Role of vagus nerves and inhalative aerosols of acetylcholine and histamine on dynamic pulmonary elastance in anesthetized spontaneously breathing and artificially ventilated dog

1982 ◽  
Vol 181 (3) ◽  
pp. 155-170 ◽  
Author(s):  
M. S. Islam ◽  
W. T. Ulmer
Keyword(s):  
Vagus Nerves ◽  
Spontaneously Breathing

Respiratory response to partial paralysis in anesthetized dogs

1984 ◽  
Vol 56 (6) ◽  
pp. 1583-1588 ◽  
Author(s):  
A. Oliven ◽  
E. C. Deal ◽  
S. G. Kelsen ◽  
N. S. Cherniack
Keyword(s):  
Motor Activity ◽  
Respiratory Muscle ◽  
Respiratory Muscles ◽  
Peak Activity ◽  
Inspiratory Time ◽  
Muscle Paralysis ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing ◽  
Partial Paralysis

The ability to maintain alveolar ventilation is compromised by respiratory muscle weakness. To examine the independent role of reflexly mediated neural mechanisms to decreases in the strength of contraction of respiratory muscles, we studied the effects of partial paralysis on the level and pattern of phrenic motor activity in 22 anesthetized spontaneously breathing dogs. Graded weakness induced with succinylcholine decreased tidal volume and prolonged both inspiratory and expiratory time causing hypoventilation and hypercapnia. Phrenic peak activity as well as the rate of rise of the integrated phrenic neurogram increased. However, when studied under isocapnic conditions, increases in the severity of paralysis, as assessed from the ratio of peak diaphragm electromyogram to peak phrenic activity, produced progressive increases in inspiratory time and phrenic peak activity but did not affect its rate of rise. After vagotomy, partial paralysis induced in 11 dogs with succinylcholine also prolonged the inspiratory burst of phrenic activity, indicating that vagal reflexes were not solely responsible for the alterations in respiratory timing. Muscle paresis was also induced with gallamine or dantrolene, causing similar responses of phrenic activity and respiratory timing. Thus, at constant levels of arterial CO2 in anesthetized dogs, respiratory muscle partial paralysis results in a decrease in breathing rate without changing the rate of rise of respiratory motor activity. This is not dependent solely on vagally mediated reflexes and occurs regardless of the pharmacological agent used. These observations in the anesthetized state are qualitatively different from the response to respiratory muscle paralysis or weakness observed in awake subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Contraction of dog trachealis muscle in vivo: role of alpha-adrenergic receptors

1980 ◽  
Vol 48 (2) ◽  
pp. 329-336 ◽  
Author(s):  
W. H. Beinfield ◽  
J. Seifter
Keyword(s):  
Adrenergic Receptors ◽  
Beta Blockers ◽  
Systemic Arterial Pressure ◽  
Alpha Adrenergic Receptors ◽  
Bilateral Vagotomy ◽  
Cervical Trachea ◽  
Spontaneously Breathing ◽  
Trachealis Muscle

Contraction, relaxation, and longitudinal tension were recorded by isometric strain gauge arches attached to cervical tracheal muscle (CTM) in 60 spontaneously breathing dogs anesthetized with pentobarbital. Intravenous norepinephrine (NE) (3 X 10(-9), 6 X 10(-9), 1.2 X 10(-8), and 2.4 x 10(-8) mol/kg) increased spontaneous mechanical activities (SMA) and caused dose related contraction of CTM in all dogs even though there was no pretreatment with beta-blockers. These activities were first potentiated by propranolol and then prevented by phentolamine. NE briefly decreased SMA and induced CTM relaxation prior to the onset of contraction in one-third of dogs. Propranolol prevented this initial relaxation. CTM responses induced by NE were 1) not significantly altered by atropine, tripelennamine, bilateral vagotomy, curarization, and complete tracheal transection below transducer sites; 2) unrelated to passive constriction of cervical trachea associated with airway elongation; and 3) independent of reflexes initiated by elevations of systemic arterial pressure. The moles per kilogram doses of acetylcholine were found to exceed those of NE when their intravenous administration caused equal CTM contractions in the same dog. These findings are consistent with the existence of alpha-adrenergic receptors in CTM.

