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ARTICLES
Year : 1975  |  Volume : 23  |  Issue : 1  |  Page : 22-24

Modulations in intraocular pressure under ketamine anaesthesia


1 Department of Pharmacology, Dr. V.M. Medical College, Sholapur, India
2 Department of physics, Dr. V.M. Medical College, Sholapur, India
3 Department of Ophthalmology, Dr. V.M. Medical College, Sholapur, India

Correspondence Address:
A G Chandorkar
Department of Pharmacology, Dr. V.M. Medical College, Sholapur
India
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Source of Support: None, Conflict of Interest: None


PMID: 1158418

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How to cite this article:
Chandorkar A G, Jain P K, Albal M V. Modulations in intraocular pressure under ketamine anaesthesia. Indian J Ophthalmol 1975;23:22-4

How to cite this URL:
Chandorkar A G, Jain P K, Albal M V. Modulations in intraocular pressure under ketamine anaesthesia. Indian J Ophthalmol [serial online] 1975 [cited 2020 Sep 19];23:22-4. Available from: http://www.ijo.in/text.asp?1975/23/1/22/31336

Table 1

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Table 1

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Ketamine (CI-581), a phencyclidine com­pound used as a new short acting intravenous or intramuscular anaesthetic agent, produces a "Dissociative" anaesthesia by affecting different cortical and subcortical areas. It possesses significant sympathomimetic and adrenocortical stimulant effects and is known to cause slight hypertensive reaction in patients under anaes­thesia.

Corssen and Hoy [4] studied its effect on intra­ocular pressure in 46 patients of various ages and have reported that unlike conventional anaesthetic agents, this drug causes a slight rise in intraocular pressure. This rise was not related to either the age of the patient or to the changes in his systemic blood pressure.

In our preliminary study of effects of Ketamine on physiological functions in human beings, we found a significant rise in intraocular pressure [3] . As the ocular anatomy and physio­logy of rabbits shows close resemblance to that of man, the present study vas undertaken to confirm the effect of Ketamine on intraocular pressure in rabbits and to study its mechanism of action, if possible.


  Methods and Result Top


Rabbits of both sexes weighing an average of 2.0 kg were used for the experiments. They exhibited no pathological condition in the eyes and their tonometric values taken after the usual technique of topical anaes­thesia (0.4% Benoxinate hydrochloride) were within normal limits.

The intraocular pressure was measured with a Schiotz tonometer with 5.5 g. weight, by the same observer and by the same instrument through out the entire study. The data was calculated by using Fried­enwald's Tables (1955).

The readings were taken before and after applica­tion of the topical anaesthesia which produced no change in intraocular pressure, and immediately after induction of anaesthesia by intra venous injection of 2, 4, and 8 mg/kg of Ketamine and after every one minute upto the arousal of animal.

The results are shown in [Table - 1]. The intraocular pressure always decreased rapidly by 2 to 8 mm. of Hg below the control values after 2 min. of induction in the rabbits which received 2 mg/kg of Ketamine intraven­ously. The mean decrease was 6.5±0.2 mm of Hg. This fall was maintained upto 6 min. and then it grad­ually returned back to the normal control values by the end of 10 min. An increase in dose to 4 mg/kg increased the extent of the mean fall by 4 mm. (10.5j--0.12 mm of Hg) at 2 min. and the effect lasted slightly longer (12 min.). The dose of 8 mg/kg, how­ever, did not increase this response either in extent or in duration than that seen with a dose of 4 mg/kg.

Increase in dose of Ketamine from 4 mg. to 8 mg/kg did not alter the plane of anaesthesia, however, the duration of anaesthesia was slightly prolonged (18 to 20 min) than with 4 mgikg dose (12 to 15 min).


  Conclusions and Discussion Top


Ketamine (2mg/kg) produced a rapid decre­ase in intraocular pressure varying from 2-8 mm of Hg. for about 7 to 8 min. which gradually returned to normal control values by 10 to 12 min. These findings are in conformity with those of Prete at el [9] who observed a fall of 2-8 mm of Hg lasting for 7 min. in 2 nag/kg dose. However, we have observed a greater fall of 8-16 mm of Hg in the intraocular pressure with increase in the dose of Ketamine to 4 mg/kg. anaesthetic agents like ether and cyclopropane cause lesser or greater modification depending upon the plane of anaesthesia. It is usually observed that under light Ketamine anaesthesia the extrinsic muscles of the eyes may be stimu­lated tending to increase the intraocular pres­sure [3],[4],[11] and that only the intra venous admi­nistration of a single dose of 3 mg-4 mg/kg of Ketamine makes it possible to obtain a suffici­ently deep plane of anaesthesia (Ketamine pro­duced more fall in intraocular pressure with increase in the dose) therefore it seems that the decrease in the intraocular pressure is in same way dependent on the depth of anaesthesia and can be modified by increase in the dose.

