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Biomedical subjects

S Castellani

Publications and source records attributed to S Castellani.

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

Repeated sympathetic stimuli elicit the decline and disappearance of prostaglandin modulation and an increase of vascular resistance in humans.

To investigate the role of prostaglandins I2 and E2 in modulating the vasoconstrictor response to sympathetic stimulation, repeated and proximate cold pressor tests were performed in 23 healthy young volunteers. Limb vascular resistance (blood flow measured by venous occlusion plethysmography), prostaglandin I2 (as 6-ketoprostaglandin F1 alpha) and prostaglandin E2 plasma levels (detected by radioimmunoassay), and plasma catecholamines (detected by high-performance liquid chromatography and electrochemical detection) were measured. A progressive increase in the duration of the vasoconstrictor response was observed with repetition of cold applications (p less than 0.001, by analysis of variance for trends). This increase was associated with a progressive decrease in cold-induced elevation of 6-ketoprostaglandin F1 alpha and prostaglandin E2 plasma levels until, after five stimulations, neither prostaglandin was detectable. The maximum detected concentration of norepinephrine did not significantly change, but its area under the curve in time showed a trend toward an increase. Epinephrine levels did not significantly change. The increase of vascular resistance was significantly correlated with the decrease of both prostaglandins (r = 0.93, p less than 0.05 for prostaglandin E2 and r = 0.89, p less than 0.05 for 6-ketoprostaglandin F1 alpha), whereas no significant correlations were found between variations of vascular resistance and catecholamines. Prostaglandin blockade induced by diclofenac sodium administration caused, from the first cold application, a pattern of the vasoconstrictor response and plasma prostaglandin and norepinephrine changes similar to that observed at the fifth cold application in untreated subjects, when prostaglandins are no longer detectable in plasma. We conclude that an increased vasoconstrictor response to sympathetic stimulation in humans may result from a diminished inhibitory influence of prostaglandins on adrenergic transmission.

Adult↗
PubMed1989

The antihypertensive and renal activities of potassium canrenoate are associated with increased renal prostaglandin excretion.

1. In a double-blind, randomized, cross-over study the effects of potassium canrenoate administration (100 mg twice daily for 10 days orally) on renal prostaglandin synthesis (prostaglandin E2 and prostaglandin F2 alpha) were evaluated in 10 normotensive females and in 10 females with essential hypertension. 2. When compared with normotensive subjects, hypertensive patients in baseline conditions showed a reduced excretion of urinary prostaglandin E2 associated with an excessive prostaglandin F2 alpha production. 3. Potassium canrenoate significantly reduced mean blood pressure in hypertensive patients [from 118.9 +/- 8.7 mmHg (1.62 +/- 0.12 kPa) to a peak minimum value of 104.7 +/- 9.8 mmHg (1.42 +/- 0.13 kPa) on the seventh day of treatment; P less than 0.01 for the whole period] but not in control subjects [from 88 +/- 9.4 mmHg (1.20 +/- 0.13 kPa) to 84.3 +/- 8.3 mmHg (1.15 +/- 0.11 kPa) on the eighth day, NS] even though potassium canrenoate significantly increased sodium excretion in both groups. Renal prostaglandin excretion was affected differently in the two groups: in control subjects excretion of both prostaglandin E2 and prostaglandin F2 alpha was increased after drug administration, whereas in hypertensive patients only prostaglandin E2 excretion was enhanced.

Adult↗
PubMed1986

Impaired cardiac PGI2 and PGE2 biosynthesis in patients with angina pectoris.

Thirty-four patients with unstable angina and 14 patients with stable effort angina were investigated for cardiac prostacyclin and prostaglandin E2 (PGE2) biosynthesis, under resting conditions and after cold pressor testing. Twenty-seven patients undergoing cardiac catheterization and coronary angiography for congenital or acquired heart diseases other than coronary artery disease were studied as a control group. Prostacyclin (as 6-keto-PGF1 alpha) and PGE2 were measured by specific radioimmunoassay of blood from the coronary sinus and aorta. During resting conditions no significant differences in plasma 6-keto-PGF1 alpha and PGE2 concentrations were found between coronary sinus and aortic blood, and no transcardiac gradient existed either in control subjects or in patients with stable and unstable angina, respectively. In control subjects cold pressor testing induced a significant increase in 6-keto-PGF1 alpha and PGE2 levels in blood from the different sampling sites, and a significant transcardiac gradient occurred (+11.2 +/- 6.4 pg/ml for 6-keto-PGF1 alpha and +5.1 +/- 3.4 pg/ml for PGE2). However, in angina patients no significant increase in 6-keto-PGF1 alpha and PGE2 plasma levels was found and no transcardiac gradient was formed after cold pressor testing. These results indicate impaired cardiac prostacyclin and PGE2 biosynthesis both in patients with stable and unstable effort angina.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Platelet MAO concentration and molecular activity: I. New methods using an MAO B-specific monoclonal antibody in a radioimmunoassay.

