MECHANISMS FOR VASOPRESSIN EFFECTS ON INTRAOCULAR-PRESSURE IN ANESTHETIZED RATS

Continuous intracameral infusions of a balanced salt solution (0.175 m u l min(-1)) have been reported to raise intraocular pressure (IOP) in anesthetized rats. Palm et al. (1995) previously reported that this e ffect was attenuated significantly by inclusion of arginine-vasopressi n (AVP, 10 ng 0.175 mu l(-1)) in the infusate. This study used experim ental and computer simulation methods to investigate factors underlyin g these changes in IOP. First, constant intracameral infusions of arti ficial cerebrospinal fluid (aCSF) at different fixed rates (0.049-0.35 mu l min(-1)) were used to estimate the outflow resistance. Secondly, IOP responses were measured during an 2 hr intracameral infusion of e ither aCSF or AVP that was the sum of a small constant component (0.05 mu l min(-1)) and a larger periodic component (0.25 mu l min(-1), cyc ling for 4 min on, then 4 min off); the mean infusion rate was 0.175 m u l min(-1). As shown previously for 0.175 mu l min(-1) constant infus ions, the periodic aCSF infusion induced a significant rise in IOP tha t was attenuated by AVP administration. Complex demodulation analysis and the estimated gain parameter of a second order transfer function f it to the periodic responses indicated that outflow resistance increas ed significantly during the infusions in both aCSF and AVP groups, but that the indices of resistance did not differ significantly between a CSF and AVP infused eyes. This finding implies that changes in outflow resistance do not explain the difference in IOP responses to intracam eral aCSF and AVP. The two responses differed significantly, though, i n damping factors, such that the aCSF responses were considerably more underdamped than the AVP responses. It is hypothesized that aCSF-indu ced increase in IOP reflects both (1) a small component reflecting inc reased outflow resistance and (2) a larger non-resistive component. Si nce the non-resistive component is insensitive to pretreatment with ac etazolamide, it is suggested that the aCSF-induced elevation in IOP re flects primarily vascular perfusion changes that are reduced by local vasoconstrictor actions of AVP. The latter mechanism likely maintains vascular perfusion of the globe when intraocular hypertension develops . (C) 1997 Academic Press Limited.