Stimulation of vagal afferents inhibits locomotion in mesencephalic cats

1993 ◽  
Vol 74 (1) ◽  
pp. 103-110 ◽  
Author(s):  
J. G. Pickar ◽  
J. M. Hill ◽  
M. P. Kaufman
Keyword(s):  
Intravenous Injection ◽  
Left Atrial ◽  
Onset Time ◽  
Vagal Afferents ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
C Fibers ◽  
Cervical Vagotomy ◽  
Reflex Arc ◽  
Stimulation Of

Using electrical stimulation of the mesencephalic locomotor region, we made decerebrate unanesthetized cats walk on a treadmill. The locomotion induced by stimulation of this midbrain area was assessed before and during activation of vagal afferents by either intravenous injection of phenylbiguanide or inflation of a balloon placed in the left atrium. Inflation of a balloon, which increased left atrial pressure by 7–25 mmHg, abolished locomotion in 9 of 10 cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by balloon inflation in each of two cats tested. Intravenous phenylbiguanide (50 or 100 micrograms/kg) or serotonin (40 micrograms/kg) injections abolished or attenuated walking induced by midbrain stimulation in 11 of 13 cats tested. In addition, intravenous phenylbiguanide injections abolished or attenuated locomotion with a shorter onset time than did systemic injections of this substance in five of six cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by phenylbiguanide injection in each of five cats tested. We conclude that locomotion can be prevented by a viscerosomatic reflex arising from the lungs and heart. The afferent arm of this reflex arc is the vagus nerve. Afferents such as slowly and rapidly adapting pulmonary stretch receptors, atrial receptors, and lung C-fibers may have had a role in preventing locomotion during the increase in left atrial pressure in our experiments. On the other hand, pulmonary C-fibers had a crucial role in preventing locomotion during intravenous injection of phenyl-biguanide. We speculate that this viscerosomatic reflex may help to explain in part the intolerance for exercise displayed by patients with congestive heart failure.

Pulmonary congestion enhances responses of lung rapidly adapting receptors to cigarette smoke in rabbit

1994 ◽  
Vol 77 (6) ◽  
pp. 2633-2640 ◽  
Author(s):  
K. Ravi ◽  
C. T. Kappagoda ◽  
A. C. Bonham
Keyword(s):  
Left Atrium ◽  
Cigarette Smoke ◽  
Left Atrial ◽  
Venous Congestion ◽  
Transient Increase ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pulmonary Congestion ◽  
Stimulation Of

We examined the effects of low-nicotine cigarette smoke, pulmonary venous congestion, and their combination on the activity of rapidly (RAR) and slowly adapting receptors (SAR) in anesthetized rabbits. Pulmonary venous congestion was achieved by inflating a balloon in the left atrium to increase left atrial pressure. We examined smoke effects on RARs (averaged over 15 breaths) at baseline left atrial pressure and at subthreshold and suprathreshold increases in left atrial pressure. At baseline, smoke significantly increased RAR activity from 12.1 +/- 4.2 to 16.2 +/- 4.2 impulses/breath (P < 0.05). At subthreshold increases in left atrial pressure (2.9 +/- 0.6 mmHg), smoke produced larger increases in RAR activity (12.3 +/- 3.3 to 22.5 +/- 4.1 impulses/breath; P < 0.05). Suprathreshold increases in left atrial pressure (9.2 +/- 1.1 mmHg) alone increased RAR activity from 10.9 +/- 3.2 to 19.8 +/- 5.9 impulses/breath (P < 0.05). Smoke had no additional effect (22.3 +/- 4.8 impulses/breath; P > 0.05). There was, however, a transient increase in RAR activity (1st 3 breaths of smoke) under all three conditions. Of nine SARs examined, only two were stimulated by smoke. We conclude that in the rabbit smoke-induced stimulation of RARs is augmented by mild pulmonary venous congestion. of RARs is augmented by mild pulmonary venous congestion.

Vagal regulation of arginine vasopressin in conscious dogs

1986 ◽  
Vol 251 (1) ◽  
pp. H19-H23 ◽  
Author(s):  
H. Morita ◽  
W. T. Manders ◽  
M. M. Skelton ◽  
A. W. Cowley ◽  
S. F. Vatner
Keyword(s):  
Arginine Vasopressin ◽  
Left Atrial ◽  
Volume Expansion ◽  
Vagal Afferents ◽  
Atrial Pressure ◽  
Conscious Dogs ◽  
Left Atrial Pressure ◽  
Rapid Infusion ◽  
Cardiopulmonary Receptors ◽  
Persistent Elevation