Mechanical role of expiratory muscles during breathing in upright dogs

1988 ◽  
Vol 64 (3) ◽  
pp. 1060-1067 ◽  
Author(s):  
G. A. Farkas ◽  
R. E. Baer ◽  
M. Estenne ◽  
A. De Troyer
Keyword(s):  
Tidal Volume ◽  
Progressive Increase ◽  
Substantial Contribution ◽  
Postural Changes ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Expiratory Muscles ◽  
Spontaneously Breathing

To examine the mechanical effects of the abdominal and triangularis sterni expiratory recruitment that occurs when anesthetized dogs are tilted head up, we measured both before and after cervical vagotomy the end-expiratory length of the costal and crural diaphragmatic segments and the end-expiratory lung volume (FRC) in eight spontaneously breathing animals during postural changes from supine (0 degree) to 80 degrees head up. Tilting the animals from 0 degree to 80 degrees head up in both conditions was associated with a gradual decrease in end-expiratory costal and crural diaphragmatic length and with a progressive increase in FRC. All these changes, however, were considerably larger (P less than 0.005 or less) postvagotomy when the expiratory muscles were no longer recruited with tilting. Alterations in the elastic properties of the lung could not account for the effects of vagotomy on the postural changes. We conclude therefore that 1) by contracting during expiration, the canine expiratory muscles minimize the shortening of the diaphragm and the increase in FRC that the action of gravity would otherwise introduce, and 2) the end-expiratory diaphragmatic length and FRC in upright dogs are thus actively determined. The present data also indicate that by relaxing at end expiration, the expiratory muscles make a substantial contribution to tidal volume in upright dogs; in the 80 degrees head-up posture, this contribution would amount to approximately 60% of tidal volume.

Phrenic afferents and ventilatory control at increased end-expiratory lung volumes in cats

1989 ◽  
Vol 66 (3) ◽  
pp. 1297-1303 ◽  
Author(s):  
S. Iscoe
Keyword(s):  
Steady State ◽  
Independent Effect ◽  
Respiratory Drive ◽  
Phrenic Motoneurons ◽  
Partial Pressure Of Co2 ◽  
Before And After ◽  
Steady State Responses ◽  
Spontaneously Breathing ◽  
State Responses

The role of phrenic afferents in controlling inspiratory duration (TI) at elevated end-expiratory lung volume (EEV) has been studied in pentobarbital-anesthetized, spontaneously breathing cats with intact vagi. Responses to increases in EEV, induced by imposition of an expiratory threshold load (ETL) of 10 cmH2O, were monitored before and after section of cervical dorsal roots C3-C7. The immediate (first-breath) effect of application of ETL was a prolongation of both TI and expiratory duration (TE). After 10 min of breathing against the ETL, average TI returned to control values but TE remained prolonged. Abolishing feedback from the diaphragm did not affect these responses. When steady-state responses to ETL were compared with those elicited by inhalation of 5–6% CO2 in O2, changes in EEV had, on average, no independent effect on respiratory drive (rate of rise of integrated phrenic activity), although phrenic activity increased greatly in some cats despite little or no change in arterial partial pressure of CO2. These data indicate that diaphragmatic receptors do not contribute to either the immediate (first-breath) or steady-state responses of phrenic motoneurons to increases in EEV in intact cats.

