Kiel J W
Department of Ophthalmology, University of Texas Health Science Center, San Antonio 78284.
Exp Eye Res. 1994 May;58(5):529-43. doi: 10.1006/exer.1994.1047.
This study tests the hypothesis that choroidal myogenic autoregulation participates in the intraocular pressure (IOP) response to mean arterial pressure (MAP) by minimizing arterial-pressure-dependent changes in choroidal blood volume. To test this hypothesis, the IOP response to MAP was quantified before and after impairing choroidal autoregulation. In a previous study, the efficacy of choroidal myogenic autoregulation was inversely related to IOP. Therefore, in one series of experiments (n = 6), the relationship between MAP and IOP was determined at normal and elevated baseline IOP (i.e., 15 and 25 mmHg, respectively). In a second series of experiments (n = 6), the relationship between MAP and IOP was determined at the normal IOP (15 mmHg) before and after administering hydralazine, an arterial vasodilator. In both series, the MAP manipulations were kept brief to avoid the confounding effects of aqueous compensation. The experiments were performed in pentobarbital anesthetized rabbits with hydraulic occluders placed on the thoracic descending aorta and inferior vena cava to raise and lower MAP, respectively. MAP was measured via a central ear artery catheter. The right eye was cannulated with two 23 gauge needles; one cannula was used to set the IOP by varying the ocular volume and the other was used to measure the IOP. The protocol consisted of inflating the occluders to cause brief (1-1.5 min) ramp increases and decreases in MAP over a wide pressure range. Baseline IOP was set prior to each occlusion, but was otherwise uncontrolled. In the first series, the MAP range was 30 to 95 mmHg and IOP changed by 6 mmHg at the normal baseline IOP and by 18 mmHg at the elevated baseline IOP. The corresponding volume shifts were 7.7 and 14.5 microliters, respectively. In the second series, the MAP range was 25 to 95 mmHg and IOP changed by 6 mmHg during control and by 14 mmHg after hydralazine. The corresponding volume shifts were 6.7 and 13.8 microliters, respectively. In both series, the prompt return of IOP to baseline upon restoration of normal MAP indicated that the volume changes were due to changes in ocular blood volume. Additional experiments confirmed that elevating the baseline IOP and administering hydralazine impaired choroidal autoregulation but did not alter the cranial venous pressure response to varying MAP.(ABSTRACT TRUNCATED AT 400 WORDS)
脉络膜肌源性自身调节通过最小化脉络膜血容量中依赖动脉压的变化,参与眼内压(IOP)对平均动脉压(MAP)的反应。为验证这一假设,在损害脉络膜自身调节之前和之后,对IOP对MAP的反应进行了量化。在先前的一项研究中,脉络膜肌源性自身调节的功效与IOP呈负相关。因此,在一系列实验(n = 6)中,分别在正常和升高的基线IOP(即分别为15和25 mmHg)下测定MAP与IOP之间的关系。在另一系列实验(n = 6)中,在给予动脉血管扩张剂肼苯哒嗪之前和之后,于正常IOP(15 mmHg)下测定MAP与IOP之间的关系。在这两个系列实验中,对MAP的操作均保持短暂,以避免房水代偿的混杂效应。实验在戊巴比妥麻醉的兔子身上进行,分别在胸段降主动脉和下腔静脉放置液压闭塞器以升高和降低MAP。通过中心耳动脉导管测量MAP。右眼用两根23号针头插管;一根插管用于通过改变眼内容积来设定IOP,另一根用于测量IOP。实验方案包括充气闭塞器,使MAP在较宽的压力范围内短暂(1 - 1.5分钟)呈斜坡式上升和下降。每次闭塞前设定基线IOP,但其他方面未进行控制。在第一系列实验中,MAP范围为30至95 mmHg,在正常基线IOP时IOP变化6 mmHg,在升高的基线IOP时IOP变化18 mmHg。相应的容积变化分别为7.7和14.5微升。在第二系列实验中,MAP范围为25至95 mmHg,在对照期间IOP变化6 mmHg,在给予肼苯哒嗪后IOP变化14 mmHg。相应的容积变化分别为6.7和13.8微升。在这两个系列实验中,当恢复正常MAP时IOP迅速恢复到基线,表明容积变化是由于眼血容量的变化所致。额外的实验证实,升高基线IOP和给予肼苯哒嗪会损害脉络膜自身调节,但不会改变颅内静脉压对不同MAP的反应。(摘要截取自400字)