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Biomedical subjects

D Mabin

Publications and source records attributed to D Mabin.

At least 19 recordsLinked to original sources
PubMed2005

Time-course effects of centrally administered native urotensin-II on motor and cardioventilatory activity in trout.

Although in most vertebrate species urotensin-II (UII) is synthesized in neurons of the central nervous system, little is known regarding the physiological actions of UII in the brain. We have investigated the effects of intracerebroventricular (ICV) administration of synthetic trout UII (1, 5, and 50 pmol) on total motor activity (ACT), ventilatory frequency (VF), ventilatory amplitude (VA), and heart rate (HR) in the unanesthetized trout. ICV injection of UII increased ACT in a dose-dependent manner, and the maximal effect was observed at a dose of 5 pmol. At doses of 1 and 5 pmol, UII did not affect VF, VA, or HR. At the highest dose tested (50 pmol), UII not only increased ACT, but also significantly activated VF, VA, and HR. In contrast, ICV injection of synthetic trout angiotensin-II (5 pmol) did not produce any effect on ACT, VF, or VA, but sharply increased HR. These data provide the first evidence that UII can act centrally to induce motor activity in a nonmammalian vertebrate species.

Animals↗
PubMed2000

Cardiovascular actions of centrally and peripherally administered trout urotensin-I in the trout.

The cardiovascular effects of centrally and peripherally administered synthetic trout urotensin (U)-I, a member of the corticotropin-releasing hormone family of neuroendocrine peptides, were investigated in unanesthetized rainbow trout Oncorhynchus mykiss. Intracerebroventricular injections of U-I (5.0 and 12.5 pmol) produced a sustained increase in mean dorsal aortic blood pressure (P(DA)) without significant change in heart rate (HR). This elevation in P(DA) was associated with an increase in cardiac output, but systemic vascular resistance did not change. Intra-arterial injection of U-I (12.5-500 pmol) evoked a dose-dependent increase in P(DA), but in contrast to the hemodynamic effects of centrally administered U-I, the hypertensive effect was associated with an increase in systemic vascular resistance and an initial fall in cardiac output. HR did not change or underwent a delayed increase. Pretreatment of trout with prazosin, an alpha-adrenoreceptor antagonist, completely abolished the rise in arterial blood pressure after intra-arterial administration of U-I, which was replaced by a sustained hypotension and tachycardia. Trout U-I produced a dose-dependent (pD(2) = 7.74 +/- 0.08) relaxation of preconstricted rings of isolated trout arterial vascular smooth muscle, suggesting that the primary action of the peptide in the periphery is vasorelaxation that is rapidly reversed by release of catecholamines. Our results suggest that U-I may regulate blood pressure in trout by acting centrally as a neurotransmitter and/or neuromodulator and peripherally as a neurohormone functioning either as a locally acting vasodilator or as a potent secretagogue of catecholamines.

Adrenergic alpha-Antagonists↗
PubMed1999

Central and peripheral administration of endothelin-1 induces an increase in blood pressure in conscious trout.

The central and peripheral cardiovascular effects of endothelin (ET)-1 and ET-3 were investigated in conscious rainbow trout. Both intracerebroventricular and intra-arterial injections of ET-1 (6. 25-25 pmol) but not ET-3 (25 pmol) caused a dose-dependent increase in mean dorsal aortic blood pressure and a concomitant decrease in heart rate. The hypertensive effects induced by intra-arterial and intracerebroventricular injection of ET-1 were associated with a significant (P < 0.05) increase in systemic vascular resistance. Intracerebroventricular injection of ET-1 induced a twofold higher pressor response than that caused by intra-arterial injection of ET-1 and provoked a barostatic gain that was reduced by 2.5- to 3-fold compared with that calculated after intra-arterial administration of the peptide. The ET receptor antagonist bosentan significantly (P < 0.05) attenuated these responses regardless of the route of administration. Finally, intra-arterial injection of ET-1 did not significantly modify plasma cortisol level. The present data demonstrate that intracerebroventricular and intra-arterial administration of very low doses of ET-1 produces hypertension in conscious trout. The lack of effect of ET-3 indicates that the hemodynamic actions of ET-1 are mediated both centrally and peripherally through ETA receptors.

Animals↗
PubMed1998

[The effects of clomipramine on diurnal sleepiness and respiratory parameters in a a case of Prader-Willi syndrome].