To determine whether removal of inhibition of arginine vasopressin (AVP) by vagal afferents results in persistent elevation of plasma AVP, effects of bilateral cervical vagal denervation (VD) on plasma AVP were examined in 10 dogs with sinoaortic baroreceptor denervation (SAD). VD increased plasma AVP levels by 98 +/- 16 from 3.8 +/- 1.0 pg/ml (P less than 0.01) at 15 min after VD. By 4 h after VD there were no significant differences from control values. Responses of plasma AVP were also examined in response to acute volume expansion in conscious dogs with all reflexes intact, SAD, and SAD plus VD. In intact and SAD dogs, when blood volume was expanded by 20% with a rapid infusion of isotonic, isooncotic 3% dextran in saline, mean left atrial pressure rose transiently and plasma AVP fell insignificantly. With more prolonged stimulation to cardiopulmonary receptors, i.e., when left atrial pressure was maintained at elevated levels for 1 h by volume loading, plasma AVP fell by 0.9 +/- 0.3 pg/ml. However, after correction for hemodilution was made, AVP did not change with volume expansion, indicating that secretion rate was unchanged. Thus acute, but not chronic, interruption of vagal pathways induces striking release of AVP, but a resetting mechanism rapidly returns plasma AVP to control levels. Furthermore, stimulation of vagally innervated receptors by means of acute volume expansion suppresses plasma AVP when the elevation in atrial pressure is sustained, but this fall in plasma AVP can be accounted for entirely by the concomitant hemodilution.

Mechanism of diuretic response associated with atrial tachycardia

1975 ◽  
Vol 229 (6) ◽  
pp. 1486-1491 ◽  
Author(s):  
J Boykin ◽  
P Cadnapaphornchai ◽  
KM McDonald ◽  
RW Schrier
Keyword(s):  
Left Atrial ◽  
Atrial Tachycardia ◽  
Free Water ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Atrial Pacing ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs

Left atrial pacing was performed in three groups of anesthetized dogs. In the first group of eight intact dogs a mean increase in atrial rate (AR) from 140 +/- 7 to 244 +/- 6 was associated with a decrease in urinary osmolality (U osmol) from 631 +/- 72 to 264 +/- 43 mosmol/kg (P less than .001), and free-water clearance (CH20) increased from -.325 +/- .06 to +.355 +/- .15 ml/min (P less than .001). At the same time left atrial pressure (LAP) increased from 6 +/- 1 to 15 +/- 1 mmHg (P less than .001). A second group of studies was performed in six hypophysectomized, steroid-replaced animals receiving 40-50 muU/kg per min of antidiuretic hormone (ADH). In these animals AR was increased from 148 +/- 17 to 250 +/- 17 but diuresis did not occur. In these studies Uosmol was 690 +/- 55 before and 704 +/- 49 mosmol/kg after atrial pacing and CH20 also did not change. Left atrial pressure increased from 10 +/- 2 to 19 +/- 2 mmHg during atrial pacing. A third group of studies was performed in five animals with bilateral cervical vagotomy. In these animals AR was increased from 159 +/- 6 to 258 +/- 17 and LAP increased from 7 +/- 1 to 16 +/- 2 mmHg. Osmolality increased from 808 +/- 72 to 1,049 +/- 65 musmol/kg (P less than .005) and CH20 was unchanged. These results, therefore, indicate that atrial tachycardia primarily increases renal water excretion by suppressing ADH release. This reflex is dependent on the integrity of cervical vagal pathways.

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

Intravenous injection of hypertonic NaCl solution stimulates pulmonary C-fibers in dogs

1991 ◽  
Vol 260 (5) ◽  
pp. H1522-H1530 ◽  
Author(s):  
T. E. Pisarri ◽  
A. Jonzon ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Intravenous Injection ◽  
Pulmonary Circulation ◽  
Bronchial Artery ◽  
Dependent Manner ◽  
Nacl Solution ◽  
Impulse Frequency ◽  
Minimum Effective Concentration ◽  
C Fibers ◽  
Hypertonic Solutions ◽  
Stimulation Of

Intravenous injection of hypertonic NaCl solution evokes reflex bradycardia and hypotension, effects thought to result from stimulation of afferent vagal endings in the lungs. To identify the afferents responsible for these effects, we recorded vagal impulses arising from endings in the lungs and lower airways of anesthetized dogs and examined the response to injection of hypertonic solutions into the pulmonary circulation. Injection of 4,800 mmol/l NaCl solution (1 ml/kg) stimulated 39 of 49 pulmonary C-fibers, their impulse frequency increasing 35-fold. Stimulation was concentration dependent, the minimum effective concentration being between 1,200 and 4,800 mmol/l. Rapidly adapting receptors were also stimulated in a concentration-dependent manner, 35 of 41 receptors being stimulated by 4,800 mmol/l NaCl solution, firing increasing fivefold. Bronchial C-fibers were not stimulated by injection into the pulmonary circulation but were by injection into the bronchial artery. Hypertonic urea solutions had qualitatively similar but smaller effects on pulmonary C-fibers and rapidly adapting receptors. The results suggest that the reflex effects of intravenous injection of hypertonic solutions result principally from stimulation of pulmonary C-fibers.

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