Biomedical subjects

C Marchesi

Publications and source records attributed to C Marchesi.

At least 73 records · Page 4Linked to original sources

PubMed1989

Abnormal thyroid stimulating hormone, prolactin, and growth hormone responses to thyrotropin releasing hormone in abstinent alcoholic men with cerebral atrophy.

The thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) responses to thyrotropin releasing hormone (TRH), the Wechsler Adult Intelligence Scale (WAIS) for cognitive impairment, and computed tomographic scans were evaluated in 15 nondepressed alcoholic men after 4 weeks of abstinence and in 10 normal controls. Both cognitive impairment and cerebral atrophy were found in 13 of the alcoholics. Eight alcoholics (seven with cerebral atrophy) had blunted TSH and PRL responses to TRH and a TRH-induced paradoxical increase of GH. This study demonstrates that besides affecting the TSH response to TRH, alcoholism often induces alterations of the PRL and GH secretory patterns in response to TRH. The severe brain damage caused by long-term alcoholism might be involved in the pathogenesis of these neuroendocrine alterations.

Adult↗

PubMed1989

Dopaminergic, but not cholinergic, involvement in regulation of hypoglycemia-induced oxytocin release in man.

The plasma oxytocin response to insulin-induced hypoglycemia was evaluated in 20 normal male subjects in the basal state (insulin tolerance test (ITT) alone) and after pretreatment with the muscarinic antagonist pirenzepine (40 mg IV 10 min before the ITT in six subjects), the nicotinic antagonist trimethaphan (0.3 mg/min IV for 30 min before the ITT in six subjects), and the dopaminergic receptor agonist bromocriptine (2.5 mg PO 1 hr before the ITT in eight subjects). The drugs did not modify arterial blood pressure nor produce side effects capable of altering oxytocin secretion. Neither pirenzepine nor trimethaphan administration changed the oxytocin response to hypoglycemia, whereas bromocriptine significantly reduced the oxytocin increase during the ITT. These data suggest the involvement of dopaminergic, but not of cholinergic, muscarinic or nicotinic, receptors in the oxytocin response to hypoglycemia.

Adult↗

PubMed1989

Effects of the GABAergic agent sodium valproate on the arginine vasopressin responses to hypertonic stimulation and upright posture in man.

In order to evaluate the possible influence of GABAergic neurotransmission on the arginine vasopressin (AVP) response to osmotic and pressure volumetric stimuli, the GABAergic drug sodium valproate was administered by mouth (200 or 400 mg 16 h, 8 h and just before tests) to eight normal men before osmotic (i.v. infusion of 0.51 , NaCl for 2 h) and orthostatic (standing upright and maintaining an orthostatic position for 20 min) tests. In both experimental conditions, the AVP rise was significantly lower in the presence than in absence of sodium valproate. The maximum AVP responses in the control orthostatic and osmotic tests were respectively 2.3 and 2.5 times higher than basal levels. When 600 mg sodium valproate was given, the maximum AVP rise in response to hypovolaemic and osmotic stimuli were respectively 1.75 and 2.1 times higher than basal value. Similar results were obtained giving 1.2 g sodium valproate. These results suggest that in man a GABAergic pathway is involved in the AVP responses to hypovolaemic and hyperosmotic stimuli.

Adult↗

PubMed1989

Simultaneous inhibition by pirenzepine of the GH responses to GnRH and TRH in insulin-dependent diabetics and in patients with major depression.

The present study was undertaken in order to establish whether muscarinic cholinergic receptors are involved in the anomalous GH response to GnRH in men with insulin-dependent diabetes mellitus and in male patients with major depression. For this purpose, 16 male diabetics, 18 depressed men and 9 normal controls were tested with GnRH (25 micrograms iv) with and without previous treatment with the muscarinic cholinergic receptor blocker pirenzepine (40 mg iv 10 min before GnRH). Additional experiments with TRH (200 micrograms iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. The administration of GnRH stimulated GH release in 12 out of the 16 diabetics and in 8 out of the 18 depressed patients, but not in the normal controls. Control and diabetic non-responders to GnRH did not respond to TRH. In contrast, all diabetic responders to GnRH, except 2, showed paradoxical GH responses to TRH. All depressed responders to GnRH and 3 of the non-responders, were responsive to TRH. The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression.

Acetylcholine↗

PubMed1988

Metergoline, naloxone, and sodium valproate did not modify arginine vasopressin response to insulin-induced hypoglycemia in man.

