The effect of the novel partial alpha2‐adrenoceptor agonist naphthylmedetomidine on the basic cardiorespiratory parameters and behavior in rhesus monkeys

Abstract

Our results suggest that naphthylmedetomidine can be used to induce sedation in primates and other small animals while avoiding the serious side effects observed after administration of the currently used full alpha(2)-AR agonists.

Short term pharmacological immobilization in macaque monkeys

“…In primates the most commonly described immobilization protocols are based on the administration of dissociative anaesthetic agents including ketamine, often combined with medetomidine (Sun et al 2003) and the combination of tiletamine with zolazepam (Bentson et al 2003). In our laboratory we have described the combined immobilization effect of medetomidine or its derivative naphthylmedetomidine with midazolam and ketamine in anthropoid apes (Hess et al 2010) and rhesus monkeys (Votava et al 2009). However, the dissociative anaesthetic agents are known to cause many adverse reactions, among which salivation and hypertonic reactions are the most disturbing.…”

“…In our laboratory we have described the combined immobilization effect of medetomidine or its derivative naphthylmedetomidine with midazolam and ketamine in anthropoid apes (Hess et al. 2010) and rhesus monkeys (Votava et al. 2009).…”

Immobilization Stress With <i>α</i>₂-Adrenergic Stimulation Induces Regional and Transient Reduction of Cardiac Contraction Through Gi Coupling in Rats

“…α 2 -AR agonists have been used as antihypertensive drugs, sedatives, and adjuncts in anesthesia and echocardiography. 19,20) However, the results of this study indicate that physicians must be cautious of excessive contractile depression following injection of α 2 -AR agonists in patients suspected of stress cardiomyopathy, and in patients who have experienced restraint or psychological stress. The genotyping of α 2 -AR and β 2 -AR might facilitate individualized therapy for patients with distinct backgrounds who are suspected of stress cardiomyopathy or heart failure.…”

“…α 2 -AR agonists are widely recognized to inhibit stimulation-evoked release of norepinephrine and epinephrine from presynaptic adrenergic nerve terminals 18) and the adrenal medulla. 19) During the progression of congestive heart failure, negative-feedback inhibition through presynaptic α 2 -AR is potentiated, which attenuates excessive norepinephrine release in patients 28) and in mice exposed to pressure overload. 29) Consistent with these findings, sustained (30 minutes) IMO did not increase norepinephrine secretion, possibly reflecting endogenous α 2 -AR-mediated feedback inhibition ( Figure 4B).…”

“…16) α 2 -AR agonists induce central hypotension in association with an inhibition of catecholamine release from presynaptic adrenergic nerve terminals and the adrenal medulla. 17,18) Moreover, α 2 -AR agonists cause sedation, 19) stabilize circulatory dynamics, and improve cardiac oxygen consumption during surgery. 20,21) Recently, Ibacache, et al identified the cardiomyocyte α 2A -and α 2C -ARs that mediate the cardiac protection conferred by ischemic preconditioning in rats.…”