Panchal Shital S, Mehta Anita A, Santani Devdas D
Department of Pharmacology, Institute of Pharmacy, Nirma University, Ahmedabad 382481, Gujarat, India.
Department of Pharmacology, L.M. College of Pharmacy, Navarangpura, Ahmedabad 9, Gujarat, India.
Taiwan J Ophthalmol. 2016 Jul-Sep;6(3):131-135. doi: 10.1016/j.tjo.2016.05.006. Epub 2016 Jun 20.
Glaucoma is characterized by increased intraocular pressure (IOP). The effect of nicorandil and pinacidil on IOP in experimentally induced acute and chronic models of glaucoma and the mechanism of action involved were studied.
New Zealand white rabbits were used for the study. After the measurement of IOP, nicorandil (1%), pinacidil (1%), and pilocarpine as standard (1%) were instilled topically into the left eye. The other eye served as control. Dextrose (5%) was used to induce acute glaucoma. IOP changes were recorded every 15 minutes until the pressure became normal. Freshly prepared α-chymotrypsin solution was introduced in the posterior chamber to induce chronic glaucoma. Rabbits with ocular hypertension were selected for the study. Similar drug solutions were used to study the effect on IOP. Glibenclamide, pilocarpine, and indomethacin (1%) were used to study the mechanism of action of both drugs. The IOPs were measured just prior to drug instillation and at suitable time intervals using a tonometer.
Pretreatment with topical nicorandil and pinacidil significantly lowered the rise in IOP in the acute model. Nicorandil and pinacidil initially caused rise in IOP for 15-30 minutes in chronic glaucoma. This was followed by reduction in IOP. Pretreatment with indomethacin and pilocarpine did not modify the effect of nicorandil and pinacidil on IOP. Pretreatment with glibenclamide blocked IOP from the lowering effect of nicorandil and pinacidil.
The oculohypotensive effect shown by these drugs appears to be attributable to enhancement of the aqueous humor outflow. This effect is perhaps mediated through potassium channels.
青光眼的特征是眼内压（IOP）升高。研究了尼可地尔和平卡地尔对实验性诱导的急性和慢性青光眼模型中眼内压的影响及其作用机制。
使用新西兰白兔进行研究。测量眼内压后，将1%的尼可地尔、1%的平卡地尔和作为标准的1%毛果芸香碱局部滴入左眼。另一只眼作为对照。用5%葡萄糖诱导急性青光眼。每隔15分钟记录眼内压变化，直至眼压恢复正常。将新制备的α-糜蛋白酶溶液注入后房诱导慢性青光眼。选择高眼压兔进行研究。使用类似的药物溶液研究对眼内压的影响。用格列本脲、毛果芸香碱和1%吲哚美辛研究两种药物的作用机制。在滴药前及适当的时间间隔使用眼压计测量眼内压。
局部应用尼可地尔和平卡地尔预处理可显著降低急性模型中眼内压的升高。在慢性青光眼中，尼可地尔和平卡地尔最初会使眼内压在15 - 30分钟内升高，随后眼内压降低。用吲哚美辛和毛果芸香碱预处理不会改变尼可地尔和平卡地尔对眼内压的影响。用格列本脲预处理可阻止尼可地尔和平卡地尔的降眼压作用。
这些药物显示的降眼压作用似乎归因于房水流出增加。这种作用可能是通过钾通道介导的。
