Effect of Diazinon PLUS on rapidly adapting receptors in the rabbit

1996 ◽  
Vol 81 (6) ◽  
pp. 2604-2610 ◽  
Author(s):  
Hillary Campbell ◽  
Krishnan Ravi ◽  
Emigdio Bravo ◽  
C. Tissa Kappagoda
Keyword(s):  
Normal Saline ◽  
Action Potentials ◽  
Left Atrial ◽  
Defense Mechanisms ◽  
Control Period ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Baseline Activity ◽  
Airway Defense ◽  
Control State

Campbell, Hillary, Krishnan Ravi, Emigdio Bravo, and C. Tissa Kappagoda. Effect of Diazinon PLUS on rapidly adapting receptors in the rabbit. J. Appl. Physiol. 81(6): 2604–2610, 1996.—The effects of Diazinon PLUS aerosol on the activities of rapidly adapting receptors (RARs) and slowly adapting receptors (SAR) of the airways were investigated in anesthetized rabbits. The effects on both the baseline activity and the responses to stimulation by increasing mean left atrial pressure were examined. Action potentials were recorded from the left cervical vagus nerve. Aerosols (particle size 3 μm) were generated by a Mini-HEART nebulizer. We observed that an aerosol of Diazinon PLUS (1:10 vol/vol dilution in normal saline) decreased the baseline RAR activity ( n= 10) significantly ( P < 0.05) from 209 ± 77 to 120 ± 40 impulses/min. In the post-Diazinon PLUS control period, the RAR activity recovered partially to 185 ± 75 impulses/min and decreased significantly to 131 ± 52 impulses/min ( P < 0.05) after a second exposure of Diazinon PLUS (undiluted) aerosol. Aerosols of normal saline in the control state did not produce a significant change in the RAR activity. A group of SAR ( n = 8) were examined under similar conditions, and it was found that only the exposure to Diazinon PLUS (undiluted) aerosol decreased the activity significantly ( P < 0.05) from 1,536 ± 206 to 1,367 ± 182 impulses/min. The effect of Diazinon PLUS on the response to increasing mean left atrial pressure was examined in seven RARs. In the control state, RAR activity increased significantly ( P < 0.05) during elevation of mean left atrial pressure. This response was abolished after exposure to Diazinon PLUS. These findings suggest that diazinon may interfere with airway defense mechanisms by reducing the activity of RARs.

N omega-nitro-L-arginine methyl ester selectively inhibits pulmonary vasodilator responses to acetylcholine and bradykinin

1991 ◽  
Vol 71 (5) ◽  
pp. 2026-2031 ◽  
Author(s):  
T. J. McMahon ◽  
J. S. Hood ◽  
J. A. Bellan ◽  
P. J. Kadowitz
Keyword(s):  
Methyl Ester ◽  
Left Atrial ◽  
Vascular Tone ◽  
Control Period ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Vascular Bed ◽  
Pulmonary Vasodilator ◽  
Pressor Responses ◽  
Pulmonary Vascular Bed

The effects of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of endothelium-derived relaxing factor (EDRF) production, on vascular tone and responses were investigated in the pulmonary vascular bed of the intact-chest cat under conditions of controlled blood flow and constant left atrial pressure. When pulmonary vascular tone was elevated with U-46619, intralobar injections of acetylcholine, bradykinin, sodium nitroprusside, isoproterenol, prostaglandin E1 (PGE1), lemakalim, and 8-bromo-guanosine 3′,5′-cyclic monophosphate (8-bromo-cGMP) dilated the pulmonary vascular bed. Intravenous administration of L-NAME elevated lobar arterial and systemic arterial pressures without altering left atrial pressure. When U-46619 was infused after L-NAME to raise lobar arterial pressure to levels similar to those attained during the control period, vasodilator responses to acetylcholine and bradykinin were reduced significantly, whereas responses to PGE1, lemakalim, and 8-bromo-cGMP were not altered, and responses to nitroprusside were increased. There was a small effect on the response to the highest dose of isoproterenol, and pressor responses to BAY K 8644 and angiotensin II were not altered. These results are consistent with the hypothesis that EDRF production may involve the formation of nitric oxide or a nitroso compound from L-arginine and that EDRF production may have a role in the regulation of tone and in the mediation of responses to acetylcholine and bradykinin in the pulmonary vascular bed of the cat.

