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J Chelly

Publications and source records attributed to J Chelly.

At least 127 records · Page 7Linked to original sources
PubMed1987

Long-range genomic map of the Duchenne muscular dystrophy (DMD) gene: isolation and use of J66 (DXS268), a distal intragenic marker.

By cloning the endpoints of a DMD-associated deletion, we have "jumped" 1100 kb from pERT87-1 (DSX164) to a new locus designated J66 (DXS268), mapping distally within the Duchenne muscular dystrophy (DMD) gene. Both J66 and JBir are mapped by field-inversion gel electrophoresis and detect abnormal SfiI fragments in DMD patients and distal DMD-associated X; autosome translocations. Our long-range map extends the physical map of the DMD gene from 800 to 2000 kb (2 Mb) and increases the mapped portion of Xp21 to approximately 8 Mb. The position of the glycerol kinase gene and the adrenal hypoplasia locus are further confined to the region between J66 and the nearest distal probe L1-4. This region spans at least 1.5 Mb. The multiallelic J66 polymorphism has immediate application in the diagnosis of DMD and generally appears to be distal to DMD mutations.

Chromosome Deletion↗
PubMed1987

Involvement of cholinergic mechanisms in the central cardiovascular actions of nicardipine in dogs.

The involvement of cholinergic mechanisms in the central cardiovascular effects of a dihydropyridine, nicardipine, was investigated in pentobarbital-anaesthetized normotensive dogs. Nicardipine (1 microgram/kg) injected intracisternally (i.c.) induced a rise in both blood pressure and heart rate. This induced hypertension was suppressed by pretreatment with intravenous (i.v.) atropine or i.c. methylatropine but not i.v. methylatropine. I.c. methylatropine reduced nicardipine-induced tachycardia. These results demonstrate the involvement of cholinergic pathways in the central cardiovascular effects of i.c. nicardipine in dogs and suggest a functional interaction between dihydropyridine binding sites and cardiovascular cholinergic mechanisms in the brain.

Animals↗
PubMed1986

Effects of norepinephrine on the dog common carotid, coronary and renal arteries: in vitro studies.

The effects of norepinephrine were studied on segments of the common carotid, left circumflex and renal arteries of dogs with the endothelium intact and removed. Norepinephrine induced a dose-dependent increase in tension in segments of the renal and carotid artery but did not produce any effect on the coronary artery. Although the absence of endothelium did not affect the magnitude of the norepinephrine-induced vasoconstriction of the renal artery, it elicited a more pronounced response in the carotid artery in which the endothelium was removed. Our data suggest that the vascular response to norepinephrine is dependent upon the specific arterial bed and, secondly, that the endothelium plays a determinant role in the magnitude of the response of the carotid artery.

Animals↗
PubMed1986

De novo DNA microdeletion in a girl with Turner syndrome and Duchenne muscular dystrophy.

The single X chromosome of a girl with Turner syndrome (45,X) and typical Duchenne muscular dystrophy was investigated at the chromosomal and DNA levels. No visible abnormality of the residual X chromosome was found upon high-resolution R-banding. The DNA was analysed by Southern blotting and hybridization with seven cloned probes mapping in the Xp21 region where the Duchenne locus is thought to be located. A molecular deletion was detected with probes pERT 87.1, pERT 87.8, and pERT 87.15. The other probes (754, C7, 99.6, and RC8) gave a normal signal. The DNA alleles seen in the two parents indicated that the deletion found in the propositus had occurred de novo on a maternal X chromosome.

Adolescent↗
PubMed1986

Suppression of renin release by antagonism of endogenous opiates in the dog.

The influence of blockade of endogenous opioids on the release of renin due to partial renal arterial constriction was determined acutely and chronically in unilaterally nephrectomized dogs. In acute preparations changes in plasma renin activity, arterial blood pressure, and heart rate were determined after 15 min of 60% renal arterial constriction before and after administration of either a saline vehicle, the opiate antagonist naloxone (0.05 mg/kg), or morphine (2 mg/kg). Acute antagonism of endogenous opiates abolished the increase in plasma renin activity and mean arterial pressure associated with renal arterial constriction. Repeated renal arterial constrictions in saline- or morphine-treated animals did not alter the humoral or hemodynamic responses. In chronic preparations long-term naloxone infusion attenuated the development of renovascular hypertension and diminished the increase in plasma renin activity. These data suggest that endogenous opioid peptides are modulators in the control of renin release and may be important participants in the pathogenesis of hypertension.

Animals↗
PubMed1983

Possible role of alpha 1- and alpha 2-adrenoceptors in the modulation of the sympathetic component of the baroreflex.

