PMID- 1723406
OWN - NLM
STAT- MEDLINE
DCOM- 19920312
LR  - 20181130
IS  - 8750-7587 (Print)
IS  - 0161-7567 (Linking)
VI  - 71
IP  - 6
DP  - 1991 Dec
TI  - Intravascular anti-IgE challenge in perfused lungs: mediator release and vascular 
      pressor response.
PG  - 2499-506
AB  - Intravascular application of goat anti-rabbit immunoglobulin E (IgE) was used to 
      stimulate parenchymal mast cells in situ in perfused rabbit lungs. Sustained 
      pulmonary arterial pressure rise was evoked in the absence of lung vascular 
      permeability increase and lung edema formation. Early prostaglandin (PG) D2 and 
      histamine release into the perfusate was documented, accompanied by more 
      sustained liberation of cysteinyl leukotrienes (LT), LTB4, and PGI2. The 
      quantities of these inflammatory mediators displayed the following order: 
      histamine greater than cysteinyl-LT greater than PGI2 greater than LTB4 greater 
      than PGD2. Pressor response and inflammatory mediator release revealed 
      corresponding bell-shaped dose dependencies. Cyclooxygenase inhibition 
      (acetylsalicylic acid) suppressed prostanoid generation, increased LT release, 
      and did not substantially affect pressor response and histamine liberation. BW755 
      C, a cyclo- and lipoxygenase inhibitor, blocked the release of cysteinyl-LT and 
      markedly reduced the liberation of the other inflammatory mediators as well as 
      the pressor response. The H1-antagonist clemastine caused a moderate reduction of 
      the anti-IgE-provoked pressure rise. We conclude that intravascular anti-IgE 
      challenge in intact lungs provokes the release of an inflammatory mediator 
      profile compatible with in situ lung parenchymal mast cell activation. Pulmonary 
      hypertension represents the predominant vascular response, presumably mediated by 
      cysteinyl-LT and, to a minor extent, histamine liberation.
FAU - Walmrath, D
AU  - Walmrath D
AD  - Department of Internal Medicine, Justus-Leibig University, Giessen, Federal 
      Republic of Germany.
FAU - Schneider, U
AU  - Schneider U
FAU - Kreusler, B
AU  - Kreusler B
FAU - Grimminger, F
AU  - Grimminger F
FAU - Ennis, M
AU  - Ennis M
FAU - Seeger, W
AU  - Seeger W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (Antibodies, Anti-Idiotypic)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - DCR9Z582X0 (Epoprostenol)
RN  - RXY07S6CZ2 (Prostaglandin D2)
SB  - IM
MH  - Animals
MH  - Antibodies, Anti-Idiotypic/*administration & dosage
MH  - Blood Pressure/physiology
MH  - Epoprostenol/metabolism
MH  - Female
MH  - Histamine Release
MH  - Immunoglobulin E
MH  - Inflammation/physiopathology
MH  - Lung/*immunology/physiology
MH  - Male
MH  - Mast Cells/immunology
MH  - Perfusion
MH  - Prostaglandin D2/metabolism
MH  - Rabbits
EDAT- 1991/12/01 00:00
MHDA- 1991/12/01 00:01
CRDT- 1991/12/01 00:00
PHST- 1991/12/01 00:00 [pubmed]
PHST- 1991/12/01 00:01 [medline]
PHST- 1991/12/01 00:00 [entrez]
AID - 10.1152/jappl.1991.71.6.2499 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 1991 Dec;71(6):2499-506. doi: 
      10.1152/jappl.1991.71.6.2499.