PubMed · 4173425
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W Sargant. 1968-07-27. Prophylactic lithium?. https://doi.org/10.1016/s0140-6736(68)92647-0
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The role of the histamine (HA) H3 receptor (estimated by binding of [3H]N-alpha-methyl HA in the brain cortex) in the response of male rats to four types of stress was evaluated: acute weak foot-shock stress (0.5 mA x 1 s x 5 times), acute intense foot-shock stress (1mA x 10 s x 5 times), acute restraint stress (60 min at 24 degrees C) and chronic variate stress. Two groups of rats received chronic treatment with a tricyclic antidepressant: amitriptyline (5 mg/kg i.p.); one group was also chronically stressed. HA-H3 receptor density rapidly decreased in acute intense foot-shock and chronic variate stress, but was unchanged in acute weak foot-shock and restraint stress. Amitripytline counteracted the chronic variate stress-induced decrease, and increased HA-H3 receptor density when chronically administered in the non-stressed control group. These results indicate that cortical HA-H3 receptor density is affected by the response to stress in function of the type, duration and intensity of the stressor.
This paper examines the biochemical and behaviour changes induced by an acute stress (five 10-s, 1-mA foot-shocks) in three groups of rats: (1) never stressed, (2) subjected to chronic variate stress for 20 days, (3) subjected to the same chronic stress and treated with 5 mg/kg per day amitriptyline. After 15 min, acute stress led to a marked reduction in cortical beta-adrenoceptor and 5-HT2 receptor density, whereas the density of the 5-HT1A receptors was unchanged. Chronic stress also increased beta-adrenoceptor and 5-HT2 receptor density and had no effect on 5-HT1A. Acute stress diminished the density of beta-adrenoceptors in chronically stressed animals, but did not alter that of the two 5-HT populations. Amitriptyline alone reduced beta-adrenoceptor and 5-HT2 receptor densities only. Acute stress applied to animals treated with amitriptyline reduced 5-HT1A receptors, and caused a further beta-adrenoceptor decrease, but had no further effect on the 5-HT2 receptors. On behaviour, chronic stress diminished reactivity to the acute stress. This reduction was fully abolished by amitriptyline. An open-field study showed that acute stress reduced motor activity, increased latency times and diminished rearing in the controls, whereas chronic stress reduced motor activity only. No significant changes in behaviour were induced by the acute stress in animals subjected to chronic stress. The combination of chronic stress with amitriptyline was accompanied by a diminution of exploratory activity that persisted after the acute stress.(ABSTRACT TRUNCATED AT 250 WORDS)
Sinus tachycardia facilitates ventricular conduction delay and sustained ventricular tachyarrhythmias during tricyclic antidepressant overdose. We hypothesized that impeding sinus tachycardia with the specific bradycardia agent, UL-FS 49, would reduce the incidence of ventricular tachyarrhythmia caused by tricyclic antidepressant overdose and tested this hypothesis in a canine model of ventricular tachycardia (VT) induced by graded amitriptyline infusion (0.5-1.0 mg/kg/min) during continuous hemodynamic monitoring. Three groups were studied. A control group (group A, n = 8) received amitriptyline infusion alone. A pretreated group (group B, n = 8) received UL-FS 49 (1 mg/kg intravenously, i.v.) 45 minutes before amitriptyline infusion. A treatment group (group C, n = 5) received UL-FS 49 (1 mg/kg) during amitriptyline infusion after onset of ventricular tachyarrhythmia. Seven (88%) in group A had ventricular tachyarrhythmia at 35 +/- 6 min of amitriptyline infusion. Ventricular tachyarrhythmia did not occur in any (0%) animal in group B. Peak sinus heart rate (HR) was significantly higher in group A (160.0 +/- 9.8 beats/min) than in group B (92.8 +/- 5.3 beats/min; p < 0.0001). Unimpeded sinus tachycardia in group A was associated with a significantly longer QRS duration (158.8 +/- 7.4 ms) as compared with group B (101.0 +/- 2.3 ms; p < 0.0001). UL-FS 49 did not influence systolic blood pressure (SBP) at baseline or during amitriptyline infusion. In group C, 3 of 5 dogs with nonsustained VT (NSVT) had effective sinus rate slowing and suppression of all NSVT after UL-FS 49. UL-FS 49 did not terminate SVT in 2 of 5 group C dogs.(ABSTRACT TRUNCATED AT 250 WORDS)