The Effect of Local Anaesthesia of the Airway on Respiratory Reflexes in the Rabbit

1973 ◽  
Vol 44 (6) ◽  
pp. 519-538 ◽  
Author(s):  
S. K. Jain ◽  
Diana Trenchard ◽  
Felicity Reynolds ◽  
M. I. M. Noble ◽  
A. Guz

1. The effect of breathing anaesthetic aerosols (lignocaine 20% and bupivacaine 5%) on respiratory reflexes was studied in rabbits. 2. The cough reflex was blocked in every experiment. 3. The inflation reflex was abolished in eleven out of twenty-six rabbits given lignocaine aerosol and in fourteen out of fifteen rabbits given bupivacaine aerosol. 4. The deflation reflex was blocked pari passu with the inflation reflex. 5. The ventilatory response to histamine was sometimes blocked; more commonly it was partially preserved. 6. The ventilatory response to phenyldiguanide was never impaired and often enhanced. 7. Bronchoconstriction produced by electrical stimulation of the peripheral cut ends of the cervical vagus nerves was unaffected. 8. Block of the above respiratory reflexes was associated with slower, deeper breathing. 9. Bupivacaine has produced more consistent and reliable results than lignocaine; the effects were reversible in both cases usually within 30 min. 10. Plasma concentrations of both anaesthetics were usually below the generally accepted toxic concentrations in man. 11. Control experiments using intravenous infusions of the anaesthetics proved that none of the effects could have been produced by systemic effects of the absorbed anaesthetic. 12. No pathological changes were found in the airways on both macroscopic and microscopic examination. 13. The experiments show that it is possible to block respiratory reflexes whose afferents arise from the airways, and to preserve a reflex arising at alveolar level.

1975 ◽  
Vol 38 (6) ◽  
pp. 1045-1050 ◽  
Author(s):  
D. S. Dain ◽  
H. A. Boushey ◽  
W. M. Gold

The effects of inhalation of 100 breaths of bupivacaine hydrochloride (5 percent solution in saline) on the cough reflex, the Breuer-Hering inflation, reflex, and the duration of apnea and bronchoconstriction produced by histamine aerosol were studied in nine anesthetized dogs. Cough was abolished in every animal; the duration of the inflation reflex was shortened from 47 +/- 4.6 s (mean plus or minus SE) to 16 +/- 3.4 s. The duration apnea produced by histamine was abolished or shortened and the rise in resistance was diminished from 170 plus or minus 22 per cent (control) to 49 +/- 6 per cent (after bupivacaine). These reflexes returned toward control values within 45 min. Bupivacaine inhibited the bronchoconstriction produced by electrical stimulation of the distal ends of cut vagus nerves both in dogs and in rabbits, but it did not alter the rise in resistance produced by histamine aerosol in vagotomized dogs. We conclude that administration of bupivacaine aerosol produces a reversible blockage of both afferent and efferent nervous activity in airways without abolishing the ability of smooth muscles to contract.


1976 ◽  
Vol 50 (6) ◽  
pp. 439-454 ◽  
Author(s):  
Brenda A. Cross ◽  
A. Guz ◽  
S. K. Jain ◽  
Sietske Archer ◽  
J. Stevens ◽  
...  

1. The effect of breathing an anaesthetic aerosol of 5% bupivacaine hydrochloride has been assessed in dog and man. 2. In the dog, the cough reflex was abolished and the Hering—Breuer inflation reflex severely impaired or abolished; breathing became slower and deeper; no pathological changes were found in the lungs of these dogs. 3. In man, no untoward effects resulted from a 10 min period of aerosol inhalation; there were no systematic effects on airway resistance or lung volumes and the cough reflex in response to either tactile or chemical (citric acid aerosol) stimulation was invariably abolished. The Hering—Breuer inflation reflex was impaired, but this was not associated with any change in resting ventilation. The V̇E/CO2 response was enhanced after aerosol anaesthesia; subjects felt an exaggerated dyspnoea. The aerosol anaesthesia abolished the afferent pathway of a reflexly elicited bronchoconstriction in one subject. There was no effect on the ability to hold the breath, or on the quality of the associated sensation. 4. Control aerosols of sodium chloride solution or phosphate buffer produced no effects. Control experiments with intravenous infusions of bupivacaine proved that none of the effects could have been produced by systemic effects of the absorbed anaesthetic. 5. Plasma concentrations of bupivacaine in man did not exceed a recognized toxic level. The experiments demonstrate a safe reversible anaesthesia of the airways in man lasting for a period of 10–20 min.