New methods for determination of specific concentration and molecular activity of monoamine oxidase (MAO) in platelets are described and evaluated in parallel with specific activity measures, performed in whole platelets and platelet extracts. Platelet MAO specific concentration is determined in platelet extracts by a radioimmunoassay, using a monoclonal antibody that recognizes human MAO B, the form that occurs in platelets, but not MAO A. All four platelet MAO measures are found to be reliable and stable, and thus are suitable for long-term comparisons of normal and clinical populations, such as those reported in Part II of this report. The new measures of enzyme concentration and molecular activity make available important information about the state of MAO B molecules in a given individual that reflects the genetic expression and control of the enzyme.

Adult↗
PubMed1986

Platelet MAO concentration and molecular activity: II. Comparison of normal and schizophrenic populations.

Platelet monoamine oxidase (MAO B) in 59 normal and 57 RDC-diagnosed medicated and unmedicated schizophrenic subjects was analyzed for whole platelet and extracted activities, specific concentration, and molecular activity. A novel radioimmunoassay using a monoclonal antibody elicited to human platelet MAO was used. Female schizophrenics showed no differences from female normals in MAO measures; however, these data could not be clearly evaluated because of confounding effects of age and drugs. Male schizophrenics treated with neuroleptics expressed significantly reduced whole platelet MAO activity, compared to untreated male patients. Compared with normal males, male schizophrenics showed significantly lowered molecular activities, along with elevated specific concentrations, which did not appear to be explained solely by drug usage. Additional mechanisms explaining the diminished molecular activity in male schizophrenics may be the presence of an endogenous irreversible inhibitor or a genetically determined, possibly structural, variant of MAO B.

Adult↗
PubMed1986

Enhanced peripheral vasoconstrictor response and increased thromboxane A2 synthesis after the cold pressor test in patients with angina at rest.

Peripheral vascular resistance (PVR) and thromboxane A2(TxA2) synthesis after the cold pressor test were investigated in different subsets of patients with angina (10 with stable effort angina, 36 with resting angina [24 in an active phase and 12 in an inactive phase], and five with Prinzmetal's variant angina) and in 41 control subjects of equivalent age and risk factors. Left ventricular end-diastolic pressure, ejection fraction, extent of coronary angiographic lesions, and baseline PVR were not significantly different among the various patient groups. In all patient groups, except those with variant angina, the cold pressor test resulted in a higher increase in PVR than in the control subjects (p less than .001 for all groups). In patients with variant angina the vasoconstrictor response was increased only in proximity (about 1 hr) to ischemic attacks. In patients with active resting angina the vasoconstrictor response was on the average four times longer than that in patients with effort angina and with inactive resting angina (p less than .001). This exaggerated vasoconstrictor response was associated with elevated TxA2 resting levels in plasma and with increased TxA2 synthesis after the cold pressor test. A linear relationship was found between the area of the vascular response and the area of TxA2 production after the cold pressor test in patients with active resting angina (r = .87, p less than .001). The increased TxA2 synthesis and the inappropriate increase of peripheral vascular response to sympathetic stimulation revert back to normal in the inactive phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1985

Spontaneous and cold pressor test-induced prostaglandin biosynthesis by human heart.

To investigate prostaglandin biosynthesis by the heart, 21 patients undergoing cardiac catheterization and coronary angiography for congenital or acquired heart diseases other than coronary artery disease were investigated. Prostacyclin (as 6-keto-PGF1 alpha), PGE2, PGF2 alpha and TxA2 (as TxB2) were measured by specific radioimmunoassay in blood from coronary sinus, aorta, and a peripheral vein under resting conditions and following cold pressor test (CPT). PGF2 alpha was always found undetectable. In resting conditions, no significant differences in plasma 6-keto-PGF1 alpha, PGE2, or TxB2 concentrations were found among coronary sinus, aorta, and peripheral venous blood and no transcardiac gradient existed (mean: +0.4 +/- 1.2 pg/ml for 6-keto-PGF1 alpha, +0.1 +/- 0.6 pg/ml for PGE2, and -0.4 +/- 9.9 pg/ml for TxB2). CPT was able to induce a significant increase in 6-keto-PGF1 alpha and PGE2 concentration in blood from the different sampling sites and a significant transcardiac gradient was found following CPT (+11.6 +/- 7.4 pg/ml for 6-keto-PGF1 alpha (p less than 0.01) and +5.2 +/- 3.6 pg/ml for PGE2 (p less than 0.001). TxB2 levels significantly increased in peripheral venous blood (from 18.3 +/- 6.2 to 29.2 +/- 20.3 pg/ml, p less than 0.05), but they did not increase either in coronary sinus (from 21.9 +/- 9.7 to 22.9 +/- 9.8 pg/ml) or in aorta (from 22.3 +/- 4.7 to 19.1 +/- 6.5 pg/ml). Present results indicate that a cardiocoronary prostacyclin and PGE2 synthesis is inappreciable under resting conditions but it becomes remarkable following sympathetic stimulation. On the contrary, no TxA2 cardiocoronary biosynthesis seems to occur in patients free from coronary artery disease.

Adult↗