Limits...
PGF2 alpha causes bronchoconstriction and pulmonary vasoconstriction via thromboxane receptors in rat lung.

Kang KH, Shim JJ, Banerjee M, Newman JH - Korean J. Intern. Med. (1996)

Bottom Line: N omega-nitro-L-arginine, 100 microns, a NO synthase inhibitor potentiated the Ppa response two-fold with significant change in airway mechanics.SQ 29548, a thromboxane receptor blocker and Cl, a protein kinase C (PKC) inhibitor, fully blocked both the vascular and airway responses to PGF2 alpha.PGF2 alpha is a constrictor of pulmonary vessels and airways in rat lungs via thromboxane SQ 29548 receptors, thansduced by intracellular PKC.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Korea University, Seoul.

ABSTRACT
We determined the vascular and airway effects of PGF2 alpha and its mechanism of action on isolated-perfused lungs of rats were isolated and perfused at 50 ml/kg/min with Krebs-Henseleit bicarbonate buffer solution containing 3% bovine serum albumin. The lungs were ventilated with 21% O2 and 5% CO2 at a tidal volume of 2 ml. frequency of 60 per minute and positive end expiratory pressure of 3 cmH2O. Following injection of 50 micrograms PGF2 alpha into the afferent pulmonary catheter, there was a marked rise in pulmonary arterial pressure (Ppa) and in resistance to airflow across the lung (RL) and a fall in dynamic lung compliance (Cdyn). Double vascular occlusion technique revealed that 29% of the rise in Ppa was due to an increase in upstream and 71% to downstream resistance. N omega-nitro-L-arginine, 100 microns, a NO synthase inhibitor potentiated the Ppa response two-fold with significant change in airway mechanics. Rat atrial natriuretic factor (r-ANF), 40 micrograms quickly reversed the changes in Ppa, RL and Cdyn. Infusion of r-ANF prior to PGF2 alpha attenuated the Ppa response by 38%, RL by 44% and Cdyn by 12%. SQ 29548, a thromboxane receptor blocker and Cl, a protein kinase C (PKC) inhibitor, fully blocked both the vascular and airway responses to PGF2 alpha. PGF2 alpha is a constrictor of pulmonary vessels and airways in rat lungs via thromboxane SQ 29548 receptors, thansduced by intracellular PKC.

Show MeSH

Related in: MedlinePlus

Pulmonary arterial pressure response to PGF2α without and with pretreatment with Nw-nitro-L-arginine(NNLA).Values are means±SE of 12 experiments.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4531997&req=5

f3-kjim-11-1-74-9: Pulmonary arterial pressure response to PGF2α without and with pretreatment with Nw-nitro-L-arginine(NNLA).Values are means±SE of 12 experiments.

Mentions: NNLA increased baseline Ppa only at doses>100 μM. Subsequent injection of PGF2α caused pulmonary edema associated with a pronounced increase (>60 mmH2O) in Ppa. The dose of NNLA we chose did not affect baseline Ppa, nor was there any change in airway mechanics after the addition of NNLA in the perfusate. 100 μM of NNLA potentiated the peak Ppa response to 50 μg PGF2α with no statistically significant change in RL and Cdyn (Fig. 3).


PGF2 alpha causes bronchoconstriction and pulmonary vasoconstriction via thromboxane receptors in rat lung.

Kang KH, Shim JJ, Banerjee M, Newman JH - Korean J. Intern. Med. (1996)

Pulmonary arterial pressure response to PGF2α without and with pretreatment with Nw-nitro-L-arginine(NNLA).Values are means±SE of 12 experiments.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4531997&req=5

f3-kjim-11-1-74-9: Pulmonary arterial pressure response to PGF2α without and with pretreatment with Nw-nitro-L-arginine(NNLA).Values are means±SE of 12 experiments.
Mentions: NNLA increased baseline Ppa only at doses>100 μM. Subsequent injection of PGF2α caused pulmonary edema associated with a pronounced increase (>60 mmH2O) in Ppa. The dose of NNLA we chose did not affect baseline Ppa, nor was there any change in airway mechanics after the addition of NNLA in the perfusate. 100 μM of NNLA potentiated the peak Ppa response to 50 μg PGF2α with no statistically significant change in RL and Cdyn (Fig. 3).

Bottom Line: N omega-nitro-L-arginine, 100 microns, a NO synthase inhibitor potentiated the Ppa response two-fold with significant change in airway mechanics.SQ 29548, a thromboxane receptor blocker and Cl, a protein kinase C (PKC) inhibitor, fully blocked both the vascular and airway responses to PGF2 alpha.PGF2 alpha is a constrictor of pulmonary vessels and airways in rat lungs via thromboxane SQ 29548 receptors, thansduced by intracellular PKC.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Korea University, Seoul.

ABSTRACT
We determined the vascular and airway effects of PGF2 alpha and its mechanism of action on isolated-perfused lungs of rats were isolated and perfused at 50 ml/kg/min with Krebs-Henseleit bicarbonate buffer solution containing 3% bovine serum albumin. The lungs were ventilated with 21% O2 and 5% CO2 at a tidal volume of 2 ml. frequency of 60 per minute and positive end expiratory pressure of 3 cmH2O. Following injection of 50 micrograms PGF2 alpha into the afferent pulmonary catheter, there was a marked rise in pulmonary arterial pressure (Ppa) and in resistance to airflow across the lung (RL) and a fall in dynamic lung compliance (Cdyn). Double vascular occlusion technique revealed that 29% of the rise in Ppa was due to an increase in upstream and 71% to downstream resistance. N omega-nitro-L-arginine, 100 microns, a NO synthase inhibitor potentiated the Ppa response two-fold with significant change in airway mechanics. Rat atrial natriuretic factor (r-ANF), 40 micrograms quickly reversed the changes in Ppa, RL and Cdyn. Infusion of r-ANF prior to PGF2 alpha attenuated the Ppa response by 38%, RL by 44% and Cdyn by 12%. SQ 29548, a thromboxane receptor blocker and Cl, a protein kinase C (PKC) inhibitor, fully blocked both the vascular and airway responses to PGF2 alpha. PGF2 alpha is a constrictor of pulmonary vessels and airways in rat lungs via thromboxane SQ 29548 receptors, thansduced by intracellular PKC.

Show MeSH
Related in: MedlinePlus