Biomedical subjects

C Polidori

Publications and source records attributed to C Polidori.

At least 55 records · Page 3Linked to original sources

PubMed1993

[The effect of the angiotensin III (Sar1, Ile7) Ang III, on water intake of Wistar rats].

A[Sar1, Ile7] AngIII, an angiotensin III analogue apparently devoid of any affinity for vascular angiotensin II (AngII) receptors, inhibits AngII-induced drinking but neither affects cellular dehydration-induced drinking nor produces any intake of water in water replete rats, suggesting that the dipsogenic effect of AngII is not of vascular origin. Thus, [Sar1, Ile7] AngIII is an interesting tool to study the central effects of AngII.

Angiotensin II↗

PubMed1992

Inhibition of cell dehydration-induced drinking by tachykinins: evaluation of possible renal effects accounting for the long-lasting inhibition.

Central injection of the tachykinins (TKs) neurokinin A (NKA), eledoisin (ELE), and kassinin (KASS) produced long-lasting inhibition (up to 6 h) of drinking induced by subcutaneous hypertonic NaCl, while substance P (SP) and physalaemin (PHYS) evoked short-lasting effects. The hypothesis that water retention or increased Na+ excretion by the kidney (induced by TKs) may reduce the need for water ingestion was tested. The results obtained both in urine collection experiments and in nephrectomized rats showed that the duration of the effect of NKA, ELE, and KASS is not due to water retention or increased Na+ excretion by the kidney. The effect of NKA, but not that of ELE and KASS, was shortened by nephrectomy, even though NKA did not modify urine volume or Na+ excretion. Indomethacin pretreatment, like nephrectomy, reduced the duration of the NKA effect, suggesting that renal prostaglandins are involved in it. On the other hand, the long-lasting effect of the three TKs cannot be easily explained in terms of slow metabolic degradation, particularly for NKA. Alternatively, it might be hypothesized that these TKs produce a modification of osmoreceptor function lasting well beyond the life of the peptide, and/or that they produce Na+ loss through emunctories different from the kidney.

Animals↗

PubMed1992

Central effects of neuropeptide K on water and food intake in the rat.

The present study investigated the effect on water and food intake in the rat of the intracerebroventricular (ICV) injection of neuropeptide K (NPK), the N-terminally extended form of neurokinin A. NPK inhibited water deprivation-induced water intake even at 31.2 ng/rat. At higher doses, it inhibited also water intake induced by ICV angiotensin II or by subcutaneous hypertonic NaCl, and food-associated drinking, the threshold dose being 125 ng/rat. In response to 125 ng/rat, food intake following 16 h food deprivation was not reduced. NPK inhibited food intake only at 500 ng/rat, a dose that evoked excessive grooming in treated animals. Thus NPK is a potent inhibitor of water deprivation-induced drinking and at higher doses it exerts a general antidipsogenic effect towards several dipsogenic determinants, without affecting food intake. On the other hand, it inhibits food intake only at high doses, 500 ng/rat or more, but this inhibition might be just related to the intense grooming evoked. The effects of NPK on ingestive behavior are markedly different from those of neurokinin A, which selectively inhibits osmotic drinking and food-associated drinking. These differences suggest that NPK itself may exert its effects on the central nervous system, not necessarily through the conversion to neurokinin A.

Analysis of Variance↗

PubMed1992

[Measurement of cardiac output by invasive methods: methods and variability].

Invasive techniques for the measurement of cardiac output include the Fick method, the marker dilution method and radiological ventriculography. The principles, methods and accuracy of these techniques are described. The reference method remains that of Fick, despite its being less widely used now because of its complicated nature and its technical limitations (need for strict baseline conditions, precision of sampling). The thermodilution method is often performed. It is easy and provides reliable results, except in conditions of low cardiac output or when there is severe tricuspid insufficiency. Radiological ventriculography is used less for the measurement of cardiac output, since it is heavily dependent upon heart rate and theoretical geometrical models. It remains valuable for the quantification of mitral and aortic regurgitation.

Cardiac Output↗

PubMed1992

[Evaluation of cardiac output by Doppler echocardiography. Basic principles and practice].

