頭蓋内圧亢進時における脳血流障害の研究—特に静脈側の血流動態について

CIRCULATORY DISTURBANCE OF THE VENOUS SYSTEM UNDER INTRACRANIAL HYPERTENSION

緒言

　外傷性頭蓋内血腫，脳腫瘍，高血圧性脳内血腫等によつて発生する急性頭蓋内圧亢進は，しばしば急激に致命的な障害を引き起こす為，脳神経外科領域の最も重要な問題の1つになつている。かかる種々の病変により，頭蓋内圧がある程度以上になると，脳血流量が減少する事は，笑気法^1），電磁血流計^2）等による臨床例，電磁血流計^3）−5），熱電対法^6）7），ラジオアイソトープ法^8）による動物実験により，既に広く知られている。しかしながら，頭蓋内圧亢進時，どのような機序で脳血流量の減少は引き起こされるのか，あるいは，脳血流量の減少を引き起こす原因は，頭蓋内血流系路のどの部分に存在するのか，といつた問題についての報告は少なく，未だ十分に解明されていないのが現状である。

　この問題に関するこれまでの動物実験を主にした報告をみてみると，頭蓋内圧亢進時の脳血流量減少の原因として，頭蓋内静脈血流路の狭窄を指摘し^{9）−16）7）}，狭窄部位としては，脳表静脈より上矢状静脈洞への移行部が疑わしい^{10）11）7）}，と想定している報告はあるが，これを実際に証明しえた報告はみあたらない。

Although many authors have suggested vascular congestion as a cause of "reduction of cerebral blood flow with increase of cerebral blood volume" under increased intracranial pressure, exact mecha-nism of the congestion is still remaining obscure at present. This experiment was designed to find out exact site of vascular stenosis which produced the vascular congestion, and further, to clarify thg mechanism of such stenosis under increased intra-cranial pressure.

(1) Method : Using adult mongrel dogs, cortical venous pressure including pressure of bridging vein, cortical arterial pressure and superior sagittal sinus pressure were measured by cannulating small cali-bred (0.3-1.0 mm in outer diameter) polyethylene tube, The intracranial pressure was elevated by inflating rubber baloon placed in the epidural space. Pressures of above mentioned vessels, systemic blood pressure and intracranial pressure were measured by standard pressure transducer, and were monitored by ink writing oscillograph.

Collapsibility of the parasagittal intradural venouschannels (lateral lacuna of the superior sagittal sinus) were also investigated by measuring flow rate through these portions under increasing in-tracranial pressure.

(2) Results : The cortical venous pressure includ-ing pressure of bridging vein was constantly 50-200 mm H₂O higher than intracranial pressure, regardless of the level of intracranial pressure. This relationship was maintained until the intra-cranial pressure was elevated higher than the cortical arterial pressure. In contrast to the cortical venous pressure, superior sagittal sinus pressure was quite stable at the level of 50-75 mm H₂O unless the intrathoracic pressure was elevated by respiratory disturbances. The cortical arterial pressure somewhat elevated as a reflection of the systemic blood pressure by intracranial hyper-tension.

As to the collapsibility of the venous pathways, the lateral lacuna was gradually compressed by increasing intracranial pressure.

(3) Conclusions :

1) By gradually increased pressure gradient be-tween superior sagittal sinus and cortical vein in-cluding bridging vein under intracranial hyper-tension and collapsibility of the lateral lacuna, it is concluded that the constriction of vascular system takes place in the lateral lacuna of the superior sagittal sinus. As the results of the lacuna, cortical venous pressure is constantly main-tained 50-200 mm H2O higher than intracranial pressure, and thus the cortical veins are protected from compression by increased intracranial pressure.

The authors propose to name this mechanism as "intracranial venous pressure regulation mecha-nism".

2) As elevation of cortical arterial pressure is slight in degree as compared with that of cortical venous pressure under intracranial hypertension, pressure gradient between cortical arteries and veins gradually decreases as the intracranial pres-sure elevates. Thus, this mechanism is the main factor to cause decrease in cerebral blood flow and increase in cerebral blood volume, and as a result, this phenomenon accelerates further elevation of the intracranial hypertension.