全身一氧化氮合酶抑制对常氧和高碳酸血症状态下视盘氧分压的影响。

Petropoulos Ioannis K, Pournaras Jean-Antoine C, Stangos Alexandros N, Pournaras Constantin J

Laboratory of Ocular Vascular Diseases, Faculty of Medicine, University of Geneva, Geneva, Switzerland.

Invest Ophthalmol Vis Sci. 2009 Jan;50(1):378-84. doi: 10.1167/iovs.08-2413. Epub 2008 Aug 1.

PURPOSE

To investigate the effect of systemic nitric oxide synthase (NOS) inhibition on optic disc oxygen partial pressure (PO(2)) in normoxia and hypercapnia.

METHODS

Intervascular optic disc PO(2) was measured in 12 anesthetized minipigs by using oxygen-sensitive microelectrodes placed <50 microm from the optic disc. PO(2) was measured continuously during 10 minutes under normoxia, hyperoxia (100% O(2)), carbogen breathing (95% O(2), 5% CO(2)), and hypercapnia (increased inhaled CO(2)). Measurements were repeated after intravenous injection of N(omega)-nitro-L-arginine methyl ester (L-NAME) 100 mg/kg. Intravenous L-arginine 100 mg/kg was subsequently given to three animals.

RESULTS

Before L-NAME injection, an increase was observed in optic disc PO(2) during hypercapnia (DeltaPO(2) = 3.2 +/- 1.7 mm Hg; 18%; P = 0.001) and carbogen breathing (DeltaPO(2) = 12.8 +/- 5.1 mm Hg; 69%; P < 0.001). Optic disc PO(2) in normoxia remained stable for 30 minutes after L-NAME injection (4% decrease from baseline; P > 0.1), despite a 21% increase of mean arterial pressure. Optic disc PO(2) increase under hypercapnia was blunted after L-NAME injection (DeltaPO(2) = 0.6 +/- 1.1 mm Hg; 3%; P > 0.1), and this effect was reversible by L-arginine. Moreover, L-NAME reduced the response to carbogen by 29% (DeltaPO(2) = 9.1 +/- 4.4 mm Hg; 49%; P = 0.01 versus before L-NAME). The response to hyperoxia was not affected.

CONCLUSIONS

Whereas systemic NOS inhibition did not affect optic disc PO(2) in normoxia, a blunting effect was noted on the CO(2)-induced optic disc PO(2) increase. Nitric oxide appears to mediate the hypercapnic optic disc PO(2) increase.

目的

研究全身一氧化氮合酶（NOS）抑制对常氧和高碳酸血症状态下视盘氧分压（PO₂）的影响。

方法

使用置于距视盘<50微米处的氧敏感微电极，对12只麻醉的小型猪的血管间视盘PO₂进行测量。在常氧、高氧（100% O₂）、卡波金呼吸（95% O₂，5% CO₂）和高碳酸血症（吸入CO₂增加）状态下，连续10分钟测量PO₂。静脉注射100 mg/kg Nω-硝基-L-精氨酸甲酯（L-NAME）后重复测量。随后给三只动物静脉注射100 mg/kg L-精氨酸。

结果

注射L-NAME前，高碳酸血症（ΔPO₂ = 3.2±1.7 mmHg；18%；P = 0.001）和卡波金呼吸（ΔPO₂ = 12.8±5.1 mmHg；69%；P < 0.001）期间视盘PO₂升高。尽管平均动脉压升高21%，但注射L-NAME后常氧状态下视盘PO₂在30分钟内保持稳定（较基线降低4%；P > 0.1）。注射L-NAME后高碳酸血症状态下视盘PO₂升高减弱（ΔPO₂ = 0.6±1.1 mmHg；3%；P > 0.1），且L-精氨酸可使此效应逆转。此外，L-NAME使对卡波金的反应降低29%（ΔPO₂ = 9.1±4.4 mmHg；49%；与注射L-NAME前相比，P = 0.01）。对高氧的反应未受影响。