犬カオリン水頭症における髄液中Atrial Natriuretic Peptideおよびcyclic GMPの経時的変動

Alteration of Atrial Natriuretic Peptide and Cyclic GMP in Cerebrospinal Fluid in Canine Kaolin-induced Hydrocephalus

　犬カオリン水頭症モデルを用いて水頭症の進行形成過程における髄液中Atrial Natriuretic Peptide（ANP）とそのセカンドメッセンジャーであるcGMP濃度および髄液圧を経時的に測定し，カオリン注入前，急性期（2週以内），慢性期（3,4週）に分けて評価した。急性期では髄液中ANP, cGMP濃度および髄液圧は注入前より有意に上昇した。慢性期では髄液中ANP濃度，髄液圧は注入前との有意差はなくなり，髄液中cGMP濃度は有意な高値を持続した。髄液中Na濃度，浸透圧は経過を通して有意な変動を示さなかった。髄液中ANP濃度と髄液圧には有意な順相関を認めた。髄液中cGMP濃度と髄液中ANP濃度，髄液中cGMP濃度と髄液圧には有意な相関はなかった。以上より，水頭症急性期の髄液中ANP濃度は髄液圧と平行して変動する傾向が示唆されたが，脳室拡大の程度や血清Na濃度との関連は明らかではなかった。水頭症における髄液中cGMP濃度の変動は髄液中ANP濃度に依存せず，他の因子により強く依存する事が示唆された。

CSF and Plasma concentrations of atrial natriur-etic peptide (ANP) and cyclic GMP (cGMP), which is regarded as a second messenger of ANP, were measured intermittently during the progress of canine kaolin-induced hydrocephalus. Data were analyzed being divided into three groups, normal, acute (within 2 weeks after intracisternal injection of kaolin suspension) and chronic (from 3 to 4 weeks after injection of kaolin suspension) stages of hydrocephalus. The presence of venricular dilata-tion was evaluated by MRI or postmortal dissection. ANP, cGMP in CSF and CSF pressure significantly increased in the acute stage of hydrocephalus. In the chronic stage, ANP in CSF and CSF pressure had no statistical difference with data of the normal stage. Cyclic GMP in CSF kept significantly high value in the chronic stage of hydrocephalus. CSF concentra-tions of Na, CSF osmolarity, plasma ANP, plasma cGMP, plasma ADH, serum Na and serum osmola-rity did not change significantly in the course of hydrocephalus. There was a significant positive correlation between ANP in CSF and CSF pressure. ANP in CSF did not correlate with degree of ventricular dilatation. Cyclic GMP in CSF did not correlate with ANP in CSF, nor with CSF pressure. These data suggest that concentration of ANP in CSF may alter directly or indirectly depending on CSF pressure in kaolin-induced hydrocephalus. And cGMP in CSF was suggested to depend not on ANP in CSF, but on other unknown factors in kaolin-induced hydrocephalus.