D C da Silva | PubMed Health

PubMed1999

Central moxonidine on water and NaCl intake.

In this study we investigated: (a) the effects of intracerebroventricular (i.c.v.) injections of moxonidine (an alpha2-adrenergic and imidazoline receptor agonist) on the ingestion of water and NaCl induced by 24 h of water deprivation; (b) the effects of i.c.v. injection of moxonidine on central angiotensin II (ANG II)- and carbachol-induced water intake; (c) the effects of the pre-treatment with i.c.v. idazoxan (an alpha2-adrenergic and imidazoline receptor antagonist) and RX 821002 (a selective alpha2-adrenergic antagonist) on the antidipsogenic action of central moxonidine. Male Holtzman rats had stainless steel cannulas implanted in the lateral cerebral ventricle. Intracerebroventricular injection of moxonidine (5 and 20 nmol/1 microl) reduced the ingestion of 1.5% NaCl solution (4.1 +/- 1.1 and 2.9 +/- 2.5 ml/2 h, respectively vs. control = 7.4 +/- 2.1 ml/2 h) and water intake (2.0 +/- 0.6 and 0.3 +/- 0.2 ml/h, respectively vs. control = 13.0 +/- 1.4 ml/h) induced by water deprivation. Intracerebroventricular moxonidine (5 nmol/1 microl) also reduced i.c.v. ANG II-induced water intake (2.8 +/- 0.9 vs. control = 7.9 +/- 1.7 ml/1 h) and i.c.v. moxonidine (10 and 20 nmol/1 microl) reduced i.c.v. carbachol-induced water intake (4.3 +/- 1.7 and 2.1 +/- 0.9, respectively vs. control = 9.2 +/- 1.0 ml/1 h). The pre-treatment with i.c.v. idazoxan (40 to 320 nmol/1 microl) abolished the inhibitory effect of i.c.v. moxonidine on carbachol-induced water intake. Intracerebroventricular idazoxan (320 nmol/1 microl) partially reduced the inhibitory effect of moxonidine on water deprivation-induced water intake and produced only a tendency to reduce the antidipsogenic effect of moxonidine on ANG II-induced water intake. RX 821002 (80 and 160 nmol/1 microl) completely abolished the antidipsogenic action of moxonidine on ANG II-induced water intake. The results show that central injections of moxonidine strongly inhibit water and NaCl ingestion. They also suggest the involvement of central alpha2-adrenergic receptors in the antidipsogenic action of moxonidine.

Adrenergic alpha-Antagonists↗

PubMed1985

[Neuropathies caused by thalidomide].

Symptoms and signs in four patients with thalidomide-induced neuropathy developing during treatment of discoid lupus were limited for long period to distal paresthesiae with altered sensory conduction velocities. Semi-thin biopsy specimens of the distal sural nerve showed depopulation of myelinized fibers, mainly affecting those of large caliber, and signs of axonal degeneration. Study of dissociated fibers showed a high proportion of E fibers. Morphometry confirmed the axonal lesion. Ultrastructural examination demonstrated anomalies of axons of amyelinic fibers (vacuoles, lamellar figures) and of Schwann cells (stacked cytoplasmic prolongations), together with numerous collagen pockets, all non-specific lesions. The disease course was slow, with disappearance of sensory symptoms in a few weeks in 3 of the 4 cases and normal clinical findings in one of the four patients one year after cessation of treatment. Definite correlations between the dose administered and the severity of the neuropathy could not be established. The still poorly understood mechanism of action is discussed.

Acute Disease↗

PubMed1981

Pilot trials on the treatment of Dermatobia hominis infections in cattle with closantel.

The therapeutic and prophylactic activities of closantel given to calves inoculated with larvae of Dermatobia hominis were studied. Calves (n = 9 principals, plus 3 nontreated controls) were given closantel at different dosages (8 to 12.5 mg/kg) and schedules of treatment. The largest dosage of closantel (12.5 mg/kg) had the most efficacious therapeutic activity (97.3%). Prophylactic activity was also seen in calves given the drug before they were experimentally inoculated.

Animals↗