The present study was carried out in order to determine whether insulin-induced hypoglycemia exerts its stimulatory effect on plasma concentrations of arginine vasopressin (AVP) by interacting with a serotonergic, a GABA-ergic or an opioid pathway. For this purpose, the effect of the serotonergic antagonist metergoline (10 mg/day for 4 days po), the GABA-ergic agonist sodium valproate (600 mg in three divided doses po) and the opioid-receptor blocker naloxone (10 mg in a iv bolus) on the AVP response during an insulin (0.15 IU/kg bw) tolerance test (ITT) was evaluated in three groups of 6 normal men each. In all men, control ITTs were performed without drug treatments. Basal and ITT-stimulated AVP secretion was not modified by drug administration, suggesting that serotonergic, GABAergic and naloxone-sensitive opioid receptors are not involved in the regulation of AVP secretion in response to insulin-induced hypoglycemia.

Adrenocorticotropic Hormone↗

PubMed1988

Dopaminergic control of TSH secretion in endogenous depression.

To evaluate whether the inhibitory control exerted by endogenous dopamine on thyroid-stimulating hormone (TSH) secretion is altered in patients with major depressive disorder, 11 depressed patients and 9 normal controls were tested with the dopaminergic receptor antagonist domperidone (10 or 20 mg i.v.). The administration of domperidone induced a significant increase in circulating TSH levels in the normal controls, but not in the depressed patients. These data excluded the possibility that the dopaminergic inhibition of TSH secretion is enhanced in depression. To establish whether domperidone failure was due to a reduced dopaminergic tone, domperidone was administered before stimulation of TSH secretion with thyrotropin-releasing hormone (TRH) (200 micrograms i.v.). The TSH response to TRH was significantly lower in the depressed than in the control subjects, regardless of domperidone priming. However, in both groups domperidone enhanced the TRH-induced TSH release by 50%. These data suggest that the dopaminergic control of TSH secretion is not altered in patients with endogenous depression and that a reduced capacity of the pituitary to secrete TSH might be responsible for the reduced TSH responsiveness to TRH and domperidone.

Adult↗

PubMed1988

[Water loading diuresis test in albino rats. Critical study of approximately 12,000 tests. 3. Loading tests using several mineral waters bottled under various experimental conditions].

The authors studied a series of more than 12,000 complex diuresis exams after water loading, in the albino rat, which permitted them to draw the following conclusions: 1). The temperature of water definitively and, probably the environmental temperature, influence the diuretic response. 2). The most favourable water loading preparations are not fasting and solid fasting during the 24 hrs. prior to loading. 3). Pretreatment with diuretic water 15 days prior to loading, favours the diuretic response to the same or the any other water: activated kidney. 4). The addition of CO2 to water, by itself, does not seem to favour diuresis. 5). Aging or conservation in bottles, always reduces, more or less sensitively, the diuretic properties of the water itself, especially during the first 2-3 months. This confirms that the diuretic properties do not only and exclusively depend on the chemical or physical composition or on the structure, but on everything together, that is modified after the moment of it's natural emergence. This loss of activity, in any case, is favourable to the indiscriminate use of these waters as both dietetic and drinking water. 6). It is probable that the different pH's of water influence it's diuretic activity. 7). Even if the more active waters, in this study, seem to be bicarbonate, sulfate bicarbonate, or bicarbonate-sulfate-alkaline-terrose, this can be attributed to the prevalence of these classes of water in this study. Instead, what emerges with certainty, from the point of view of the molar concentration, is that while there are which are minimally mineralized and oligominerals with scarce or no diuretic activity, there are mediomineral and hypotonic mineral waters with up to 100 mmol/liter, and with conspicuous diuretic activity, even after more or less long periods of conservation in bottles. 8). For all of the above-mentioned reasons, we feel that a useful orientation can also be gained for the use of the discussed water for human needs.

Animals↗

PubMed1988

[Diagnosis of depression in chronic alcoholism: methodological aspects].

The incidence of depression ranges between 3% and 98% in chronic alcoholism. This discrepancy has been attributed to the lack in univocal diagnostic criteria and to poor attention to the moment when the observation takes place. In patients with chronic alcoholism, accurate clinical examinations are required to make a diagnosis of depression; furthermore, the presence of continuous alcohol abuse, or the condition of initial of prolonged abstinence must be considered. Using these criteria the diagnosis of depression in chronic alcoholism will probably become more reliable and will be possible to carry out a more appropriate therapy.