In anaesthetized and bilaterally vagotomized dogs, reflex bradycardia elicited by intravenous injection of noradrenaline was facilitated by AR-C 239, a new alpha 1-adrenoceptor blocking drug and inhibited by the alpha 2-adrenoceptor antagonist, yohimbine. Both alpha-blocking drugs were administered into the vertebral artery. In another group of bilaterally vagotomized dogs, unilateral electrical stimulation of the carotid sinus nerve induced a frequency-dependent decrease in mean blood pressure solely mediated through the sympatho-inhibitory component of the baroreflex. Administration of the alpha 1-adrenoceptor blocking drugs, AR-C 239 and prazosin (5 micrograms/kg) into the vertebral artery decreased basal mean blood pressure and increased depressor responses to the carotid sinus nerve stimulation, whereas the intracisternal injection of phenylephrine (30 micrograms/kg), a preferential alpha 1-agonist, increased mean blood pressure but inhibited the hypotension resulting from electrical stimulation. In addition, the injection into the vertebral artery of yohimbine (100 micrograms/kg), an alpha 2-adrenoceptor blocking agent which caused no change in mean arterial pressure, inhibited the decrease in the sympathetic component. In conclusion, these results suggest the possible participation of the two types of alpha-adrenoceptors in the modulation of the sympathetic component of the baroreflex: alpha 1-adrenoceptor stimulation could inhibit, whereas alpha 2-adrenoceptor activation facilitates the reflex activity in the sympathetic fibres.

Animals↗
PubMed1982

Possible role of central alpha 1-adrenoceptors in the control of the autonomic nervous system in normotensive and spontaneously hypertensive rats.

The cardiovascular effects of AR-C 239, a new and selective alpha 1-adrenoceptor blocking drug were studied in normotensive and spontaneously hypertensive rats (SHR). AR-C 239 (300 micrograms/kg i.v.) did not change the heart rate in control (without pretreatment) and bilaterally vagotomized normotensive rats, but induced significant bradycardia in rats pretreated with a beta-adrenoceptor blocking drug. This bradycardic effect was inhibited by atropine or bilateral vagotomy. In SHR, the administration of AR-C 239 reduced heart rate in the control, bilaterally vagotomized and beta-blocked rats. Blood pressure was decreased in the same way in the two rat strains. It is suggested that central alpha 1-adrenoceptors could participate in the control of vagal tone in normotensive and SH rats, and of sympathetic activity in the SHR only.

Adrenergic alpha-Antagonists↗
PubMed1982

Hemodynamic and metabolic effects of prostacyclin after coronary bypass surgery.

The hemodynamic and metabolic effects of prostacyclin (PGI2) were assessed in 12 patients who underwent coronary bypass surgery. PGI2 were injected intravenously at a rate of 2.5 ng/kg/min for 10 minutes, followed by three consecutive 10-minute injections of 5, 10 and 20 ng/kg/min. PGI2 infusion decreased systolic and diastolic arterial pressures by 17% (p less than 0.001) and increased cardiac index by 17% (p less than 0.001) without changing the heart rate. Right atrial, pulmonary arterial and pulmonary wedge pressures remained essentially unchanged. Total vascular resistance decreased by 37% (p less than 0.001). Rate-pressure product, an index of myocardial oxygen consumption, decreased by 13% (p less than 0.01), while stroke work index did not change. A 36% decrease in arterial PO2 (p less than 0.001) was the most consistent metabolic effect induced by PGI2 infusion. However, oxygen transport increased by 11% (p less than 0.05), suggesting that no decrease in peripheral oxygen supply was produced. Thus, PGI2 improved cardiac function and performance by a predominant effect on total vascular resistance. It may be valuable in the management of patients who undergo coronary artery surgery.

Adult↗
PubMed1981

Role of alpha 1- and alpha 2-adrenoceptors in the modulation of the baroreflex vagal bradycardia.

Yohimbine (100 micrograms/kg), an alpha 2-adrenoceptor blocking agent when injected into the vertebral artery of anaesthetized dogs decreased the vagally mediated bradycardia induced by carotid sinus nerve stimulation. Intracisternal administration of phenylephrine (30 micrograms/kg) an alpha 1-adrenoceptor agonist decreased, whereas AR-C 239 (5 micrograms/kg) and prazosin (5 micrograms/kg) two potent alpha 1-adrenoceptor antagonists injected into the vertebral artery, potentiated the bradycardiac response. These results suggest the presence of two types of alpha-adrenoceptors to modulate the baroreceptor pathway: alpha 1-adrenoceptors inhibit and alpha 2-adrenoceptors facilitate the transmission of baroreceptor impulses.

Adrenergic alpha-Antagonists↗
PubMed1980

[Interaction between clonidine and alpha-blockers (author's transl)].

The inhibitory effects of clonidine on the heart seem to be due to stimulation of alpha 2 adrenoceptors. alpha-Adrenoceptor blocking agents with selective affinity for alpha 2-adrenoceptors antogonize these effects. Since the alpha-adrenoceptor blocking drugs which, at the usual dosage level, antagonize the hypotensive action of clonidine are unknown in man, caution should be exercised for such an association clonidine-alpha-blocker.