N omega-nitro-L-arginine attenuates endothelium-dependent pulmonary vasodilation in lambs

1991 ◽  
Vol 260 (4) ◽  
pp. H1299-H1306 ◽  
Author(s):  
J. R. Fineman ◽  
M. A. Heymann ◽  
S. J. Soifer
Keyword(s):  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Vascular Tone ◽  
Pulmonary Arterial Pressure ◽  
Competitive Inhibitor ◽  
Pulmonary Vasodilation ◽  
Pulmonary Arterial ◽  
Spontaneously Breathing ◽  
Dose Dependent Increase

To investigate the role of endothelium-derived relaxing factor (EDRF) in the regulation of resting pulmonary vascular tone and endothelium-dependent pulmonary vasodilation, we studied the hemodynamic effects of N omega-nitro-L-arginine (a new stereospecific EDRF inhibitor) in 10 spontaneously breathing lambs and then compared the hemodynamic responses to five vasodilators during pulmonary hypertension induced by the infusion of U-46619 (a thromboxane A2 mimetic) or N omega-nitro-L-arginine. N omega-nitro-L-arginine caused a significant dose-dependent increase in pulmonary arterial pressure. Pretreatment with L-arginine blocked this increase, but pretreatment with D-arginine did not, suggesting that N omega-nitro-L-arginine is a competitive inhibitor of L-arginine for EDRF production. During U-46619 infusions, acetylcholine, ATP-MgCl2, isoproterenol, sodium nitroprusside, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-bromo-cGMP) decreased pulmonary arterial pressure. During N omega-nitro-L-arginine infusions, the decrease in pulmonary arterial pressure caused by acetylcholine and ATP-MgCl2 (endothelium-dependent vasodilators) was significantly attenuated, but the decrease caused by isoproterenol, sodium nitroprusside, and 8-bromo-cGMP (endothelium-independent vasodilators) was unchanged. This study supports the hypothesis that EDRF in part mediates resting pulmonary vascular tone and endothelium-dependent pulmonary vasodilation. N omega-nitro-L-arginine is useful for studying EDRF inhibition in intact animals.

Failure of tracheal distension to inhibit breathing in anesthetized dogs

1980 ◽  
Vol 48 (5) ◽  
pp. 794-798 ◽  
Author(s):  
T. C. Lloyd ◽  
J. A. Cooper
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
Potential Role ◽  
Minute Volume ◽  
Abdominal Compression ◽  
Frequency Increase ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing

Using anesthetized spontaneously breathing dogs, we compared the respiratory effects of tracheal distension with the effects of changes in lung volume before and after vagotomy. We used an endotracheal tube with a long cuff to distend the trachea to pressures of 10, 20, and 40 cmH2O. Lung volume increases were imposed by expiratory threshold loading, and volume was decreased by abdominal compression, both of which caused outward rib cage displacement. During expiratory loading, the tidal volume was unchanged but respiratory frequency and minute volume fell and an active expiratory effort appeared; whereas frequency and minute volume rose, but tidal volume fell during abdominal compression. Tracheal distension evoked no discernible change in breathing. Following vagotomy, tidal volume and minute volume fell, and frequency rose slightly, during expiratory loading but abdominal compression was without effect. After vagotomy, 40 cmH2O tracheal distension caused a slight frequency increase. We concluded that the potential role of tracheal deformation in the reflex control of breathing is insignificant in comparison with the other airways.

Diaphragmatic failure during group B streptococcal sepsis in piglets: the role of thromboxane A2

1995 ◽  
Vol 78 (2) ◽  
pp. 491-498 ◽  
Author(s):  
T. D. Murphy ◽  
R. L. Gibson ◽  
T. A. Standaert ◽  
D. E. Woodrum
Keyword(s):  
Group B Streptococcus ◽  
Thromboxane A2 ◽  
Treated Group ◽  
Arachidonic Acid Metabolism ◽  
Group 4 ◽  
Group 2 ◽  
Txa2 Receptor Antagonist ◽  
Group B ◽  
Spontaneously Breathing

