1) 카드뮴(Cd) 중독가토(中毒家兎)의 전신동맥혈압(全身動脈血壓) 및 이곡혈관(耳穀血管)의 말초저항(末梢抵抗)은 비(非)중독 대조군에 비(比)하여 증가(增加)되었다. 2) Cd중독군 혈관의 전기자극 반응은 대조군혈관의 것에 비(比)하여 현저히 감약되어 있었다. 그러나 norepinephrine에 대(對)하여는 전자(前者)에서 super-sensitivity를 나타내었다. 3) Arachidonate에 의하여 전기자극반응이 대조군혈관에서는 억제되었으나 Cd중독군에서는 증가되었다. 그리고 PGE2 및 PGE2α에 의하여는 양군혈관 모두 반응이 억제되었다. 4. Indomethacin전처치 혈관은 대조군에서는 영향을 받지 않았으나 Cd중독군은 월등히 증가되었다. 5) 비(非)중독군 혈관을 PSS로 관류시는 전기자극반응이 영향을 받지 아니하였으나
1) Experiments were undertaken to elucidate the mechanism which elevates the systemic arterial blood pressure by cadmium (Cd). 2) The mean arterial pressure and peripheral resistance of central ear artery in Cd-poisoned rabbit were significantly increased in comparison with those in control. 3) The vascular pressure response to electrical stimulation in Cd-poisoned group was less than that in control. However, in the former group it showed the supersensitivity to norepinephrine. 4) The response to electrical stimulation was diminished by sodium arachidonate in the ear artery, on the contrary, it was rather enhanced in the vessel of Cd-poisoned group. The responses in both groups were reduced by pretreatment with either PGE2 or PGE2α. 5) The response to electrical stimulation was not affected in control, but enhanced in Cd-poisoned group by pretreatment with indomethacin. 6) When the ear artery of control group was perfused with physiological salt solution (PSS) the response to electrical stimulation was not changed by indomethacin, it was much enhanced without affecting on the response to norepinephrine when K+-free PSS, was used. These results demonstrate the evidence that the alteration of regulatory mechanism on the vessels was causally related to the elevation of arterial pressure and the increase in peripheral resistance in Cd-poisoned rabbits.