Adrenergic alpha-Antagonists↗
PubMed1980

Pharmacological properties of AR-C239, 2-[2-[4(o-methoxyphenyl)-piperazine-1-Yl]-ethyl]4,4-dimethyl-1,3(2H-4H) isoquinolinedione, a new alpha-adrenoceptor blocking drug.

In pentobarbital-treated dogs and rats, AR-C239, a new and potent alpha-adrenoceptor blocking drug, competitively antagonized pressor responses to adrenaline and inhibited pressor responses to noradrenaline, phenylephrine, tyramine, and dimethylphenylpiperazinium. Injected intravenously into closed-chest dogs, AR-C239 (3-50 micrograms/kg) induced a progressive fall in blood pressure, heart rate, and sympathetic nerve activity. The drug appears to be devoid of direct vasodilator action, and the fall in blood pressure results from the peripheral alpha-blockade. AR-C239 did not change the tachycardia induced by stimulation of the cardiac nerve in dogs and, at least in this preparation, seems to be a specific alpha 1-adrenoceptor blocking drug. When administered into the cisterna magna of dogs, AR-C239 did not have any centrally mediated cardiovascular actions and heart rate. AR-C239 did not modify the functioning of the baroreflex arc. Due to its specificity for alpha 1-Adrenoceptors, AR-C239 may be useful for characterizing alpha-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1980

[Nitroglycerin and anaesthesia in phaeochromocytoma (author's transl)].

Six patients who have undergone surgery for phaeochromacytoma have been separated in 2 groups. In group I (n = 3) a nitroglycerin infusion of 7.8 microgram . kg-1 . mn-1 has been used before the removal of the tumor and no vasodilator drug was infused in group II. During the dissection, mean arterial pressure was significantly lower in group I (129 +/- 12 mm Hg) than in group II (172 +/- 17 mm Hg) (p < 0.05). After removal of the tumor the decrease in mean arterial pressure was lower in group I than in group II. In group I the maximal rise in mean arterial pressure (73 +/- 18 mm Hg) was significantly reduced compared to group II (134 +/- 20 mm Hg). These results show that nitroglycerin is an interesting substance to decrease the variations of arterial blood pressure and this effect is important to prevent cardiac complications during and after surgery.

Adrenal Gland Neoplasms↗
PubMed1980

[Clinical use of nitroglycerin as an hypotensive agent during general anesthesia for caesarean section. Report of a case (author's transl)].

Nitroglycerin in aqueous solution has been used as hypotensive agent during a caesarean section, in a patient who presented an arterial hypertension not controled by administration of four antihypertensive agents (acebutolol, clonidine, dihydralazine, alpha-methyl-dopa). Nitroglycerin continuous infusion started two hours before caesarean section at the dose of one milligramme over one hour and stopped several hours after.

Adult↗
PubMed1979

Effects of L-glutamic acid and kainic acid on central cardiovascular control.

L-Glutamic acid and kainic acid injected into the cisterna magna of dogs, produced a dose-dependent increase in blood pressure and a decrease in heart rate. In contrast, intravenous injection of both compounds was ineffective. The hypertension was probably due to an increase in sympathetic tone as guanethidine prevented the rise in blood pressure induced by central administration of L-glutamic acid and kainic acid. Kainic acid was 1 000 fold more potent than L-glutamic acid.

Animals↗
PubMed1979

[Action of N-butylnorsympathone on the effects of cardioaccelerator nerve stimulation in the dog].

In Dogs anaesthetized with pentobarbital (30 mg . kg-1), N-butylnorsympathone (20 mg . kg-1 i.v.) reduced the bradycardia induced by stimulating the cardiac nerve (1, 2, 5, 10 Hz). Phentolamine (1 mg . kg-1 i.v.) or yohimbine (0.3 mg . kg-1 i.v.), two potent alpha-adrenoceptor blocking agents known to block presynaptic alpha-adrenoceptor induced a recovery of the effect of cardiac nerve stimulation. Prazosine (0.050 mg . kg-1 i.v.) an alpha-adrenoceptor blocking agent known to be ineffective on presynaptic alpha-adrenoceptors did not induce a recovery. However neither phentolamine or yohimbine were able to prevent the effects of N-butylnorsympathone. Neither haloperidol (0.050 to 2 mg . kg-1 i.v.) or pimozide (0.20 to 1 mg . kg-1 i.v.) induced a recovery or prevented the effects of N-butylnorsympathone. These results suggest that N-butylnorsympathone may stimulate presynaptic receptors which do not resemble classical presynaptic alpha-adrenoceptors or dopamine receptors.

Animals↗