The association of Prader-Willi-syndrome with breathing disturbances such as sleep apnea syndrome and/or hypoxemia during REM sleep, REM sleep abnormalities and excessive daytime sleepiness is well known. We report the case of an 11-year-old boy who presented with Prader-Willi syndrome, obesity (body mass index [BMI] = 45.6), severe obstructive sleep apnea syndrome and significant daytime sleepiness on multiple sleep latency test. Behavioral disorders did not allowed the use of continuous positive pressure in this patient. Therefore, clomipramine (20 mg per day) was administered. Sleep examination over 8 months showed: slight weight loss (BMI = 44.4), persistence of severe obstructive sleep apnea syndrome, slight improvement in nocturnal hypoxemia, and disappearance of excessive daytime drowsiness with mean sleep latency of 15 min 37 s (less than 2 min before treatment) and no diurnal REM sleep periods. However, clomipramine had no effect on hyperphagia.

Child↗
PubMed1998

Contrasting cardiovascular effects following central and peripheral injections of trout galanin in trout.

Little is known about the role of galanin (Gal) in fish. In the present study, cardiovascular effects of central and peripheral administrations of a synthetic replicate of trout Gal (tGal) were investigated in the unanesthetized trout. Intracerebroventricular injection of 0.1, 0.5, 1.0, and 3.0 nmol/kg body mass of the peptide demonstrated that the two highest doses tested produced a significant (P < 0.001) and equivalent increase in mean dorsal aortic blood pressure (PDA) without changing heart rate (HR). At a dose of 1.0 nmol/kg, the systemic vascular resistance (Rs) increased, but no change was detected in cardiac output compared with that produced by intracerebroventricular injection of vehicle only. In contrast, intra-arterial injections of 0.1, 0.5, and 1.0 nmol/kg body mass of tGal produced a dose-dependent decrease in PDA with a threshold dose for significant effects observed at a dose of 0.5 nmol/kg. None of the doses tested changed HR. At a dose of 1 nmol/kg, a significant decrease in Rs (P < 0.001) was the factor responsible for the fall in PDA. Intra-arterial injection of porcine Gal (1 nmol/kg) produced a change in PDA similar to that of the same dose of tGal, but HR increased slightly. Pretreatments of trout with the cyclooxygenase inhibitors indomethacin and meclofenamate did not inhibit the vasodepressor effects of tGal. However, after intra-arterial injection of NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, the hypotensive action of Gal was reduced threefold, suggesting the possible involvement of the nitric oxide system in mediating the vasodilatory effect of Gal. In conclusion, our results have shown that tGal may have contrasting cardiovascular regulatory functions in trout depending on whether its site of action is the brain or the peripheral circulation.

Animals↗
PubMed1998

[Victor Segalen's death: a medical view-point].

Victor Segalen, born in Brest in 1878, naval physician and writer, died in Huelgoat forest, in Brittany. Accident or self-murder? After analysis of his personality, psychic antecedents, events of his death, and evidences of friends, his suicide seems probable. It is possible that Yvonne, his wife, and Hélène Hilpert, a woman-friend, expected this end. The accident was asserted. Comparison with death of his heroes reinforces suicide hypothesis.

France↗
PubMed1997

Role of dorsal vagal motor nucleus in angiotensin II-mediated tachycardia in the conscious trout Oncorhynchus mykiss.

Responses of heart rate (HR) and mean arterial blood pressure (MABP) were examined following microinjection of angiotensin II ([Asn1,Val5]AI) within the dorsal vagal motor nucleus (DVN) of the conscious trout's brainstem. AII (15-125 fmol) preferentially and significantly increased HR in a dose-dependent manner, but the rise in MABP was not dose-dependent and was only significant (P < 0.05) after injection of AII at a dose of 62.5 fmol. The cardiovascular action of AII was site-specific, since administrations of the peptide at a dose of 62.5 fmol, but outside the boundaries of the DVN, were devoid of any effect on HR or MABP. All the responses to DVN injections of AII were totally prevented by DVN injection of 1 nmol of losartan, a mammalian non-peptide AII subtype 1 (AT1) receptor antagonist. The ability of DVN injection of AII to induce a tachycardic response was negatively correlated to HR basal values. In conclusion, these results indicate that, at femtomolar doses, AII exerts a central neurocardioregulatory role, involving a localized receptor closely related to the mammalian AT1 receptor subtype within the DVN of the trout.

Angiotensin II↗
PubMed1997

Assessment of a newly recognized association. Carotid sinus hypersensitivity and denervation of sternocleidomastoid muscles.

