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猫视网膜缺血后充血:腺苷受体阻断的影响。

Post-ischemic hyperemia in the cat retina: the effects of adenosine receptor blockade.

作者信息

Roth S

机构信息

Department of Anesthesia and Critical Care, University of Chicago, IL 60637, USA.

出版信息

Curr Eye Res. 1995 Apr;14(4):323-8. doi: 10.3109/02713689509033533.

Abstract

Significant hyperemia results after 1 h of retinal ischemia in cats. Adenosine receptor blockade significantly attenuates the increase in retinal blood flow that occurs in response to systemic hypoxia. Synthesizing these findings, I hypothesized that adenosine receptor antagonism would attenuate the increase in blood flow that follows retinal ischemia. In these experiments, blood flows were measured with radioactively labeled microspheres in the retina and choroid of adult cats anesthetized with chloralose and acepromazine. Ischemia was induced for 1 h in both eyes by elevation of intraocular pressure above systolic arterial pressure. Blood flows were measured before ischemia and 5 min after the return of normal intraocular pressure. In each animal, after baseline blood flows were determined and approximately 10-15 min before ischemia was induced, one eye received 0.1 ml of intravitreal 0.01M 8-sulfophenyltheophylline, a polar adenosine receptor antagonist, while the opposite eye, the control, received an equal volume of intravitreal saline. Arterial blood gas tensions, systemic arterial pressure, hematocrit, and anesthetic level were kept constant during the experimental protocol. Compared with control eyes, hyperemia was significantly attenuated in the retinal circulation after ischemia in eyes injected with 8-sulfophenyltheophylline. Increase in post-ischemic choroidal blood flow was not affected. Although adenosine is involved in the vasodilatation that occurs when blood flow is restored after retinal ischemia, adenosine receptor blockade did not completely abolish hyperemia, implying that blockade was incomplete or other vasoactive substances also affect post ischemic hyperemia in the retina.

摘要

猫视网膜缺血1小时后会出现显著的充血。腺苷受体阻断可显著减弱因全身性缺氧而导致的视网膜血流量增加。综合这些发现,我推测腺苷受体拮抗作用会减弱视网膜缺血后血流量的增加。在这些实验中,用放射性标记的微球测量用氯醛糖和乙酰丙嗪麻醉的成年猫视网膜和脉络膜中的血流量。通过将眼内压升高至收缩期动脉压以上,使双眼缺血1小时。在缺血前和眼内压恢复正常后5分钟测量血流量。在每只动物中,在确定基线血流量后且在诱导缺血前约10 - 15分钟,一只眼睛接受0.1 ml玻璃体内注射的0.01M 8 - 磺苯基茶碱(一种极性腺苷受体拮抗剂),而对侧眼睛作为对照接受等量的玻璃体内生理盐水。在实验过程中,动脉血气张力、全身动脉压、血细胞比容和麻醉水平保持恒定。与对照眼相比,注射8 - 磺苯基茶碱的眼睛缺血后视网膜循环中的充血显著减弱。缺血后脉络膜血流量的增加未受影响。虽然腺苷参与了视网膜缺血后血流恢复时发生的血管舒张,但腺苷受体阻断并未完全消除充血,这意味着阻断不完全或其他血管活性物质也影响视网膜缺血后的充血。

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