Group B Streptococcus (GBS) causes an impairment of diaphragmatic pressure generation (Pdi) in 2-wk-old piglets, whereas 4-wk-old piglets are unaffected. In this study, we examined the effect on 4-wk-old piglets of a higher dose of GBS than previously utilized. We sought to determine whether an eicosanoid product of arachidonic acid metabolism accounted for the decrease in Pdi during GBS infusion and whether thromboxane A2 (TxA2) is the putative eicosanoid mediator of decreased Pdi during GBS infusion. Measuring Pdi during phrenic nerve stimulation, we studied four groups of anesthetized spontaneously breathing 4-wk-old piglets. Group 1 (GBS) was infused with live GBS, which caused a decrease in Pdi by 1 h at 20-, 30-, 50-, and 100-Hz stimulation frequencies. Group 2 [GBS + indomethacin (Indo)] was pretreated with Indo before GBS infusion. In the GBS + Indo group, Pdi did not decrease throughout 4 h of GBS infusion. Because Indo proved to be protective of Pdi during GBS infusion, we examined the role of TxA2, the only eicosanoid present at 1 h in the serum of GBS-infused piglets. Group 3 was infused with the TxA2 analogue U-46619 only for 1 h. Group 4 was treated with the TxA2-receptor antagonist SQ-29548 before and concomitant with GBS infusion for 1 h; the SQ-29548 was then discontinued, and GBS was continued for 1 h more. In the U-46619-infused group, Pdi decreased at 1 h, and in the SQ-29548-treated group, Pdi did not decrease during GBS infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Control of bile flow in the cholecystectomized dog

1963 ◽  
Vol 204 (5) ◽  
pp. 825-828 ◽  
Author(s):  
Michael E. Fritz ◽  
Frank P. Brooks
Keyword(s):  
Bile Flow ◽  
Anticholinergic Drug ◽  
Vagus Nerves ◽  
Intestinal Hormones ◽  
Insulin Hypoglycemia ◽  
Intravenous Insulin ◽  
Bilateral Vagotomy ◽  
The Common ◽  
Choleretic Effect

Rate of flow and composition of bile were measured in three unanesthetized, cholecystectomized dogs. One of these animals and one other dog were also studied after bilateral vagotomy. Bile flow and output of solids were increased by intravenous insulin and feeding. Tolbutamide had a similar choleretic effect. The anticholinergic drug, pipenzolate methylbromide blocked the choleretic effect of insulin. After bilateral vagotomy, the choleretic effect of both feeding and insulin-hypoglycemia was lost. Commercial pancreozymin had a choleretic action which may indicate a role of intestinal hormones in the response to feeding. Intraduodenal injection of hydrochloric acid was followed by an increase in only the volume of bile. Glucagon produced a hydrochloresis and an increase in bilirubin output. The results suggest that normal bile production in the dog after eating may be controlled in part by a mechanism involving the vagus nerves. The data also show that the insulin-hypoglycemia-induced choleresis differs from that of secretin. The composition of hepatic bile obtained from the common duct is consistent with an absorptive function of the ductal epithelium in the dog without a gallbladder.

Right atrium mediates a vasomotor reflex

1981 ◽  
Vol 241 (3) ◽  
pp. R163-R166
Author(s):  
R. F. Munzner ◽  
D. G. Ward ◽  
D. S. Gann
Keyword(s):  
Right Atrium ◽  
Carotid Arteries ◽  
Right Atrial ◽  
Vagus Nerves ◽  
Vascular Responses ◽  
The Right ◽  
Vasomotor Reflex ◽  
Atrial Receptors ◽  
Volume Pulsation

To examine the role of right atrial receptors in mediating reflex vascular responses we measured, in cats anesthetized with chloralose/urethan, changes in mean arterial pressure (MAP) in response to volume pulsation of the right atrium (+/- 1 ml, 1 Hz). Changes in MAP were measured 1) with pressure in the carotid arteries normal and vagus nerves intact: right atrial pulsation led to a very small and transient fall in MAP; 2) with pressure in the carotid arteries at 75 mmHg and the vagus nerves intact: right atrial pulsation led to a larger and sustained fall in MAP; 3) with pressure in the carotid arteries at 75 mmHg and the vagus nerves cooled or sectioned bilaterally: right atrial pulsation of the right atrium led only to a very small and transient fall in MAP. These data suggest strongly that signals from right atrial receptors traveling in the vagus nerves mediate a reflex change in MAP that is normally masked by signals from carotid receptors.

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