Biochemical Alterations of Jungular Venous Blood after the Complete Cerebral Ishemia: Lactate and Latate/Pyruvate Ratios of Canine Jugular Venous Blood following Complete Cerebral Bloody-ischemia.
- Author:
Joo Myung KIM
1
;
Soon Guan CHOI
;
Duck Young CHOI
;
Kwang Seh RHIM
Author Information
1. Department of Neurosurgery, College of Medicine, Chung-Ang University, Korea.
- Publication Type:Original Article
- MeSH:
Acidosis, Lactic;
Alkalosis, Respiratory;
Aneurysm;
Animals;
Arterial Pressure;
Biochemistry;
Blood Gas Analysis;
Brain;
Brain Injuries;
Chemistry;
Cisterna Magna;
Humans;
Hypertension, Pulmonary;
Hyperventilation;
Intracranial Pressure;
Ischemia;
Lactic Acid*;
Needles;
No-Reflow Phenomenon;
Prognosis;
Pyruvic Acid;
Reference Values;
Rupture;
Uric Acid
- From:Journal of Korean Neurosurgical Society
1977;6(2):311-320
- CountryRepublic of Korea
- Language:Korean
-
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 overstimated. Hansdorfer er al.(1973) reported that lactate, pyruvate, uric acid and alpha-HBDH of central venous blood obtained form 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 mmHg above systemic arterial pressure by infusion of blood and mock CSF mixture into the cisterna 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 0.165mM(P<0.05). 2. The more severe the neurological deficits of the animals, the highest 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.
