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E. C. Delgado, C. Marques-Neves, I. Rocha, J. Sales-Luis, L. Silva-Carvalho; Effects of Amlodipine in an Experimental Model of Isolated Rabbit Eye. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2289.
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To characterize the reactivity of rabbit ocular vasculature to amlodipine, a calcium channel blocker, in a rabbit model of isolated eye circulation.
Rabbit external ophthalmic arteries (n=12) were cannulated and perfused with warmed tyrode. The three way polypropylene catheter was further connected to a continnuous infusion pump and to a pressure transducer, and the effect of intraluminal pressure as a measure of total vascular resistance was assessed. In group A (n=6) two intraarterial injections of amlodipine (3 mg/ml) followed by phenylephrine (250 µg/ml) were done. In group B (n=6) two intraarterial injections of ET-1 (27 µg/ml) followed by amlodipine (3 mg/ml) were performed. Changes on perfusion pressure between control values and the maximum value on chemical stimulation were evaluated. For statistical analysis the paired t-test was used and differences considered significant when p<0.05. Fast Fourier Transform was also applied to analyze the frequency components of the perfusion pressure signal.
Without any drug administration intrinsic vasomotricity was observed in the 12 rabbit models. The medium frequency of the oscillations was 0.06 Hz (SEM 0.012) and the medium amplitude was 1.2 mm Hg (SEM 0.012). In group A amlodipine elicited vasodilation and both frequency and amplitude of the oscillations decreased. In group B ET-1 induced a strong and long lasting vasoconstritor tone. Vasomotricity became more evident, showing a higher frequency and amplitude of the oscillations. With amlodipine we obtained vasodilation and a notable decrease in frequency and amplitude of the oscillations.
Amlodipine acted as a vasodilator of ocular vasculature and decreased intrinsic vasospasm in our experimental model. Intraarterial ET-1 increased vascular resistance and caused a faster rate of pulsatility in external ophthalmic artery and its collaterals in the isolated rabbit eye. With amlodipine after ET-1 vascular resistance decreased and intrinsic vasomotricity became less evident which might indicate a protective action against vasospasm. Since the neural control was abolished by death, it proves that vasoactive responses to amlodipine and ET-1 are independent of central and autonomic regulation and due to local mechanisms. Frequency-domain analysis of intraarterial pressure using the Fast Fourier Transform was found to be valuable for quantifying the patterns of intrinsic vasomotricity.
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