TY - JOUR
T1 - Near infrared spectroscopic monitoring of secondary cerebral energy failure after transient global hypoxia-ischemia in the newborn piglet
AU - Chang, Yun Sil
AU - Park, Won Soon
AU - Lee, Munhyang
AU - Kim, Ki Soo
AU - Shin, Son Moon
AU - Choi, Jung Hwan
PY - 1999
Y1 - 1999
N2 - The present study was done to establish whether the secondary cerebral energy failure could be reproduced in the newborn piglet subjected to transient global hypoxia-ischemia, and whether the evolution of secondary cerebral energy failure could be monitored by measuring the changes of Cyt aa3 using NIRS. Fifteen anesthetized, ventilated newborn piglets (< 3 day) were divided into 2 groups. Eight of hypoxia-ischemia (HI) group were induced transient HI by breathing 8% oxygen and complete occlusion of bilateral common carotid arteries for 30 min followed by release of occluders and reoxygenation and maintained for up to 48 h. Seven were given sham operation and maintained for 48 h also. Monitoring of cerebral Hb, HbO, HbT and Cyt aa3 were continued throughout the experiment using near infrared spectroscopy. Na+, K+-ATPase activity, lipid peroxidation products (conjugated dienes), tissue high energy phosphates (ATP and phosphocreatine) levels and brain glucose and lactate levels were determined blocheroically in the cerebral cortex harvested at the termination of experiment. HbT as an index of a cerebral blood volume increased at 2 h after resuscitation significantly in HI group. During hypoxiaischemia Cyt aa3 fell to -2.0 ± 0.5 μ l-1 (p < 0.01), returned to baseline on resuscitation, but decreased again progressively from 33 h, and finally fell to -2.2 ± 0.9 μmol l-1 (p < 0.01) at 48 h in spite of normal physiologic values. There were no changes in control animals. Cerebral level of ATP and PCr in HI group decreased significantly compared to control and ATP concentrations were correlated with the final levels of Cyt aa3. In HI group, cerebral Na+, K+-ATPase activity decreased, but the cerebral level of conjugated dienes, glucose, lactate was not different compared to controls. These findings suggest that secondary cerebral energy failure was successfully reproduced in the newborn piglets after transient hypoxia-ischemia and the continuous in vivo NIRS monitoring can be used as a useful tool for the monitoring of delayed cerebral injury.
AB - The present study was done to establish whether the secondary cerebral energy failure could be reproduced in the newborn piglet subjected to transient global hypoxia-ischemia, and whether the evolution of secondary cerebral energy failure could be monitored by measuring the changes of Cyt aa3 using NIRS. Fifteen anesthetized, ventilated newborn piglets (< 3 day) were divided into 2 groups. Eight of hypoxia-ischemia (HI) group were induced transient HI by breathing 8% oxygen and complete occlusion of bilateral common carotid arteries for 30 min followed by release of occluders and reoxygenation and maintained for up to 48 h. Seven were given sham operation and maintained for 48 h also. Monitoring of cerebral Hb, HbO, HbT and Cyt aa3 were continued throughout the experiment using near infrared spectroscopy. Na+, K+-ATPase activity, lipid peroxidation products (conjugated dienes), tissue high energy phosphates (ATP and phosphocreatine) levels and brain glucose and lactate levels were determined blocheroically in the cerebral cortex harvested at the termination of experiment. HbT as an index of a cerebral blood volume increased at 2 h after resuscitation significantly in HI group. During hypoxiaischemia Cyt aa3 fell to -2.0 ± 0.5 μ l-1 (p < 0.01), returned to baseline on resuscitation, but decreased again progressively from 33 h, and finally fell to -2.2 ± 0.9 μmol l-1 (p < 0.01) at 48 h in spite of normal physiologic values. There were no changes in control animals. Cerebral level of ATP and PCr in HI group decreased significantly compared to control and ATP concentrations were correlated with the final levels of Cyt aa3. In HI group, cerebral Na+, K+-ATPase activity decreased, but the cerebral level of conjugated dienes, glucose, lactate was not different compared to controls. These findings suggest that secondary cerebral energy failure was successfully reproduced in the newborn piglets after transient hypoxia-ischemia and the continuous in vivo NIRS monitoring can be used as a useful tool for the monitoring of delayed cerebral injury.
KW - Cerebral metabolism
KW - Hypoxia-ischemia
KW - Near infrared spectroscopy
KW - Newborn piglet
KW - Secondary cerebral energy failure
UR - https://www.scopus.com/pages/publications/0345628625
U2 - 10.1080/01616412.1999.11740921
DO - 10.1080/01616412.1999.11740921
M3 - Article
C2 - 10100211
AN - SCOPUS:0345628625
SN - 0161-6412
VL - 21
SP - 216
EP - 224
JO - Neurological Research
JF - Neurological Research
IS - 2
ER -