Stimulation of cervical sympathetic trunk induces a persistent reduction in intraocular pressure [8] , a reaction accompanied some times but not always by a rise in the resistance to aqueous outflow [2] . It would seem likely that the fall in the pressure is due to a reduction in the rate of formation of aqueous following vasoconstriction in the ciliary process [7] . In the rabbit sympathetic stimulation causes a predominant vasoconstrictor response and a fall in intraocular pressure [5].

Ketamine causes sympathetic stimulation. Takki et al [10] and Dundee and associates [6] have reported it to cause an increase in blood cate­cholamine levels. Both adrenaline, noradrenalin and total catecholamines were increased, even to the extent of 50%. Hence it could be presumed that this Ketamine induced catechola­mine release might be causing vasoconstriction of ocular blood vessels, thus reducing the for­mation of aqueous humour. This may ultima­tely be responsible for the Transient reduction in the intraocular pressure.

The small decrease (2 mm) in intraocular pressure seen in some animals may be due to the result of summation of increased intraocular pressure due to stimulation of extra-ocular muscle and decrease in intraocular pressure due to vasoconstriction of ocular blood vessels. Increase in the dose of Ketamine may be pro­ducing an absolute absence of myocontractile stimuli on extrinsic muscles of the eyes by having a depressant action on corticothalamic pathways influencing the postulated diencephalic regulatory centres of intraocular pressure [1] in addition to the vasoconstriction of ocular blood vessels, thus producing a greater decrease in intraocular pressure than seen with 2 mg/kg dose of ketamine.


  Summary Top


Effect of Ketamine a "dissociative anaes­thetic agent" was studied on intraocular pressure in rabbits by using Schiot'z tonometer. A transient fall of 2-8 mm of Hg, (mean 6.5±0.2) was observed for about 6-8 min. with 2 mg/kg dose. An increase in dose to 4 mg/kg. produced a greater fall of 8 to 16 mm. (mean 10.5±0.12). A dose of 8 mg/kg, however, did not produce further reduction in the intraocular pressure.

The mechanism of this reduction seems probably due to vasoconstriction of ocular blood vessels leading to the decreased formation of aqueous and relaxation of extrinsic muscles of the eye due to depression on corticothalamic pathways and diencephalic regulatory centres of intraocular pressure or both.


  Acknowledgement Top


We are grateful to Dean, Dr. V.M. Medical, Sholapur for the facilities given to undertake this work and to Dr. R.J. Modi of Parke-Davis (India) Ltd., for the liberal supply of Ketamine.

 
  References Top

1.
Alajmo, B. and Rubino, A., 1952; Oculodience­phalic physio-pathology and clinical aspects. Tip. Ariani, Florence.  Back to cited text no. 1
    
2.
Casey., 1966; Invest. Ophthal. 5, 33. Quoted by Duke-Elder, in Ref. 5. S. 1968.  Back to cited text no. 2
    
3.
Chandorkar, A.G. Jain, P.K. Bulakh, P.M. Reddy, B.V. Albal, M.V., 1974; proc. of the International Union of Physiol Sci. XXVI International Congress New-Delhi, 11, 307.  Back to cited text no. 3
    
4.
Corssen, G. and Hoy, H.E., 1967; J. Pediat. ophthal. 4, 200-203.  Back to cited text no. 4
    
5.
Duke-Elder, S., 1968; System of ophthalmology 4, 297. Henry Kimpton, London.  Back to cited text no. 5
    
6.
Dundee, J.W. Bovill, J.G. Clarke, R.S. J., and Pandit, S.K., 1971; Anaesthesia. 26, 86.  Back to cited text no. 6
    
7.
Langham, M.E., and Rosenthal, A.R., 1966: Amer. J. Physiol. 210, 786.  Back to cited text no. 7
    
8.
Paterson., 1966; Exp. Eye Res. 5, 37. Quoted by Duke-Elder, S. 1968; System of ophthalmology, 4, 297 Henry Kimpton. London.  Back to cited text no. 8
    
9.
Prete, C. Del. Friedmann, E. Vergano, F., 1969; Minerva Anesthesiologiea. 35(1) 105.  Back to cited text no. 9
    
10.
Takki, S. Nikki, P. Jaattela, A., and Taumisto, T., 1972, Brit. J. Anaesth. 44, 1318.  Back to cited text no. 10
    
11.
Yoshikawa, K. and Murai, Y., 1971, Anasth. Analg. 50, 199.  Back to cited text no. 11
    



 
 
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