The measurement of cardiac output by the Doppler-echocardiography method is of considerable interest since, in contrast to other available techniques, it offers the possibility of the measurement of output at each valve orifice, thus providing a quantitative approach to valve regurgitation. The 4 basic data items required are: the surface area of the valve orifice, trans-valvular Doppler velocity spectrum, duration of ejection and of filling, and heart rate. A large number of studies have analysed the various investigation techniques and have shown their excellent correlation with reference invasive methods. In the light of experience acquired in our Echocardiography Laboratory, we recommend, in accordance with data from the literature, the exclusive use of pulsed Doppler and measurement of valve orifices by two-dimensional imaging at the point of insertion of the aortic and sigmoid cusps as well as at the mitral ring. A simplified method for the measurement of mitral surface area on the basis of TM records is suggested.

Cardiac Output↗

PubMed1992

[Measurement of mitral flow at the extremity of the valves. Validation of a simplified method based on 101 cases].

The measurement of cardiac output at the extremity of the mitral cusps, by Doppler-echocardiography, is of fundamental value, in particular for the evaluation of valve regurgitation. However, it comes up against a theoretical difficulty resulting from constant variation in the surface area of this orifice during diastole. After reviewing the main measurement methods available in the literature, a simplified method based upon the diameter of the ring and calculation of a mean diastolic intercusp distance by TM is suggested. Evaluation of this technique in 101 patients free of valve of leak showed its feasibility to be close to 100% and the correlation with aortic (r = 0.90), pulmonary (r = 0.91) and mitral ring (r = 0.88) outputs was entirely satisfactory. Our method would thus seem to be a good compromise between digitalised integration methods for the measurement of mitral surface area--optimal but complex--and the aim of simplification compatible with routine clinical use.

Adult↗

PubMed1992

[Clinical evaluation after myocardial infarction. Its role, date and methods].

Although global mortality in the year following myocardial infarction is about 10%, this figure varies from less than 1% to more than 50% in some very high risk cases. The principal objective of clinical evaluation during the acute phase is to establish a prognosis and propose a rational strategy for myocardial revascularisation (by bypass grafting or angioplasty) in patients with a poor prognosis. An essential feature of this evaluation is to reduce health care costs and hospital stay to a minimum. Coronary angiography is the only investigation which allows assessment of the coronary circulation and is probably the best method of evaluating global and regional left ventricular function, two essential prognostic factors: on the other hand, it does not provide information about the presence of residual ischaemia or persistent myocardial viability in the infarcted territory. Some very high risk patients should undergo systematic coronary angiography to determine the possibilities for myocardial revascularisation: early post-infarction angina, left ventricular failure, chronic angina, elderly but valid patients... The indications of coronary angiography should also extend to patients with non-Q wave infarction, to young patients with myocardial infarction on thrombolysed infarcts: results of coronary angiography should then be compared with those of standard exercise stress testing. It is only in other situations, concerning a minority of patients, in which two attitudes may be considered: the first, to perform coronary angiography very early (within 24-48 hours of admission) allowing early discharge from hospital of many cases, completed later by standard exercise stress testing: any revascularisation procedure is considered at that time and requires a second hospital admission. The second attitude consists in performing coronary angiography between the 7th and 10th day only if some paraclinical changes are present: exercise stress testing then has an essential role; to improve its negative predictive value for absence of long-term coronary events it should be associated with radionuclide investigation of myocardial perfusion (thallium, MIBI) or with an evaluation or residual myocardial viability (labelled fatty acids, cyclotron). This attitude also allows early identification of "good candidates" for myocardial revascularisation.

Coronary Angiography↗

PubMed1991

The release of atrial natriuretic factor induced by central carbachol injection may be mediated by muscarinic M1 receptors.

