ATP-dependent K+ channel activation reduces loss of opioid dilation after brain injury

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 274, Issue 5 43-5, 1998, Pages

  Armstead, William M ^a,b  

^a UNIVERSITY OF PENNSYLVANIA   (United States)

^b CHILDREN S HOSPITAL OF PHILADELPHIA   (United States)

Author keywords

Cerebral circulation; Cyclic nucleotides; Newborn; Nitric oxide; Opioids

Indexed keywords

1 (2 HYDROXY 5 TRIFLUOROMETHYLPHENYL) 5 TRIFLUOROMETHYL 2(3H) BENZIMIDAZOLONE; ADENOSINE TRIPHOSPHATE; CROMAKALIM; CYCLIC GMP; CYCLIC NUCLEOTIDE; METENKEPHALIN; NITROPRUSSIDE SODIUM; OPIATE; POTASSIUM CHANNEL;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN CIRCULATION; BRAIN INJURY; CEREBROSPINAL FLUID; CONTROLLED STUDY; HEMODYNAMICS; NEWBORN; NONHUMAN; PIA ARTERY; PRIORITY JOURNAL; SWINE;

EID: 0031804774     PISSN: 03636135     EISSN: None     Source Type: Journal    
DOI: 10.1152/ajpheart.1998.274.5.h1674     Document Type: Article

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