Effect of hypoxia on lung lymph flow in newborn lambs with left atrial hypertension

1988 ◽  
Vol 254 (3) ◽  
pp. H487-H493
Author(s):  
J. U. Raj ◽  
T. A. Hazinski ◽  
R. D. Bland
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Control Period ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Fluid Filtration ◽  
Alveolar Hypoxia ◽  
Lung Lymph ◽  
Lung Lymph Flow

To determine the effect of left atrial hypertension on the vascular response to hypoxia in the newborn lung, we measured pulmonary artery and left atrial pressures, lung blood flow and lymph flow, and concentrations of protein in lymph and plasma of 13 lambs that spontaneously breathed air for 2-6 h (control period), followed by 8-11% O2 mixed with 3-5% CO2 and N2 for 2-4 h (experimental period). In eight studies, the lambs were made hypoxic first, after which we elevated their left atrial pressure by 10-12 Torr for 2-3 h. In 10 additional studies, we reversed the sequence by raising left atrial pressure first followed by addition of hypoxia. In lambs with normal left atrial pressure, alveolar hypoxia increased both pulmonary blood flow and lymph flow, with an associated reduction in lymph-to-plasma protein ratio (L/P). When left atrial pressure was increased in the presence of hypoxia, lymph flow increased by a small amount and L/P decreased further. In lambs with preexisting left atrial pressure elevation, addition of alveolar hypoxia increased both blood flow and lymph flow with no significant change in L/P. These results suggest that in newborn lambs with normal left atrial pressure, alveolar hypoxia increases lung lymph flow mainly by increasing microvascular filtration pressure, whereas in lambs with elevated left atrial pressure, hypoxia increases lymph flow by another mechanism, perhaps by increasing the perfused surface area for fluid filtration.

scholarly journals LEFT ATRIAL PRESSURE CORRELATION WITH PERSISTENT IATROGENIC ATRIAL SEPTAL DEFECT AFTER MITRACLIP IMPLANTATION

2021 ◽  
Vol 77 (18) ◽  
pp. 1200
Author(s):  
Prince Sethi ◽  
Nikhil Parimi ◽  
Prakash Acharya ◽  
Amandeep Goyal ◽  
Emmanuel Daon ◽  
...  
Keyword(s):  
Atrial Septal Defect ◽  
Left Atrial ◽  
Septal Defect ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Iatrogenic Atrial Septal Defect

scholarly journals The Effect of Furosemide on Left Atrial Pressure in Dogs with Mitral Valve Regurgitation

2011 ◽  
Vol 25 (2) ◽  
pp. 244-250 ◽  
Author(s):  
S. Suzuki ◽  
T. Ishikawa ◽  
L. Hamabe ◽  
D. Aytemiz ◽  
H. Huai-Che ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Left Atrial ◽  
Mitral Valve Regurgitation ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Valve Regurgitation

Relationship of Pulmonary Venous Flow Pattern to Mean Left Atrial Pressure and Phasic Pressure Change

Cardiology ◽  
1996 ◽  
Vol 87 (3) ◽  
pp. 224-229 ◽  
Author(s):  
Jer-Min Lin ◽  
Yi-Heng Li ◽  
Kwan-Lih Hsu ◽  
Juey-Jen Hwang ◽  
Yung-Zu Tseng
Keyword(s):  
Flow Pattern ◽  
Left Atrial ◽  
Pressure Change ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Venous Flow ◽  
Pulmonary Venous Flow ◽  
Relationship Of

scholarly journals Continuous Left Atrial Pressure Monitoring During MitraClip

2015 ◽  
Vol 8 (7) ◽  
pp. e117-e119 ◽  
Author(s):  
Mackram F. Eleid ◽  
Saurabh Sanon ◽  
Guy S. Reeder ◽  
Rakesh M. Suri ◽  
Charanjit S. Rihal
Keyword(s):  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pressure Monitoring

Doppler echo evaluation of pulmonary venous-left atrial pressure gradients: human and numerical model studies

2000 ◽  
Vol 279 (2) ◽  
pp. H594-H600 ◽  
Author(s):  
Michael S. Firstenberg ◽  
Neil L. Greenberg ◽  
Nicholas G. Smedira ◽  
David L. Prior ◽  
Gregory M. Scalia ◽  
...  
Keyword(s):  
Numerical Modeling ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
High Fidelity ◽  
Pressure Gradients ◽  
Bernoulli Equation ◽  
Venous Flow ◽  
Model Studies ◽  
Pulmonary Venous Flow

The simplified Bernoulli equation relates fluid convective energy derived from flow velocities to a pressure gradient and is commonly used in clinical echocardiography to determine pressure differences across stenotic orifices. Its application to pulmonary venous flow has not been described in humans. Twelve patients undergoing cardiac surgery had simultaneous high-fidelity pulmonary venous and left atrial pressure measurements and pulmonary venous pulsed Doppler echocardiography performed. Convective gradients for the systolic (S), diastolic (D), and atrial reversal (AR) phases of pulmonary venous flow were determined using the simplified Bernoulli equation and correlated with measured actual pressure differences. A linear relationship was observed between the convective ( y) and actual ( x) pressure differences for the S ( y = 0.23 x + 0.0074, r = 0.82) and D ( y = 0.22 x + 0.092, r = 0.81) waves, but not for the AR wave ( y = 0.030 x + 0.13, r = 0.10). Numerical modeling resulted in similar slopes for the S ( y = 0.200 x − 0.127, r = 0.97), D ( y = 0.247 x − 0.354, r= 0.99), and AR ( y = 0.087 x − 0.083, r = 0.96) waves. Consistent with numerical modeling, the convective term strongly correlates with but significantly underestimates actual gradient because of large inertial forces.

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