Alcoholism↗

PubMed1987

Pirenzepine inhibits growth hormone, but not thyrotropin response to thyrotropin-releasing hormone in patients with endogenous depression.

In order to evaluate whether in endogenous depression the anomalous growth hormone (GH) response to thyrotropin-releasing hormone (TRH) is mediated by muscarinic cholinergic receptors, 12 patients were tested with TRH (200 micrograms iv) with and without previous treatment with the muscarinic cholinergic receptor blocker pirenzepine (40 mg iv 10 min before TRH). Control tests with normal saline also were performed. Administration of normal saline did not alter serum GH levels. In contrast, TRH injections significantly increased serum GH concentrations by about three-fold. This response was inhibited by pretreatment with pirenzepine. Another neuroendocrine marker of endogenous depression, the low TSH increase in response to TRH (delta less than or equal to 7 microU/ml), was observed in our patients. Pretreatment with pirenzepine did not modify this response. These data indicate that in patients with endogenous depression a muscarinic cholinergic mechanism is involved in the GH response but not in the TSH response to TRH.

Adult↗

PubMed1987

Involvement of a dopaminergic mechanism in the response of growth hormone to thyrotropin releasing hormone in patients with major depression.

In an attempt to establish whether, in patients with major depression, dopaminergic receptors are involved in the release of growth hormone (GH) induced by thyrotropin releasing hormone (TRH), eleven subjects were tested with TRH (200 micrograms in an i.v. bolus) with or without concomitant treatment with domperidone (10 mg in an i.v. bolus 10 min before TRH), an antidopaminergic agent which does not readily cross the blood-brain barrier. In 7 out of the 11 patients, TRH strikingly increased GH levels (responders) (the mean peak level was 9 times higher than basal value), whereas it was without effect in the remaining 4 patients (non-responders). When the responders were treated with domperidone before TRH injection, TRH-induced GH increase was still present, but it was significantly lower (the mean peak level was 5.3 times higher than basal value) than in the TRH test (p less than 0.02). These data suggest that the paradoxical response of GH or TRH in patients with major depression involves a dopaminergic mechanism active at sites situated outside the blood-brain barrier.

Adult↗

PubMed1987

Muscarinic cholinergic and histaminergic H1 and H2 receptors are not involved in the LH response to naloxone in man.

The role of muscarinic-cholinergic and H1-, H2-histaminergic receptors as possible mediators of the LH response to the opioid antagonist naloxone was evaluated in 18 normal men. Subjects were divided in 3 groups of 6 men; the increment of LH in the plasma elicited by naloxone was evaluated after giving naloxone alone or together with dexchlorpheniramine, cimetidine or pirenzepine (respectively H1-, H2-histaminergic and muscarinic-cholinergic receptor antagonists). LH release was significantly stimulated by naloxone in all subjects; this response was not altered by histaminergic or cholinergic blockade. These results confirm the stimulatory effect of naloxone on LH release in man, without evidence of the involvement of H1-, H2-histaminergic or muscarinic-cholinergic pathways.

Adult↗

PubMed1987

Lysine-vasopressin does not affect basal and LH-RH-stimulated LH and FSH release during the menstrual cycle of normal women.

In order to test possible effects of lysine-vasopressin (LVP) on basal and LH-RH-stimulated LH and FSH release, an intravenous bolus of LVP (0.06 IU/kg body weight) was injected alone or 10 min before LH-RH (100 micrograms i.v.) in 33 normal women in the follicular, periovulatory and luteal phase of their menstrual cycle. The administration of LVP modified neither the basal secretion of the gonadotropins nor the LH-RH-induced LH and FSH release. These data suggest that in humans, vasopressin is not involved in the control of gonadotropin release at the level of the anterior pituitary.

Adult↗

PubMed1987

Oxytocin enhances thyrotropin-releasing hormone-induced prolactin release in normal menstruating women.

