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Publication Title | INTERACTION OF CANNABIS AND GENERAL ANAESTHETIC AGENTS IN MICE

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Br. J. Pharmac. (1974), 50, 593-599

INTERACTION OF CANNABIS AND GENERAL ANAESTHETIC AGENTS IN MICE

G.B. CHESHER, D.M. JACKSON & G.A. STARMER

Department of Pharmacology, University of Sydney, Sydney 2006, Australia

1 A cannabis extract (I) (in a concentration equivalent to 10mg A9-tetrahydro- cannabinol(THC)/kg) prolonged pentobarbitone anaesthesia in mice maximally 20 min to 2 h aftermedication.Theeffectwas stilsignificantafter8h,butlessthanat2hours.

2 Thecannabisextract(1)(equivalentto10mg A9-THC/kg)prolongedbothpentobarbitone and ether anaesthesia in mice when administered 20 min before the anaesthetic. After eight consecutivedailydosesofcannabis,thepentobarbitoneanaesthesiawas stilsignificantlylonger thana controlgroup, whileetheranaesthesiawas notsignificantlyprolonged.

3 Asecondcannabisextract(I)withadifferentratioofcannabinoids(alsoadministeredin dosageequivalentto10mg A9-THC/kg)failedtoaffectpentobarbitoneanaesthesiainmice. This extract presented about 4% the dose of cannabidiol as extract I.

4 A8-THC,A9-THCandcannabidiolprolongedpentobarbitoneanaesthesiawithcannabidiol beinggenerallymore activethanA9-THC.Cannabinol(10mg/kg)was inactive.

5 The effects of cannabidiol and A9-THC were found to be additive, and there was a consistent trend for cannabinol to reduce the effectiveness of A9-THC and cannabidiol when givenincombination.

6 Premedicationwithphenoxybenzamine,phentolamine,propranolol,iproniazid,protripty- line, desipramine, reserpine, ai-methyl tyrosine or parachlorophenylalanine did not affect the extract I-induced prolongation of pentobarbitone anaesthesia.

7 Itisconcludedthatcannabismay affectpentobarbitoneandetheranaesthesiainmiceat leastpartiallybya directdepressanteffect,andthatthecannabis-inducedprolongationof anaesthesiaisprobablyunrelatedtoanyeffecton central5-hydroxytryptamineorcatechol- amine neurones.

Introduction

One of the earliest reported properties of cannabis To elucidate these effects further we have made extractsandofpurecannabinoidsistheirability acomparativestudyoftheeffectoftwocannabis

toprolongbarbiturateanaesthesiainmice(Loewe, 1944;Garriott,Forney,Hughes&Richards,1968; Gil, Paton & Pertwee, 1970; Paton & Pertwee, 1972)andinrats(Kubena& Barry,1970).Some controversy exists as to whether this effect is due to a direct depressant action of cannabis on the central nervous system or isdue to an interference by cannabis in the metabolism of the barbiturate by the microsomal enzymes. Paton & Pertwee (1972) advanced the latter explanation when they reported the failure of a cannabis extract to prolong anaesthesia induced by ether, which isnot metabolized by microsomal enzymes. On the other hand Kubena & Barry (1970) reported that A9-tetrahydrocannabinol (A9-THC) did prolong barbitone anaesthesiainrats.Barbitone,likeether, doesnotundergomicrosomaldegradation,andis

excretedunchanged.

extractsonbothpentobarbitone-andether- inducedanaesthesiainmice.Theeffectsof A8-THC, A9-THC, cannabinol and cannabidiol on the duration of pentobarbitone anaesthesia were alsostudied.

Cannabis affects the levels and turnover of endogenous catecholamines and of 5-hydroxy- tryptamine in brain (Bose, Saifi & Bhagat, 1963,

1964; Holtzman, Lovell, Jaffe & Freedman, 1969; Colombine,Westfall& McCoy, 1970;Christensen, Freudenthal, Gidley, Rosenfeld, Boegli, Testino, Brine,Pitt& Wall,1971;Maltre,1971).Although there is some conflict in the reports of these effects, it seems that in moderate doses cannabis causes an increase in the levels of 5-hydroxy- tryptamine and a reduction in the turnover of both5-hydroxytryptamineandnoradrenaline.It was considered of interest, therefore, to determine

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