We investigated the effect of selective muscarinic antagonists on atrial natriuretic factor (ANF) release induced by intracerebroventricular (i.c.v) injection of carbachol in the rat. The muscarinic antagonists were given by i.c.v. injection 1 min before carbachol, 1 micrograms/rat. 4-Diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), a rather selective M1 and M3 receptor antagonist, was the most potent inhibitor of carbachol-induced ANF release, its ID50 being 0.18 nmol/rat. Pirenzepine, a selective M1 antagonist, also potently inhibited the effect of carbachol, its ID50 being 2.74 nmol/rat. The M3-selective antagonist, p-fluoro-hexahydro-sila-diphenidol, was much weaker than pirenzepine, with an ID50 of 57.52 nmol/rat. The selective M2 receptor antagonist, methoctramine, on the other hand, was a very weak inhibitor of carbachol-induced ANF release. The rank order of potency as well as the - log ID50 of the antagonists tested were consistent with their pA2 values for muscarinic M1 receptors, suggesting that this receptor subtype may mediate the central effect of cholinergic mechanisms in the control of ANF release.

Animals↗

PubMed1991

Natriuresis, kaliuresis and antidiuresis induced by central carbachol injection are mediated by muscarinic M1 receptors.

The present study investigated the effect of selective muscarinic antagonists on natriuresis, kaliuresis and antidiuresis induced by intracerebroventricular (i.c.v.) injection of carbachol in the rat. The muscarinic antagonists were given by i.c.v. injection 1 min before carbachol (1 microgram/rat). 4-Diphenylacetoxy-N-methyl-piperidine methiodide (4-DAMP), a rather selective M1 and M3 receptor antagonist, was the most potent inhibitor of carbachol-induced natriuresis, kaliuresis and antidiuresis, its ID50 being respectively 0.12, 0.04 and 0.56 nmol/rat. Pirenzepine, a selective M1 antagonist, potently inhibited the above mentioned carbachol effects, its ID50 being 1.85, 3.25 and 1.49 nmol/rat, respectively. On the other hand, the M2-selective antagonist methoctramine and the M3-selective antagonist p-fluoro-hexahydro-sila-difenidol were very weak inhibitors. Methoctramine at doses up to 60 nmol/rat produced non statistically significant inhibition of carbachol-induced natriuresis, kaliuresis and antidiuresis. Para-fluoro-hexahydro-sila-diphenidol showed an ID50 of 64.4 nmol/rat on carbachol-induced natriuresis, while at the maximum dose employed, 100 nmol/rat, the inhibition of carbachol-induced kaliuresis and antidiuresis was lower than 50%. The rank order of potency of the antagonists tested proved to be related to their pA2 values for muscarinic M1 receptors, suggesting that this receptor subtype mediates the central effects of cholinergic mechanisms on water and electrolyte excretion.

Animals↗

PubMed1991

The tachykinin NH2-senktide inhibits alcohol intake in alcohol-preferring rats.

The present study evaluated the effect of the intracerebroventricular injection of the tachykinins, substance P, neurokinin A and [Asp5.6,MePhe8]substance P(5-11) (also referred to as NH2-senktide), on the alcohol intake of genetically selected, alcohol-preferring rats. Animals were offered both water and 8% ethanol 2 h/day; tachykinins were administered just before access to fluids. Neurokinin A and substance P did not modify alcohol intake at doses up to 1000 and 2000 ng/rat, respectively. On the other hand, NH2-senktide potently suppressed alcohol intake at doses of 31.2-500 ng/rat. At the same doses, however, it did not significantly affect water intake. This finding suggests that its effect on alcohol intake might be rather selective and not due to general impairment of the behavior. Activation of tachykinin NK-3 receptors, for which NH2-senktide is a highly selective agonist, produces angiotensin II release in the brain; however, the effect of NH2-senktide on alcohol intake is probably not mediated by angiotensin II, as suggested by the fact that it is not modified by captopril pretreatment.

Alcohol Drinking↗

PubMed1991

Effect of capsaicin neonatal treatment on the salt intake of the adult rat.

