Zhu Y, Gidday J M
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Invest Ophthalmol Vis Sci. 1996 Jan;37(1):86-92.
To determine whether retinal blood flow increases in response to perinatal hypoglycemia and whether the vasodilator adenosine is involved in mediating the hyperemic response.
Retinal fluorescein videoangiography was undertaken in intact eyes of isoflurane-anesthetized piglets using intracarotid injections of sodium fluorescein. Angiograms were recorded to videotape and analyzed off-line by image analysis software to determine stimulus-induced changes in mean arteriovenous transit times, and arteriolar and venular diameters, from which retinal blood flow was calculated. Two groups of animals were rendered hypoglycemic (blood glucose = 19 +/- 1 mg/dl) by insulin (25 IU/kg, intravenously), and angiograms were obtained at 10-minute intervals for 0.5 hour of hypoglycemia. One group (n = 5) served as controls. In the other (n = 5), the nonspecific adenosine receptor antagonist 8-phenyltheophylline (8PT) was administered intravenously approximately 15 minutes before hypoglycemia to examine the role of adenosine in the hemodynamic response to hypoglycemia.
Acute hypoglycemia was associated with an increase in mean retinal blood flow of 94 +/- 18% (P < 0.002). However, in animals pretreated with 8PT, this hyperemic response was severely attenuated, primarily by an effect on arteriovenous transit time. In these latter animals, mean retinal blood flow only increased 19 +/- 10% in response to hypoglycemia (P = 0.13 versus normoglycemic baseline; P = 0.007 versus untreated hypoglycemic animals). All other hemodynamic variables were similar between animal groups.
Acute hypoglycemia causes a compensatory increase in retinal blood flow in the perinatal period. Because the adenosine receptor antagonist 8PT attenuated this hyperemic response, it is concluded that adenosine is involved in eliciting the increase in retinal blood flow that accompanies hypoglycemia.
确定围产期低血糖时视网膜血流量是否增加，以及血管舒张剂腺苷是否参与介导充血反应。
对异氟烷麻醉的仔猪的完整眼睛进行视网膜荧光血管造影，通过颈内动脉注射荧光素钠。将血管造影记录到录像带上，并通过图像分析软件离线分析，以确定刺激引起的平均动静脉通过时间、小动脉和小静脉直径的变化，据此计算视网膜血流量。两组动物通过静脉注射胰岛素（25 IU/kg）使其血糖降低（血糖 = 19 ± 1 mg/dl），在低血糖持续0.5小时期间，每隔10分钟获取一次血管造影图像。一组（n = 5）作为对照。另一组（n = 5）在低血糖发生前约15分钟静脉注射非特异性腺苷受体拮抗剂8-苯基茶碱（8PT），以研究腺苷在低血糖血流动力学反应中的作用。
急性低血糖与视网膜平均血流量增加94 ± 18%相关（P < 0.002）。然而，在预先用8PT处理的动物中，这种充血反应严重减弱，主要是对动静脉通过时间的影响。在这些动物中，视网膜平均血流量对低血糖的反应仅增加19 ± 10%（与正常血糖基线相比，P = 0.13；与未处理的低血糖动物相比，P = 0.007）。动物组之间的所有其他血流动力学变量相似。
围产期急性低血糖导致视网膜血流量代偿性增加。由于腺苷受体拮抗剂8PT减弱了这种充血反应，得出结论：腺苷参与引发低血糖时伴随的视网膜血流量增加。
