Mechanisms of pulmonary vasoconstriction induced by chemotactic peptide FMLP in isolated rabbit lungs

1992 ◽  
Vol 72 (4) ◽  
pp. 1549-1556 ◽  
Author(s):  
H. Tanaka ◽  
J. D. Bradley ◽  
L. J. Baudendistel ◽  
T. E. Dahms
Keyword(s):  
Reactive Oxygen Species ◽  
Polymorphonuclear Leukocytes ◽  
Reactive Oxygen ◽  
Cyclooxygenase Inhibitors ◽  
Oxygen Species ◽  
Chemotactic Peptide ◽  
Middle Segment ◽  
Pulmonary Vasoconstriction ◽  
Lipoxygenase Products ◽  
Reactive Oxygen Species Scavenger

The chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) has been shown to constrict both bronchial and coronary vascular smooth muscle through the action of cyclooxygenase or lipoxygenase products. We observed that intravenous FMLP increased pulmonary vascular resistance (PVR) in isolated buffer-perfused rabbit lungs. FMLP increased the PVR (primarily in the middle segment of the pulmonary vascular bed) at concentrations greater than or equal to 10(-7) M. Maximum vasoconstriction occurred at 5 min and then slowly declined to a level that remained above baseline at 30 min. Tachyphylaxis was observed in response to FMLP. When polymorphonuclear leukocytes (PMNs) were added to the perfusate, FMLP caused a greater increase in PVR. PMN depletion with dimethylmyleran significantly reduced the PVR response to FMLP. Pretreatment with two dissimilar cyclooxygenase inhibitors, meclofenamate and ibuprofen, and the leukotriene synthesis blocker MK 886 had no effect on the FMLP-induced vasoconstriction. However, the reactive oxygen species scavenger catalase significantly reduced the vasoconstriction. These results suggest that FMLP induces vasoconstriction that is dependent on PMNs and mediated by reactive oxygen species with no involvement of cyclooxygenase or lipoxygenase products.

scholarly journals Recent advances in oxygen sensing and signal transduction in hypoxic pulmonary vasoconstriction

2017 ◽  
Vol 123 (6) ◽  
pp. 1647-1656 ◽  
Author(s):  
Ievgen Strielkov ◽  
Oleg Pak ◽  
Natasha Sommer ◽  
Norbert Weissmann
Keyword(s):  
Reactive Oxygen Species ◽  
Transient Receptor Potential ◽  
Oxygen Sensing ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Reactive Oxygen ◽  
Receptor Potential ◽  
Complex Iii ◽  
Oxygen Species ◽  
Pulmonary Vasoconstriction ◽  
Transient Receptor

Hypoxic pulmonary vasoconstriction (HPV) is a physiological reaction, which adapts lung perfusion to regional ventilation and optimizes gas exchange. Impaired HPV may cause systemic hypoxemia, while generalized HPV contributes to the development of pulmonary hypertension. The triggering mechanisms underlying HPV are still not fully elucidated. Several hypotheses are currently under debate, including a possible decrease as well as an increase in reactive oxygen species as a triggering event. Recent findings suggest an increase in the production of reactive oxygen species in pulmonary artery smooth muscle cells by complex III of the mitochondrial electron transport chain and occurrence of oxygen sensing at complex IV. Other essential components are voltage-dependent potassium and possibly L-type, transient receptor potential channel 6, and transient receptor potential vanilloid 4 channels. The release of arachidonic acid metabolites appears also to be involved in HPV regulation. Further investigation of the HPV mechanisms will facilitate the development of novel therapeutic strategies for the treatment of HPV-related disorders.

Gossypol induced apoptosis of polymorphonuclear leukocytes and monocytes: Involvement of mitochondrial pathway and reactive oxygen species

2009 ◽  
Vol 31 (2) ◽  
pp. 320-330 ◽  
Author(s):  
Martha Barba-Barajas ◽  
Georgina Hernández-Flores ◽  
José M. Lerma-Díaz ◽  
Pablo C. Ortiz-Lazareno ◽  
Jorge R. Domínguez-Rodríguez ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Polymorphonuclear Leukocytes ◽  
Reactive Oxygen ◽  
Mitochondrial Pathway ◽  
Oxygen Species ◽  
Induced Apoptosis

Interactions of Cyclooxygenase Inhibitors with Reactive Oxygen Species

2006 ◽  
Vol 1 (2) ◽  
pp. 115-125 ◽  
Author(s):  
Sheikh A. Saeed ◽  
Muhammad A. Mesaik ◽  
J. Quadri ◽  
S. Tasneem ◽  
A. Motiwala ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Cyclooxygenase Inhibitors ◽  
Oxygen Species

Mechanisms of increased pulmonary microvascular permeability induced by FMLP in isolated rabbit lungs

1992 ◽  
Vol 73 (5) ◽  
pp. 2074-2082 ◽  
Author(s):  
H. Tanaka ◽  
J. D. Bradley ◽  
L. J. Baudendistel ◽  
T. E. Dahms
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Weight Ratio ◽  
Dry Weight ◽  
Microvascular Permeability ◽  
Cyclooxygenase Inhibitors ◽  
Myeloperoxidase Activity ◽  
Oxygen Species ◽  
Chemotactic Peptide ◽  
Isolated Lung ◽  
Baseline Values

We observed that the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L- phenylalanine (FMLP) induced pulmonary edema when polymorphonuclear leukocytes (PMNs) were added to isolated constant-flow buffer-perfused rabbit lungs. This study was designed to test the hypothesis that PMNs activated by FMLP induced lung injury by the modulation of reactive oxygen species (ROS), cyclooxygenase products, or cysteinyl leukotrienes (LTs). Addition of FMLP alone did not increase microvascular permeability (Kf). When PMNs were added to the isolated lung, FMLP caused an 80% increase in Kf. Wet-to-dry weight ratio was also significantly increased with PMNs + FMLP compared with FMLP only. There was a significant positive correlation between total myeloperoxidase activity in lung tissue and Kf values after FMLP (30 min). Pretreatment with two dissimilar cyclooxygenase inhibitors, meclofenamate or ibuprofen, had no effect on the PMN + FMLP-induced increase in Kf. However, the ROS inhibitor catalase and the nonantioxidant LT synthesis blocker MK 886 inhibited the PMN + FMLP increase in Kf. Perfusate levels of LTs (LTC4, -D4, and -E4) were significantly increased from baseline values 30 min after FMLP. Both MK 886 and catalase suppressed the elevation of LTs after PMN + FMLP. These results indicate that FMLP increased a pulmonary microvascular permeability in isolated buffer-perfused rabbit lungs that is PMN dependent and mediated by LT produced possibly by a result of ROS production.

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