PMID- 1987772
OWN - NLM
STAT- MEDLINE
DCOM- 19910215
LR  - 20181130
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 138
IP  - 1
DP  - 1991 Jan
TI  - Effects of recombinant tumor necrosis factor-alpha on cultured pulmonary artery 
      and lung microvascular endothelial monolayers.
PG  - 93-101
AB  - Whole animal studies suggest that tumor necrosis factor-alpha (TNF alpha) plays a 
      central role in the endotoxin response. In vitro studies show that TNF alpha and 
      endotoxin induce a similar range of metabolic changes to endothelial cells. 
      However both endotoxin- and TNF alpha-induced cytotoxicity is not a feature of 
      all endothelial cells lines. In recent studies, the authors have shown that 
      endotoxin causes different responses in endothelial cells taken from two levels 
      of the lung's circulation--main pulmonary artery and lung microvasculature. 
      Endotoxin exposure caused cell death for cells cultured from the large pulmonary 
      artery but not for those taken from lung periphery. The present study examined 
      the effect of TNF alpha on endothelial cells cultured from two levels of the 
      lungs' circulation--the main pulmonary artery and the lung microvasculature. End 
      points examined included lactate dehydrogenase (LDH), prostacyclin, and 
      prostaglandin E2 (PGE2) release and phase contrast microscopy. Exposure to TNF 
      alpha resulted in a dose-dependent increase in LDH release and number of detached 
      cells for cells of the pulmonary artery, whereas cells from the microvasculature 
      seemed unaffected. At both levels, however, TNF alpha caused increased release of 
      both prostacyclin and PGE2. The authors conclude that TNF alpha causes different 
      effects in endothelial cells cultured from two levels of the same organ.
FAU - Meyrick, B
AU  - Meyrick B
AD  - Department of Pathology, Vanderbilt University Medical Center, Nashville, TN 
      37232-2650.
FAU - Christman, B
AU  - Christman B
FAU - Jesmok, G
AU  - Jesmok G
LA  - eng
GR  - HL 19153/HL/NHLBI NIH HHS/United States
GR  - HL 27274/HL/NHLBI NIH HHS/United States
GR  - HL 34208/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Antibodies)
RN  - 0 (Prostaglandins)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - J2VZ07J96K (Polymyxin B)
SB  - IM
MH  - Animals
MH  - Antibodies/immunology
MH  - Cell Count
MH  - Cells, Cultured
MH  - Endothelium, Vascular/cytology/*drug effects/metabolism
MH  - Hot Temperature
MH  - L-Lactate Dehydrogenase/metabolism
MH  - Microcirculation
MH  - Polymyxin B/pharmacology
MH  - Prostaglandins/metabolism
MH  - Pulmonary Artery/cytology/*drug effects/metabolism
MH  - *Pulmonary Circulation
MH  - Recombinant Proteins
MH  - Tumor Necrosis Factor-alpha/immunology/*pharmacology
PMC - PMC1886052
EDAT- 1991/01/01 00:00
MHDA- 1991/01/01 00:01
PMCR- 1991/07/01
CRDT- 1991/01/01 00:00
PHST- 1991/01/01 00:00 [pubmed]
PHST- 1991/01/01 00:01 [medline]
PHST- 1991/01/01 00:00 [entrez]
PHST- 1991/07/01 00:00 [pmc-release]
PST - ppublish
SO  - Am J Pathol. 1991 Jan;138(1):93-101.