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S. Nakabayashi, T. Nagaoka, T. Tani, K. Sogawa, A. Yoshida; Retinal Artery Response to Acute Extreme Blood Pressure Elevation With Inflation of Balloon Catheter in Cats. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5009.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate whether nitric oxide (NO) regulates retinal circulation during acute increases in systemic blood pressure in cats.
NG-nitro-L-arginine-methylester (L-NAME, n=5), a NOS inhibitor; or phosphate-buffered saline (PBS, n=5) was injected intravitreously. Arterial hypertension was induced for 5 minutes with inflation of a balloon catheter in the descending aorta. The vessel diameter (D) and blood velocity (V) were measured simultaneously in the first-order retinal arterioles by laser Doppler velocimetry (CLBF model 100, Canon) every minute. The retinal blood flow (RBF) was calculated, and the mean arterial blood pressure (MABP) was measured during inflation of the balloon catheter.
In the PBS group, the MABP and V immediately increased and reached the highest level 3 to 4 minutes after the beginning of inflation (mean±SE, 89.0±8.4% and 39.9±8.9%, respectively). The D decreased at 2 minutes but returned to the baseline value (-6.1±1.9%; p<0.01) 3 to 5 minutes after inflation. The RBF first increased (29.4±4.6%, p<0.01) at 1 minute but returned to the baseline value at 2 minutes. The RBF again started to increase at 3 minutes, and the increase was maintained at the end of inflation. In the L-NAME group, the MABP (70.8±6.3%, p<0.01) and V (24.7±6.9%; p<0.01) increased similarly to the PBS group. The D decreased at 1 minute and reached the lowest level (-9.2±2.5%; p<0.01) at 2 minutes. The D was maintained at the lower value for 3 to 5 minutes of the inflation. In contrast to the PBS group, the RBF did not change during inflation. The D and RBF in the L-NAME group were significantly lower than in the PBS group at 1, 4, and 5 minutes after inflation.
These results indicated that the retinal arterioles constrict first by a myogenic response in the early phase of an extreme increase in blood pressure and then dilate by the release of NO probably from the endothelium. These finding also suggested that flow-induced vasodilation may overcome the myogenic contraction resulting in increased RBF out of the range of autoregulation in response to acute extreme increases in RBF.
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