The effects of oxytocin (OT) on basal thyrotropin-releasing hormone (TRH)-stimulated thyrotropin (TSH) and prolactin (PRL) secretion were evaluated in normal menstruating women during follicular, periovulatory, and luteal phases. Two different studies were performed. In one study, 15 subjects were treated with OT or saline; in the other study, 20 women were tested with TRH alone or in combination with OT. Results during follicular, periovulatory, and luteal phases were similar. OT did not produce any effect on basal serum TSH and PRL levels and on the TRH-stimulated TSH secretion, whereas it significantly enhanced the PRL response to TRH. At all examined phases during the menstrual cycle, the mean peak PRL response was reached within 20 minutes after TRH injection, and the peak was about three times higher than basal value when TRH was given alone and about four times when OT was present. These data suggest that in normal women OT is not involved in the control of basal and TRH-stimulated TSH secretion and of basal PRL release. In contrast, the enhancement of the TRH-induced PRL release suggests that OT plays a role in the control of the acutely stimulated PRL secretion. Because results were similar regardless of the phase of the menstrual cycle, estrogen and/or progesterone do not appear to be involved in the effect of OT on the TRH-induced PRL release.

Adult↗

PubMed1987

[Recording of signals in ambulatory electrocardiography].

The different techniques for the acquisition of electrocardiographic signal in ambulatory monitoring are described in this paper. Direct and, frequency modulation systems are explained in details with their relative advantages and disadvantages. The basis of digital sampling and real time analysis of ECG signals are also explained.

Electrocardiography↗

PubMed1987

[Methods of the elaboration of data of the cardiological importance].

This paper deals with some introductory topics of signal processing and decision making in cardiology. In both instances the matter is referred to general schemes well suited to host different applications. Signal processing is divided in some phases: acquisition, storing, analysis and each of them is described with applications to specific signals. In a similar manner the methods for decision making have been simplified to a scheme including a "knowledge base" and an "inference method". The scheme is used to classify various implementations. Bayes analysis and expert systems have been introduced with some details.

Data Interpretation, Statistical↗

PubMed1987

[Analysis of the market and future trends of the instrumentation for ambulatory electrocardiography].

An inquiry has been made among most manufacturers of ambulatory ECG instrumentation. Both playback and real time systems have been considered. The inquiry, based on a questionnaire, was mainly aimed at identifying possible standard technical solutions emerging from the analysis of various implementations, and at verifying whether techniques for performance evaluation are in common use. Main conclusions of this study include: playback systems are still in competition with real time systems; automatic analysis has not yet reached adequate accuracy; analysis of ST-T interval, while performed by most systems, is not evaluated because common standard of quality is lacking.

Algorithms↗

PubMed1987

[Ambulatory electrocardiography in patients with angina pectoris].

In the diagnosis of ischemic heart disease, long-term ECG recording has several distinct advantages. It allows one to relate patient symptoms to cardiac disturbances and to detect asymptomatic events, reveals the possible ischemic genesis of arrhythmias, and it is the most suitable method to assess the acute and chronic effectiveness of treatment and the evolution of the disease. In spite of these advantages, Holter monitoring has several limitations: the analysis of a single lead, is responsible in most systems for the low sensitivity in detecting ischemia occurring in unexplored regions; the period of 24-48 hours may not be sufficient for screening patients due to the unpredictable spontaneous variability of the disease; a common standard of analysis is still lacking even if the European Communities concerted action in Ambulatory Monitoring could represent the solution to this problem. Nevertheless the role of Holter monitoring appears essential in the ambulatory screening of patients with suspected ischemia for a better characterization of patients with ascertained myocardial ischemia, and for the evaluation of treatment and of the evolution of the disease.

Angina Pectoris↗

PubMed1986

Prognostic value of ventricular arrhythmias and transient ST-T changes after myocardial infarction: a two-year follow-up with ambulatory ECG recording.

The aim of this study is to evaluate the frequency and prognostic significance of ventricular arrhythmias (VA) and of ST-T changes found during 24-h ECG recording in patients who survived an acute myocardial infarction. Eighty-nine patients (2 females and 87 males) discharged from hospital after acute myocardial infarction were studied. Mean age was 52.2 years (SD +/- 10) with a range of 26-68. Serial observations were carried out at 1, 2, 3, 6, and 12 months after the acute event. Eight patients died during the first two years of follow-up, of these, 2 deaths were of noncardiac origin: one was due to gastric carcinoma and the other to pulmonary neoplasm. Of the 6 cardiac deaths, 4 were sudden and unexpected and 2 were due to reinfarction. Statistical analysis of the results obtained in the first three months of follow-up has not shown any significant correlation between pathologic patterns and cardiac death. In the second period we found a statistically significant relationship between cardiac death and multiform VPBs (p less than 0.05), CVA (p less than 0.05), and ST-T changes (p less than 0.05). More significant was the correlation between cardiac death and the presence at the same time of ST-T changes and multiform VPBs (p less than 0.01).

Adult↗