The present study investigated the involvement of capsaicin-sensitive sensory neurons on salt intake control in the rat, following capsaicin neonatal treatment. Capsaicin did not affect salt appetite induced by intramuscular injection of deoxycorticosterone enantate, or by intracranial injection of renin. Moreover, it did not alter salt preference of rats given access to a variety of NaCl concentrations, or the need-free salt intake of multidepleted male rats. On the other hand, in response to furosemide-induced sodium depletion, the salt intake of capsaicin-treated rats was lower than that of controls. However, furosemide-induced Na+ excretion of capsaicin-treated rats proved to be lower than that of controls, thus suggesting that difference in salt intake might be secondary to lower sensitivity of capsaicin-treated rats to the natriuretic action of furosemide. Salt intake is known to be influenced by sensory information from the oral cavity, from the liver and from the intravascular compartment. The absence of effect of capsaicin neonatal treatment suggests that sensory fibers relevant to salt intake control may not be capsaicin sensitive. On the other hand, our findings indicate that capsaicin treatment alters the renal response to furosemide and stimulate further studies on the effects of capsaicin on renal function.

Animals↗

PubMed1991

The hypothalamic paraventricular nucleus is a site of action for the central effect of tachykinins on plasma vasopressin.

The intracerebroventricular injection of eledoisin (ELE), or of other tachykinins with potent agonist activity at neurokinin B (NK-3) receptors, increases plasma vasopressin in the rat. The effect is antagonized by saralasin pretreatment, thus suggesting that it is mediated by angiotensin receptor activation. Since the magnocellular part of the hypothalamic paraventricular nucleus (PVN) is very rich in NK-3 receptors, the present study was aimed at investigating the role of this nucleus in the effect of ELE on plasma vasopressin. Direct injection of ELE into the PVN increased plasma vasopressin levels more potently than the injection of the same doses into the lateral ventricle. Lesioning of the magnocellular part of the PVN completely abolished the increase in plasma vasopressin induced by the injection of ELE 100 ng/rat into the lateral ventricle. Pretreatment into the PVN either with saralasin or with captopril resulted in a marked suppression of the effect of ELE on plasma vasopressin. These findings indicate the PVN as a site of action for the central effect of tachykinins on plasma vasopressin and suggest that the angiotensin mediation of the effect might take place in the same nucleus.

Amino Acid Sequence↗

PubMed1991

Tachykinin receptor subtypes involved in the central effects of tachykinins on water and salt intake.

The present study was aimed at investigating which tachykinin receptor subtypes mediate the inhibitory effects of tachykinins a) on salt intake induced by sodium depletion, b) on water intake induced by subcutaneous hypertonic NaCl administration and c) on water intake induced by central angiotensin II injection. The study was carried out by evaluating the potency of action, following intracerebroventricular injection, of several peptides, including both naturally occurring tachykinins and synthetic peptides selective for a given receptor subtype. The results obtained show different rank orders of potency of the agonists in the different behavioral tests, thus suggesting that different receptor subtypes are involved in the effects of tachykinins on water and salt intake. NK-3 receptors appear to be involved in the inhibitory effect of tachykinins on depletion-induced salt appetite. NK-2 receptors apparently mediate the inhibitory effect of tachykinins on drinking induced by hyperosmotic NaCl administration, while NK-1 receptors are probably involved in the inhibition of angiotensin II-induced drinking.

Amino Acid Sequence↗

PubMed1990

Selective antagonists provide evidence that M1 muscarinic receptors may mediate carbachol-induced drinking in the rat.

The present study served to investigate the ability of seven selective muscarinic antagonists to inhibit carbachol-induced drinking in the rat. The muscarinic antagonists were given by intracerebroventricular (i.c.v.) injection 1 min before the i.c.v. injection of carbachol (1 microgram/rat). The M2 antagonist, methoctramine, was inactive up to 80.3 nmol/rat. The M3 antagonist, p-fluoro-hexahydro-sila-difenidol, elicited a modest (42%) but statistically significant inhibition of drinking only at 80 nmol/rat. On the other hand, the selective M1 antagonists, (R)-trihexphenidyl, o-methoxy-sila-hexocyclium and pirenzepine, produced a marked and dose-dependent inhibition of carbachol-induced drinking, their ID50 values being 0.51, 7.36 and 9.31 nmol/rat. Also the M1/M3 antagonists, 4-diphenylacetoxy-N-methylpiperidine methiodide and hexahydro-sila-difenidol, were potent inhibitors of carbachol-induced drinking, their ID50 values (0.28 and 11.09 nmol/rat) being related to their pA2 values for M1 receptors in rabbit vas deferens. These data suggest that carbachol-induced drinking may be mediated by activation of muscarinic M1 receptors.

