset and surgery was 34 hours (6 min-72 max). All patients with primary arch disease had surgical repair with the aid of deep hypothermia and circulatory arrest (17-96 min). Type A dissections were treated with standard CPBP at 28 degrees C. Surgical techniques included direct suture of intimal tear alone, direct suturing of the two aortic stumps; interposition of Dacron tubular prosthesis; Bentall repair; separated valve and aortic replacement; an original aortic bulb aortoplasty with valve repair; arch replacement with resuturing of one or more aortic trunks. Human fibrin glue (Tissucol) was employed either as haemostatic agent, widely spread over the suture lines or as tissue adhesion agent between dissected aortic layers. Human fibrin glue is adopted because it gathers high glueing capacity and maintenance of the elastic property of the vessel wall. Hospital mortality (30 days) has been 25% in ascending aortic dissections (16/66 patients) and 50% in patients with arch disease (18/37 patients) who needed circulatory arrest. Late mortality 5/83 (6%). Reoperations for aortic valve insufficiency or re-dissection have been 7 (8.4%). Early diagnosis (increasing reliability of 2D-Echo and CT scans), aggressive surgery, meticulous myocardial and cerebral protection and introduction in clinical use of biological glues seem to be the milestones of present and further improvements in surgical results.

Acute Disease↗
PubMed1991

Analysis of risk factors for surgical wound infections following vascular surgery.

Although surgical wound infections (SWI) following implantation of prosthetic devices can be catastrophic and often require removal of the prosthesis, few studies have identified risk factors for these infections. We conducted a prospective multicenter study to identify risk factors for SWI. Of 561 vascular surgery patients enrolled in the study, 23 (4.1%) developed SWI. Multivariate analysis using logistic regression analyses identified surgery on lower extremities, delayed surgery, diabetes mellitus, past history of vascular surgery, and short antimicrobial prophylaxis (three doses of cefamandole) as independent risk factors for SWI. Consequences of SWI were serious; two (9%) died, 11 (48%) required reoperation, and five (22%) had their prosthesis removed. A risk index was developed using the independent risk factors for SWI identified by logistic regression analyses. When no risk factors were present, no SWI was observed (0 of 100), and the rate of SWI increased from 2.5% when one risk factor was present to 53.8% (7 of 13) when greater than or equal to 4 risk factors were present.

Cefamandole↗
PubMed1991

Arginine reinstates the somatotrope responsiveness to intermittent growth hormone-releasing hormone administration in normal adults.

It is well known that in normal adults the growth hormone (GH) response to GH-releasing hormone (GHRH) is inhibited by previous administration of the neurohormone. In 7 healthy volunteers (age 20-34 years) we studied the GH responses to two consecutive GHRH boluses (1 microgram/kg i.v. every 120 min) alone or coadministered with arginine (30 g i.v. over 30 min). The GH response to the first GHRH bolus (area under the curve, mean +/- SEM: 506.3 +/- 35.1 micrograms/l/h) was higher (p = 0.0001) than that to the second one (87.1 +/- 14.6 micrograms/l/h). The latter response was clearly increased (p = 0.0001) by coadministering arginine (980.5 +/- 257.5 micrograms/l/h). When every GHRH bolus was combined with arginine a marked potentiation of GH response to both boluses was found. However, the second combined administration of arginine and GHRH induced a GH increase which was lower compared to the first one (p = 0.016). In conclusion, our results show that arginine potentiates the GHRH-induced GH secretion preventing the lessening of somatotrope responsiveness to the neurohormone alone. As there is evidence that this phenomenon is due to an enhanced somatostatin release, these findings give further evidence of a somatostatin-suppressing effect of arginine.

Adult↗
PubMed1990

Paroxysmal nocturnal dystonia presenting as excessive daytime somnolence.

We describe the clinical and electrophysiologic findings in seven patients referred for evaluation of excessive daytime somnolence. These patients had none of the usual causes of excessive daytime somnolence but during sleep exhibited stereotypic body movements, tachycardia, respiratory disturbances, somniloquy, and transient arousals in a repetitive fashion. These episodes induced fragmentation of sleep. The polysomnograms revealed an increase in wakefulness and stage I decreased rapid eye movement during sleep in addition to the episodes of abnormal body movements. No epileptiform features were present either in the electroencephalogram or in the nocturnal polysomnogram. Four of the seven patients were treated with anticonvulsants, with both subjective and objective improvement on subsequent follow-up polysomnograms. Because of the pronounced functional deficits associated with the sleep disorder in these patients, it is of great importance to recognize the disorder and treat it appropriately.

Adult↗
PubMed1990

Primary pigmented micronodular disease of the adrenals.

Primary pigmented micronodular disease is a peculiar form of ACTH-independent Cushing's syndrome characterized by the familial occurrence, the frequent association with malformations and the pathological adrenocortical picture consisting in micronodules with cellular deposition of lipofuscinic pigment. We describe here a case occurring in a 14-year-old girl.

Adipose Tissue↗