Detail of "6740-88-1"

Reference

Biphasic response of the SA node of the dog heart in vivo to selective administration of ketamine

Biphasic response of the SA node of the dog heart in vivo to selective administration of ketamine. Nakajima, T.; Azumi, T.; Iwasaki, H.; Kaneshiro, S.; Yatabe, Y. (Sch. Dent., Niigata Univ., Niigata, Japan). Arch. Int. Pharmacodyn. Ther., 228(1), 108-17 (English) 1977. CODEN: AIPTAK. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Effect of ketamine (I) [6740-88-1] on the sinoatrail (SA) node of the dog heart was studied in vivo using a selective perfusion technique of the SA node artery. Injections of I in doses from 100 mg to 3 mg into the artery produced a depression of the SA nodal activity by a direct action. This depression was followed by the sudden appearance of a stimulatory phase. Bilateral vagotomy and sympathectomy or prior administration of a ganglion blocker failed to inhibit the occurrence of the I-induced tachycardia, while it was completely abolished in reserpinized dogs or by a prior injection of a beta-blocking agent into the SA node artery. Thus, an activation of a peripheral adrenergic mechanism may play an important role in the induction of the excitatory effect of I injected into the SA node artery.

Phencyclidine analogs and precursors: rotarod and lethal dose studies in the mouse

Phencyclidine analogs and precursors: rotarod and lethal dose studies in the mouse. Vaupel, D. B.; McCoun, Donald; Cone, Edward J. (Add. Res. Cent., Natl. Inst. Drug Abuse, Baltimore, MD, USA). J. Pharmacol. Exp. Ther., 230(1), 20-7 (English) 1984. CODEN: JPETAB. ISSN: 0022-3565. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) A series of phencyclidine (PCP) related analogs, carbonitrile synthetic precursors and 2 monohydroxylated metabolites were compared pharmacol. in mice for their ability to produce ataxia using the rotarod method and toxicol. for their acute 4-h lethality. The slope of the PCP dose-ataxic response curve was steeper than those of diazepam, pentobarbital, morphine and ketocyclzocine but not the slope of the sigma agonist, N-allylnormetazocine curve. Responses for all analogs, metabolites and precursors produced curves parallel to that of phencyclidine (PCP) [77-10-1]. Ataxia potencies of all PCP-related compds. ranged from 0.05 to 2.15 ′ PCP and durations of action ranged from 18 to 65 min. N-Ethyl-1-phenylcyclohexylamine [2201-15-2], 1-[1-(2-thienyl)cyclohexyl]-piperidine [42084-81-1], and 1-[1-(2-thienyl)cyclohexyl]-pyrrolidine [22912-13-6] were most potent and least potent were 1-(1-phenylcyclohexyl)-4-methylpiperidine [2201-42-5], the 1-(1-phenylcyclohexyl)morpholine [2201-40-3] and 1-[1-(2-thienyl)cyclohexyl]morpholine [21602-66-4] and trans-4-phenyl-4-piperidinocyclohexanol [78165-07-8]. 77-10-1 which is the cas registry number of some chemical is mentioned. Modifying the piperidine or arom. ring of PCP analogs affected the potency. PCP, it's analogs, metabolites and precursors caused seizures and respiratory depression. However, the precursors failed to elicit the stereotyped movements and hyperactivity that preceded seizures produced by the other compds. Overall potencies for lethality relative to PCP covered a narrow range (0.16-1.83) with the carbonitrile precursors being the most potent. Therapeutic indexes relatively large margins of safety for 1-[1-(2-thienyl)cyclohexyl]piperidine, N-ethyl-1-phenylcyclohexylamine and ketamine [6740-88-1] and the smallest were for 1-(1-phenylcyclohexyl)-4-methylpiperidine, the metabolite cis-4-phenyl-4-piperidinocyclohexanol [78165-06-7] and the 3 precursors. Thus, PCP analogs, but not the metabolites or precursors, produce similar effects. .