Angiotensin II↗

PubMed1990

Sensitivity of spontaneously hypertensive and of Wistar Kyoto rats to the antidipsogenic action of eledoisin.

This study investigated the sensitivity of spontaneously hypertensive rats (SHR) and of Wistar Kyoto rats (WKR) to the antidipsogenic action of the tachykinin eledoisin (ELE). Drinking was evoked by: (a) intracerebroventricular (i.c.v.) injection of angiotensin II, (b) subcutaneous (s.c.) administration of hypertonic NaCl (1.5 M; 1 ml/100 g b.wt.) or (c) 18 h of water deprivation with free access to food. In accordance with previous studies, the dipsogenic effect of all three treatments was exaggerated in the SHR. And when treated with i.c.v. ELE (12.5-25 ng/rat) they were far less sensitive than WKR to its antidipsogenic action on angiotensin-induced drinking. Smaller differences in strain sensitivity were also observed for the effect of ELE on cell dehydration- and on water deprivation-induced drinking, but only at the dose of 200 and 50 ng/rat, respectively. The different sensitivity of the SHR to the antidipsogenic effect of ELE supports the idea that tachykininergic mechanisms for control of water intake are differently regulated in the SHR than they are in the normotensive WKR.

Angiotensin II↗

PubMed1989

Vasopressin release induced by intracranial injection of tachykinins is due to activation of central neurokinin-3 receptors.

The present study investigated the effect on vasopressin release of the intracerebroventricular injection of tachykinins in rats. The selective neurokinin (NK)-3 receptor agonists [MePhe7]neurokinin B and [Asp5,6MePhe8]substance P(5-11) evoked vasopressin release. Also eledoisin, physalaemin and kassinin, which show good affinity for central NK-3 receptors, released vasopressin. On the other hand, neurokinin A, substance P and the selective NK-1 agonist [Pro9,Met(O2)11]substance P were devoid of activity. At doses releasing vasopressin, central injection of NK-3 selective agonists and of the natural tachykinins never produced hypotension. Present results indicate that activation of central NK-3 receptors is involved in vasopressin release induced by tachykinins, and rule out the possibility that the effect might be consequent to hypotension due to passage of tachykinins into the peripheral circulation.

Animals↗

PubMed1989

Methoctramine, a selective M2 alpha muscarinic receptor antagonist, does not inhibit carbachol-induced drinking in the rat.

Methoctramine, a selective M2 alpha muscarinic receptor antagonist, was examined for its ability to inhibit carbachol-induced drinking in the rat. Intracerebroventricularly (i.c.v.) administered methoctramine was devoid of activity up to a dose of 100 nmol/rat, whereas higher doses were toxic under our experimental conditions. 4-DAMP, pirenzepine and hexahydrosiladifenidol were also tested. The rank potency order for the compounds (4-DAMP greater than pirenzepine = hexahydrosiladifenidol) was similar to that for their affinity at M1 receptors, as found in experiments in vitro. The putative M1 agonist McN-A-343 was inactive up to doses of 13.9 micrograms/rat. Our data suggest that M2 alpha receptors do not mediate cholinergic drinking in the rat. The question whether M1 or M2 beta muscarinic receptors are involved in this response still awaits a firm answer.

Angiotensin II↗

PubMed1989

Label distribution after injection of labelled tachykinins into the rat lateral cerebroventricle.

The present study investigated the label distribution in several brain regions, as well as in the peripheral circulation, following injection of labelled tachykinins [( 3H]-substance P, [3H]-eledoisin or [125I]-neurokinin A) into the lateral cerebroventricle of the rat. A widespread label distribution, extending as far as to the brainstem, was detected. Hypothalamus, striatum and hippocampus were the most labelled regions by the 3 labels; however the patterns of distribution of the 3 labelled tachykinins showed marked differences. Distribution in the brain was rapid, reaching a maximum usually within 2 min after injection and declining slightly afterwards. Large amounts of label (1/6-1/15 of the total amount injected) were detected in serum even at 2 min after injection and increased thereafter, reaching a maximum at 10-15 min.

Animals↗