BACKGROUND: Carotid sinus syndrome has been reported recently to be associated with chronic denervation of the sternocleidomastoid muscles. To further understand the relationship between carotid mechanoreceptors and sternocleidomastoid denervation, the present study investigated the relation between the results of carotid sinus massage and electromyographic activity of the sternocleidomastoid muscles in patients without syncope. METHODS AND RESULTS: Patients were selected prospectively if they fulfilled strict exclusion criteria, particularly the absence of a history of syncope, pacemaker implantation, or drugs known to modify the behavior of the autonomic nervous system. A right and left carotid massage was performed for 10 seconds in 30 patients (22 men; mean age, 67.3 +/- 6.5 years). The results (monitoring for heart rate and blood pressure) were classified as normal, doubtful, or hypersensitive carotid sinus. Sternocleidomastoid electromyography activity was recorded from the right and left sides, and the results were classified as normal, moderate denervation, and severe denervation. Carotid sinus massage was normal in 13 patients (43%), doubtful in 9 (30%), and abnormal in 8 (27%). Electromyographic activity of the sternocleidomastoids was normal in 13 patients (43%) and revealed moderate denervation in 7 (24%) and severe chronic denervation in 10 (33%). The results of carotid sinus massage and sternocleidomastoid electromyography were highly concordant in each patient (kappa = .592, P < .00001) and in each side (right, kappa = .381, P < .03; left, kappa = .390, P < .01). CONCLUSIONS: Carotid sinus hypersensitivity and chronic denervation is a common finding in individuals older than 50 years of age. These two entities are significantly related, suggesting a pathophysiological relation of one to the other.

Aged↗
PubMed1997

Patients homozygous for the 17p11.2 duplication in Charcot-Marie-Tooth type 1A disease.

Charcot-Marie-Tooth type 1A disease is an inherited sensorimotor neuropathy that is most often associated with a duplication of chromosome 17p11.2. This region contains the gene of the peripheral myelin protein 22 (PMP22), which is responsible by a gene dosage effect for the Charcot-Marie-Tooth type 1A phenotype with 17p11.2 duplication. We performed a clinical, electrophysiological, and genetic study of a consanguinous Charcot-Marie-Tooth type 1A family with 4 affected siblings, 3 of whom were homozygous for the 17p11.2 duplication, the other a heterozygote. Comparison of phenotypes showed that the severity of the disease was variable among the homozygotes, one of whom was no more severely affected than the heterozygous sibling who was paucisymptomatic. These results suggest that the severity of the disease is not determined solely by the number of copies of the PMP22 gene.

Adult↗
PubMed1997

[Distal nerve compression of the leg. Clinical and electrophysiologic study].

Rare distal compressions of lower limb nerves include tarsal tunnel syndrome, entrapment of the first branch of the lateral plantar and medial calcaneal nerves, interdigital neuroma, compression of the deep peroneal nerve on the dorsum of the foot, entrapment of the superficial peroneal and sural nerves. Nerve conduction and electromyographic studies are essential to evaluate these peripheral nerve injuries in order to differentiate focal lower extremity nerve entrapments from ischemic mononeuropathies, lumbar radiculopathies or plexopathies, and generalized peripheral neuropathies. This review summarizes the clinical and electrophysiological findings for each of these rare entrapment syndromes and provides the necessary clues to obtain a correct differential diagnosis with other more common causes of foot and ankle pain and paresthesias.

Diagnosis, Differential↗
PubMed1997

Clinical and electrophysiological phenotype of a homozygously duplicated Charcot-Marie-Tooth (type 1A) disease.

Type 1A of Charcot-Marie-Tooth disease (CMT1A) is associated with a microduplication of chromosome 17 (region 17p11.2) which contains PMP22, an important gene for peripheral nerve myelination. Patients carrying two duplications are expected to have a more severe phenotype, close to the Dejerine-Sottas syndrome. In this article, we report a family of 5 CMT1A patients in whom the unrelated father and mother carry a 17p11.2 duplication. The 2 daughters carry only one duplication (one given by the father, the other given by the mother), but the son carries two 17p11.2 duplications. Interestingly, the clinical phenotype of the son is more severe (scoliosis) compared to those of his sisters, but his motor nerve conduction velocities are in the range of a heterozygote CMT1A patient. The mechanisms leading to a more severe phenotype for CMT1A are discussed and may not be strictly related to lower nerve conduction velocities.

Adult↗
PubMed1996

New insights into the pathophysiology of carotid sinus syndrome.

