scholarly journals Behavioral toxicity of sodium cyanide following oral ingestion in rats: Dose-dependent onset, severity, survival, and recovery

2018 ◽  
Vol 114 ◽  
pp. 145-154 ◽  
Author(s):  
Nathaniel C. Rice ◽  
Noah A. Rauscher ◽  
Jeffrey L. Langston ◽  
Todd M. Myers
Keyword(s):  
Sodium Cyanide ◽  
Oral Ingestion ◽  
Behavioral Toxicity ◽  
Dose Dependent

Lesions of area postrema attenuate but do not prevent anorectic action of peripheral serotonin in rats

1995 ◽  
Vol 269 (6) ◽  
pp. R1314-R1320 ◽  
Author(s):  
V. Adipudi ◽  
K. J. Simansky
Keyword(s):  
Food Intake ◽  
Dose Response ◽  
Area Postrema ◽  
Behavioral Analysis ◽  
High Dose ◽  
Reduce Food Intake ◽  
Circumventricular Organ ◽  
Behavioral Toxicity ◽  
Dose Dependent ◽  
Dose Response Function

These studies assessed the effect of selectively ablating the area postrema (AP) on the action of peripheral serotonin [5-hydroxytryptamine (5-HT)] to reduce food intake in rats. Intraperitoneal 5-HT (0, 2.0, 4.0, and 8.0 mumol/kg) reduced the intakes of sweetened mash during a 30-min test in controls (APC) and in AP-lesioned rats (APX). The anorexia was dose dependent in controls but the dose-response function was flat after AP lesions. In another study, 2.0 mumol/kg 5-HT reduced intakes of both groups by approximately 25%, but AP lesions blunted the effect at 8.0 mumol/kg 5-HT (APX, -30% vs. APC, -85%). Behavioral analysis revealed that, compared with controls, AP lesions eliminated the decrease in frequency of feeding and reduced the incidence of resting and of an aberrant posture observed after 8.0 mumol/kg. Thus peripheral 5-HT decreases food intake in rats with AP lesions. Multiple mechanisms appear to be involved in the ability of peripheral 5-HT to reduce feeding. A high dose of 5-HT promotes responses associated with satiation but also produces behavioral toxicity; these effects involve the AP. Lower doses appear to engage processes that do not rely on the function of this circumventricular organ.

Respiratory influence of peripheral chemoreceptor stimulation in maturing rabbits

1987 ◽  
Vol 63 (4) ◽  
pp. 1671-1680 ◽  
Author(s):  
C. M. Schramm ◽  
M. M. Grunstein
Keyword(s):  
Steady State ◽  
Sodium Cyanide ◽  
Co2 Production ◽  
Base Line ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Respiratory Effects ◽  
Line Level ◽  
Dose Dependent ◽  
Respiratory Depressant

To evaluate whether the influence of peripheral chemoreceptor (PCR) stimulation is centrally modulated by hypoxia, the respiratory effects of sodium cyanide (NaCN) infusion were compared during room air and 10% O2 inhalation in 18 lightly anesthetized, tracheotomized rabbits of varying postnatal age (1–33 days). During normoxia, noncumulative infusions of NaCN (5–400 micrograms/kg body wt) produced dose-dependent ventilatory (VE) stimulation. Maximal VE stimulation (VEmax) and ventilatory sensitivity to NaCN [i.e., log dose producing 50% of VEmax (log ED50)] did not significantly vary with age, with the average VEmax and log ED50 values amounting to 238% above base line and 1.564 micrograms/kg, respectively. During hypoxia, after initial stimulation (average: 152%), VE progressively decreased and stabilized to 67% above the normoxic base-line level. In contrast to normoxia, subsequent NaCN administration during steady-state hypoxia produced dose-dependent VE depression, occasionally manifested by abrupt apnea. The NaCN effect during hypoxia was significantly related to age (P less than 0.05), as well as to the estimated change in CO2 production during hypoxia (P less than 0.01). Both the respiratory depressant effects of hypoxia alone and in combination with NaCN were abolished after denervation of the peripheral chemoreceptors. These findings demonstrate that while PCR stimulation during normoxia produces ventilatory stimulation, the influence of enhanced PCR input during hypoxia is centrally modulated to produce ventilatory depression.

scholarly journals Behavioral intoxication following voluntary oral ingestion of tetramethylenedisulfotetramine: Dose-dependent onset, severity, survival, and recovery

2017 ◽  
Vol 63 ◽  
pp. 21-32 ◽  
Author(s):  
Nathaniel C. Rice ◽  
Noah A. Rauscher ◽  
Jeffrey L. Langston ◽  
Todd M. Myers
Keyword(s):  
Oral Ingestion ◽  
Dose Dependent

Increased Expression of u-PA and u-PAR on Monocytes by LDL and Lp(a) Lipoproteins – Consequences for Plasmin Generation and Monocyte Adhesion

1999 ◽  
Vol 81 (04) ◽  
pp. 594-560 ◽  
Author(s):  
Florence Ganné ◽  
Marc Vasse ◽  
Jean-Louis Beaudeu ◽  
Jacqueline Peynet ◽  
Arnaud François ◽  
...  
Keyword(s):  
Fold Increase ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Atheromatous Plaque ◽  
Monocyte Adhesion ◽  
Blood Monocytes ◽  
Proteolytic Cascade ◽  
Ecm Degradation ◽  
Dose Dependent Increase ◽  
Dose Dependent

SummaryMonocyte-derived foam cells figure prominently in rupture-prone regions of atherosclerotic plaque. As urokinase/urokinase-receptor (u-PA/u-PAR) is the trigger of a proteolytic cascade responsible for ECM degradation, we have examined the effect of atherogenic lipoproteins on monocyte surface expression of u-PAR and u-PA. Peripheral blood monocytes, isolated from 10 healthy volunteers, were incubated with 10 to 200 µg/ml of native or oxidised (ox-) atherogenous lipoproteins for 18 h and cell surface expression of u-PA and u-PAR was analysed by flow cytometry. Both LDL and Lp(a) induced a dose-dependent increase in u-PA (1.6-fold increase with 200 μg/ml of ox-LDL) and u-PAR [1.7-fold increase with 200 μg/ml of ox-Lp(a)]. There is a great variability of the response among the donors, some of them remaining non-responders (absence of increase of u-PA or u-PAR) even at 200 μg/ml of lipoproteins. In positive responders, enhanced u-PA/u-PAR is associated with a significant increase of plasmin generation (1.9-fold increase with 200 μg/ml of ox-LDL), as determined by an amidolytic assay. Furthermore, monocyte adhesion to vitronectin and fibrinogen was significantly enhanced by the lipoproteins [respectively 2-fold and 1.7-fold increase with 200 μg/ml of ox-Lp(a)], due to the increase of u-PAR and ICAM-1, which are receptors for vitronectin and fibrinogen. These data suggest that atherogenous lipoproteins could contribute to the development of atheromatous plaque by increasing monocyte adhesion and trigger plaque weakening by inducing ECM degradation.

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