대뇌혈류 완전차단시 경정맥혈액의 생화학적 기준치의 변화 : I. 뇌동맥류 출혈시 개의 경정맥혈액의 Lactate와 Lactate/Pyruvate값의 변화 Lactate and latate/pyruvate ratios of canine jugular venous blood following complete cerebral bloody-ischemia = Biochemical Alterations of Jugular Venous Blood after the Complete Cerebral Ischemia

국문 초록 (Abstract)

개를 뇌동맥류출혈과 유사한 상태로 대뇌혈류를 5분간 완전히 차단시킨 결과 다음과 같다.
1) 경정맥 혈중 lactate와 pyruvate는 post-ischemic insult후 24시간에 최고로 증가하였고(p<0.05) 신경증상이 심한 동물일 수록 증가폭은 컸다.
2) 심한 신경증상을 보였던 동물의 경정맥혈중 lactate는 72시간까지도 기준치보다 유의하게 높았으나 (p<0.05) pyruvate는 48시간 후부터 정상범위였다.
3) 모든 동물은 post-ischemic insult 24시간까지 채취한 동맥혈에서 호흡성 알카리증을 보였다(p<0.05).
4) Gas 분석으로 미루어 보면 72시간까지 혼수상태에 있던 동물에서도 luxury perfusion은 일으켰다는 증거는 없었다.
5) 경정맥혈의 lactate/pyruvate 비율은 postischemic insult 후48시간까지는 유의한 변화가 없다가 72시간에서 유의한 (p<0.05) 증가가 있었다.
6) 뇌동맥류 출혈과 유사한 상태로 대뇌혈류를 5분간 차단시켰을 때 미세순환계의 재관류장애현상을 볼 수 있었다.

다국어 초록 (Multilingual Abstract)

If in the aneurysmal rupture patients the brain metabolic parameters obtained from blood chemistry were significant and useful in clinical practice, it cannot be overestimated. Hansdo¨rfer et al. (1973) reported that lactate, pyruvate, uric acid and alpha-HBDH of central venous blood obtained from the patients with brain contusion in basal metabolic state were significantly increased and they were useful in evaluating the prognosis of the patients. Zooping (1970) and Broderson (1974) also had tried to evaluate the prognosis and brain metabolic status of the comatous patients with blood gas analysis and CSF biochemistry.
They encouraged us to estimate lactate and lactate/pyruvate ratios of canine jugular venous blood combined with gas analysis.
Complete cerebral bloody-ischemia similar with initial stage of aneurysmal rupture was induced by the instanteneous elevation, of intracranial pressure 30 ㎜Hg above systemic arterial pressure by infusion of blood and mock CSF mixture into the cisterna magna. The resultant vasopressor response was not modified and. the animals expired with cardiac arrest or pulmonary hypertension were discarded. At the end of the 5 minutes ischemic period, the needle tip which was inserted in to cisterna magna was removed without decreasing intracranial pressure. At 3 hours, 24 hours, 48 hours and 72 hours after ischemic period jugular venous and arterial blood were sampled for determination of lactate and pyruvate, and blood gas analysis.
The following results were obtained. ie;
1. Both lactate and pyruvate of canine jugular venous blood were increased from 3 hours and reached peak level at 24 hours after insult. Standard value of lactate and pyruvate were 1.416mM and 0.075mM and peak values were 2.429 and 0.l65mM. (P 0.05).
2. The more severe the neurological deficits of the animals, the higher levels of lactate and pyruvate were observed.
3. The lactate concentrations in 48 hours and 72 hours sample slopped down from 24 hours peak level but were significantly higher than those of standard.
4. Pyruvate returned to the normal range within 48 hours after insult.
5. L/P ratios were not changed significantly until 48 hours after insult but steeply elevated in 72 hours sample.
6. In gas analysis all the animals show respiratory alkalosis after insult.
7. In arterial Boundary zones multiple focal ischemia were found in necropsy which was thought as reflecting no-reflow phenomenon.
We concluded that elevation of lactate and pyruvate in early stage must be due to the hyperventilation after insult and lactate of late stage reflected CSF lactic acidosis.