BACKGROUND: The pathophysiology of carotid sinus syndrome remains poorly understood. Currently, two main hypotheses are provided: a lesion at the level of carotid sinus receptors or a central defect at the level of the nuclei of the autonomic nervous system. The objective of our study was to present arguments in favor of one of these two hypotheses. METHODS AND RESULTS: Test selection was guided by the following hypothesis: a degenerative central or local lesion could be associated with dysfunctions in the structures surrounding or comprising the baroreflex centers or their pathways. To test this hypothesis, brain stem auditory-evoked potentials; somatosensory-evoked potentials; blink reflexes; sympathetic skin responses; and styloglossus, sternocleidomastoid, and superior trapezius muscle electromyography were systematically performed from the right and left sides in 17 patients with carotid sinus syndrome and in 17 sex- and age-matched control subjects. Similar responses were found in the two groups for the "central" tests. Contrasting with this result, the electromyographic analysis of the sternocleidomastoid muscle differed significantly between the groups: 13 (76%) had pathological responses in the carotid sinus syndrome group compared with only 4 (23.5%) in the control group (P < .01). Furthermore, the abnormality was found on the right and left sides in 9 patients (53%) in the study group and in none of the control group (P < .005). CONCLUSIONS: This study strongly suggests that the neuromuscular structures surrounding the carotid mechanoreceptors are involved in the carotid sinus syndrome; however, the exact mechanism remains speculative.

Aged↗
PubMed1996

[Presymptomatic injury of the recurrent laryngeal nerve in benign thyroid disease: contribution of electromyography].

Diagnosis of recurrent laryngeal nerve palsy is usually possible through a clinical, laryngoscopical and electromyographical approach, but at a critical stage of the nerve injury. We observed four cases of benign thyroïd tumoral processes with a preoperative electromyographic examination showing neurogenic abnormalities in the thyroarytenoid muscle without any clinical symptoms. We presume that only laryngeal electromyography permits the diagnosis of mild, even asymptomatic laryngeal recurrent nerve injury. A recurrent laryngeal nerve palsy occurs in thyroid tumors, most often in malignant conditions, rarely in benign ones. Nevertheless early forms of nerve injury with benign thyroïd pathology could be underrated. Since the functional prognosis of symptomatic laryngeal nerve palsy is doubtful, laryngeal electromyography, through its ability to diagnose early nerve injury, provides helpful indications in thyroïd benign tumoral diseases for the therapeutic decision.

Adult↗
PubMed1995

Oxygen consumption during sleep in atopic dermatitis.

Measurements of oxygen consumption (VO2) were made during sleep in 10 patients with atopic dermatitis. Two groups of healthy children acted as controls. All subjects were studied in bed in an environmental temperature of 24-26 degrees C, and sleep was confirmed during continuous electroencephalographic monitoring. Mean (SD) values of VO2 in sleeping patients who were not scratching ranged from 4.0 (0.4) to 7.4 (0.7), which was not statistically significantly different from control values which ranged from 3.24 (0.3) to 5.56 (0.4). During scratching (while asleep), which occurred in nine out of 10 patients with atopic dermatitis, the mean values of VO2 ranged from 4.5 (0.04) to 10.4 (2.7), and this was significantly higher than the non-scratching patients and the control values. Scratching during sleep in children with atopic dermatitis is associated with increased VO2.

Adolescent↗
PubMed1994

Intracerebroventricular administration of angiotensin II increases heart rate in the conscious trout.

The central effect of angiotensin II on cardiovascular activity has been investigated in conscious trout bearing an intracerebroventricular (i.c.v.) cannula and an intra-arterial catheter. I.c.v. injection of the angiotensin II agonist [Asn1,Val5]AII (6.2-50 pmol) induced a dose-dependent increase in heart rate and arterial blood pressure. Central administration of the angiotensin II antagonist DuP 753 (5 nmol) 30 min before i.c.v. injection of [Asn1,Val5]AII totally prevented the tachycardia and reduced the hypertension induced by the angiotensin II agonist. Intra-arterial injection of arginine-vasotocin (12.5 pmol) caused a bradycardia associated with a marked increase in arterial blood pressure. I.c.v. injection of [Asn1,Val5]AII totally blocked the bradycardia induced by arginine-vasotocin and this effect was prevented by central administration of DuP 753. In contrast, [Asn1,Val5]AII did not affect the increase in blood pressure induced by arginine vasotocin. Suppression of the vagal tone by atropine treatment totally blocked the central effect of [Asn1,Val5]AII. These results show that angiotensin II acts directly on the trout brain to increase blood pressure and heart rate. The effect of angiotensin II is mediated through a receptor related to the mammalian AT1 receptor type.

Angiotensin II↗