Cerebral hemodynamics after traumatic brain injury of immature brain

被引:12
作者
Armstead, WM
机构
[1] Childrens Hosp Philadelphia, Dept Anesthesia, Philadelphia, PA 19104 USA
[2] Univ Penn, Dept Anesthesia, Philadelphia, PA 19104 USA
[3] Univ Penn, Dept Pharmacol, Philadelphia, PA 19104 USA
关键词
newborn; cerebral circulation; brain injury; fluid percussion; cerebral hemodynamic effects; cerebral oxygenation; K+ channels; K-ATP channel function; dilator responsiveness;
D O I
10.1016/S0940-2993(99)80087-6
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
These studies were designed to characterize the cerebral hemodynamic effects of fluid percussion brain injury (FPI) in the newborn pig equipped with a closed cranial window. Reductions in cerebral blood flow, pial artery diameter, and cerebral oxygenation following FPI were greater in newborn (1-3 days old) vs. juvenile (3-4 weeks old) pigs, suggesting that newborns were exquisitely sensitive to brain injury. Additionally, in piglets, there was decremented dilation to nitric oxide, cGMP, and cAMP dependent stimuli following FPI. The membrane potential of vascular muscle is an important contributor to vascular tone and the activity of K+ channels is an important regulator of membrane potential. Recent studies indicate that altered dilator responsiveness and cerebral hemodynamic control following FPI results from impaired K+ ATP sensitive (K-ATP) and calcium sensitive (K-Ca(+2)) channel function. Impaired K-ATP channel function results, at least in part, from protein kinase C activation by the peptide endothelin-l. These observations indicate that the effects of brain injury on cerebral hemodynamics in the newborn are multifaceted and multifactorial.
引用
收藏
页码:137 / 142
页数:6
相关论文
共 48 条
[11]  
CROCKARD HA, 1977, SURG NEUROL, V7, P281
[12]   THE ROLE OF NITRIC-OXIDE IN OPIOID-INDUCED PIAL ARTERY VASODILATION [J].
DEVINE, JO ;
ARMSTEAD, WM .
BRAIN RESEARCH, 1995, 675 (1-2) :257-263
[13]   REDUCED CEREBRAL BLOOD-FLOW, OXYGEN DELIVERY, AND ELECTROENCEPHALOGRAPHIC ACTIVITY AFTER TRAUMATIC BRAIN INJURY AND MILD HEMORRHAGE IN CATS [J].
DEWITT, DS ;
PROUGH, DS ;
TAYLOR, CL ;
WHITLEY, JM .
JOURNAL OF NEUROSURGERY, 1992, 76 (05) :812-821
[14]   CYCLOOXYGENASE PRODUCTS OF ARACHIDONIC-ACID METABOLISM IN CAT CEREBRAL-CORTEX AFTER EXPERIMENTAL CONCUSSIVE BRAIN INJURY [J].
ELLIS, EF ;
WRIGHT, KF ;
WEI, EP ;
KONTOS, HA .
JOURNAL OF NEUROCHEMISTRY, 1981, 37 (04) :892-896
[15]  
FADEN AI, 1988, J PHARMACOL EXP THER, V245, P742
[16]   NEUROPEPTIDES AND CENTRAL-NERVOUS-SYSTEM INJURY - CLINICAL IMPLICATIONS [J].
FADEN, AI .
ARCHIVES OF NEUROLOGY, 1986, 43 (05) :501-504
[17]   ANIMATE MODELS OF HUMAN HEAD-INJURY [J].
GENNARELLI, TA .
JOURNAL OF NEUROTRAUMA, 1994, 11 (04) :357-368
[18]   BENEFICIAL-EFFECTS OF THE KAPPA-OPIOID RECEPTOR AGONIST U-50488H IN EXPERIMENTAL ACUTE BRAIN AND SPINAL-CORD INJURY [J].
HALL, ED ;
WOLF, DL ;
ALTHAUS, JS ;
VONVOIGTLANDER, PF .
BRAIN RESEARCH, 1987, 435 (1-2) :174-180
[19]   EFFECTS OF NALOXONE ON SYSTEMIC AND CEREBRAL RESPONSES TO EXPERIMENTAL CONCUSSIVE BRAIN INJURY IN CATS [J].
HAYES, RL ;
GALINAT, BJ ;
KULKARNE, P ;
BECKER, DP .
JOURNAL OF NEUROSURGERY, 1983, 58 (05) :720-728
[20]   POSSIBLE PROTECTIVE EFFECT OF ENDOGENOUS OPIOIDS IN TRAUMATIC BRAIN INJURY [J].
HAYES, RL ;
LYETH, BG ;
JENKINS, LW ;
ZIMMERMAN, R ;
MCINTOSH, TK ;
CLIFTON, GL ;
YOUNG, HF .
JOURNAL OF NEUROSURGERY, 1990, 72 (02) :252-261