Biomedical subjects

N Caron

Publications and source records attributed to N Caron.

22 records · Page 2Linked to original sources

PubMed1977

Therapeutic effects of 9-beta-D-arabinofuranosyladenine and 2'-deoxycoformycin combinations on intracerebral leukemia.

Drug combinations of 9-beta-D-arabinofuranosyladenine and 2'-deoxycoformycin were active in the therapy of mice with intracerebral implants of the L1210 tumor. In in vivo mouse brain adenosine deaminase studies, inhibition of 9-beta-D-arabinofuranosyladenine deamination for periods of up to 24 hr was found after a single i.p. dose of 0.002 mmole/kg.

Adenosine Deaminase Inhibitors↗

PubMed1977

Effects of 2'-deoxycoformycin, 9-beta-D-arabinofuranosyladenine 5'-phosphate, and 1-beta-D-arabinofuranosylcytosine triple combination therapy on intracerebral leukemia 1210.

The triple combination of 2'-deoxycoformycin (2'-dCF), 9-beta-D-arabinofuranosyladenine 5'-phosphate, and 9-beta-D-arabinofuranosylcytosine was found to be very effective in the therapy of C57BL X DBA/2 F1 mice with intracerebral L1210. At the dosages and dosage scheduling used, the double combination of 2'-dCF and 9-beta-D-arabinofuranosyladenine 5'-phosphate gave minimal but significant increases in life-span. When 9-beta-D-arabinofuranosylcytosine was given at suboptimal dosage to mice with intracerebral L1210, the host toxicity caused by 2'-dCF and 9-beta-D-arabinofuranosyladenine 5'-phosphate in combination was decreased by a factor of 2, allowing a more prolonged therapy. "Cures" were obtained with the triple combination at dosages of 9-beta-D-arabinofuranosylcytosine that did not "cure". The supernatant adenosine deaminase from C57BL X DBA/2 F1 mouse brains was purified and the Ki for 2'-dCF using 9-beta-D-arabinofuranosyladenine as substrate was determined to be not more than 2 X 10(-11) M.

Adenosine Deaminase↗

PubMedDate not supplied

[Atrial natriuretic factor: retrospective and perspectives].

Since the hypotensive and natriuretic properties of crude cardiac extracts were first demonstrated in 1981 in the rat, the effector molecule has been isolated, purified and synthesized. The hormonal factor is produced by atrial myocytes in mammals and stored as a prohormone. Secretion mainly results from a volemic stress inducing an atrial stretch. Secretion includes a maturation step. A peptide of 28 amino-acids (ANP) is then released into the bloodstream. ANP has a half-life of a few minutes. ANP binds to specific receptors expressed at the target cell surface. B-receptors mediate the biological actions of ANP by an increase in cGMP while C-receptors are involved in clearance of the peptide. The kidney as well as the cardiovascular and endocrine systems are the main target sites for ANP. The renal effects of ANP are expressed by an enhanced diuresis and natriuresis which may result from an increased glomerular filtration rate and/or a reduced tubular reabsorption of salt and water. Renal hemodynamics may also be modified due to a renal specific vasodilator effect of ANP. The reduction of systemic blood pressure may result from changes in cardiac output and/or in peripheral vascular resistance. Several neurohumoral interactions of ANP also contribute to sustain the cardiovascular and renal effects described above. In view of these properties, ANP is of particular interest in order to understand the homeostasis of salt and water under physiological as well as or physiopathological conditions. In this regard, therapeutic prospects are intensively investigated. Finally, evolutionary perspectives are actually considered from studies in lower vertebrates.

Animals↗

PubMedDate not supplied

Dose-response analysis of acute hypotensive and renal effects of atrial natriuretic peptide in the rat.

Acute treatments with synthetic atrial natriuretic peptides induce hypotension, in which several mechanisms, including renal effects, are involved. The implication of the renal vasculature and the excretory capacities in the hypotensive action of atrial natriuretic peptides are not ascertained as yet. To address this issue, the rapid time sequence of the acute effects of atrial natriuretic peptides upon renal blood flow, mean arterial pressure, heart rate, and salt and water excretion, as well as a dose-response analysis, were investigated in 38 anesthetized euvolemic rats. Doses varying from 0.25 to 2.50 micrograms of atrial natriuretic peptide were injected i.v. in 30 sec. Each dose induced a brisk and transient increase in renal blood flow, which was maximal (13%) above 1 microgram of atrial natriuretic peptide. A small reduction in mean arterial pressure, timely related to renal vasodilation, occurred at first. It was followed by a second reduction in mean arterial pressure, which was concomitant to the maximal increases in diuresis and natriuresis. It persisted over a longer period of time. The maximal hypotensive effect (-15 mmHg) was observed above 1.5 micrograms of atrial natriuretic peptide. All effects were dose-dependent. There were no changes in heart rate. In conclusion, atrial natriuretic peptides transiently induced dose-dependent increases in renal blood flow and salt and water excretion, while the mean arterial pressure decreased stepwisely. The biphasic hypotensive effect was time-related to the renal vasodilator and diuretic effects, respectively.

Animals↗