1959 ◽  
Vol 148 (2) ◽  
pp. 437-449 ◽  
Author(s):  
E. L. Blair ◽  
A. A. Harper ◽  
C. Kidd ◽  
T. Scratcherd
Keyword(s):  

1991 ◽  
Vol 71 (6) ◽  
pp. 2255-2261 ◽  
Author(s):  
A. D. Fryer ◽  
M. Wills-Karp

The effect of antigen challenge on the function of neuronal M2-muscarinic autoreceptors in the lungs was studied in anesthetized guinea pigs. Guinea pigs were injected intraperitoneally with saline (control group) or ovalbumin (10 mg/kg) on days 1, 3, and 5. One group of sensitized animals was challenged on days 20–25 with aerosolized ovalbumin for 5 min/day (challenged group), while another group of the sensitized animals was not challenged (sensitized group). On day 26 the animals were anesthetized, paralyzed, tracheostomized, and artificially ventilated. Pulmonary inflation pressure (Ppi), tidal volume, blood pressure, and heart rate were recorded. Both vagus nerves were cut, and electrical stimulation of the distal portions caused bronchoconstriction (measured as an increase in Ppi) and bradycardia. In the control group, pilocarpine (1–100 micrograms/kg iv) attenuated vagally induced bronchoconstriction by stimulating inhibitory M2-muscarinic receptors on parasympathetic nerves in the lungs. Conversely, blockade of these receptors with the antagonist gallamine (0.1–10 mg/kg iv) produced a marked potentiation of vagally induced bronchoconstriction. These results confirm previous findings. In the challenged guinea pigs, pilocarpine did not inhibit vagally induced bronchoconstriction. Furthermore, gallamine did not potentiate vagally induced bronchoconstriction to the same degree as in the controls. In the group of animals that was sensitized but not challenged, the potentiation of vagally induced bronchoconstriction by gallamine was identical to the controls. There was no increase in baseline Ppi in the sensitized or challenged animals compared with the controls.(ABSTRACT TRUNCATED AT 250 WORDS)


1978 ◽  
Vol 76 (3) ◽  
pp. 557-558 ◽  
Author(s):  
J. B. WAKERLEY ◽  
M. B. TER HAAR

A.R.C. Institute of Animal Physiology, Babraham, Cambridge, CB2 4AT (Received 1 November 1977) Thyrotrophin releasing hormone (TRH) can have a stimulatory effect on the release of both prolactin and thyrotrophin (TSH; Deis & Alonso, 1973), although in the rat, supraphysiological doses of TRH are required to affect the secretion of prolactin (Burnet & Wakerley, 1976). A more important factor in the control of the release of prolactin is considered to be prolactin release inhibiting factor (PIF), which is thought to act through the catecholamine, dopamine (MacLeod, 1976). Stimuli which cause the concomitant release of TSH and prolactin are thought to have a direct effect at the hypothalamic level such that neurones releasing TRH are excited, whereas those releasing PIF are inhibited. In the present work, we have tested this hypothesis using the suckling stimulus to elicit the simultaneous release of prolactin and TSH (Blake, 1974; Burnet & Wakerley, 1976). If


1991 ◽  
Vol 261 (1) ◽  
pp. G104-G110
Author(s):  
L. E. Hierlihy ◽  
J. L. Wallace ◽  
A. V. Ferguson

The role of the vagus nerve in the development of gastric mucosal damage was examined in urethan-anesthetized male Sprague-Dawley rats. Electrical stimulation was applied to the vagus nerves for a period of 60 min, after which macroscopic gastric damage was scored and samples of the stomach were fixed for later histological assessment. Damage scores were assigned blindly based on a 0 (normal) to 3 (severe) scale. Stimulation of vagal afferents or efferents in isolation did not result in significant damage to the gastric mucosa (P greater than 0.1). In contrast, stimulation of both intact vagus nerves resulted in significant gastric mucosal damage (mean damage score, 2.0 +/- 0.33, P less than 0.01). A second series of experiments demonstrated this gastric damage to be induced within 30-60 min; extending the stimulation period to 120 min did not worsen the gastric damage scores significantly (P greater than 0.1). In a third study, stimulation of both intact vagus nerves after paraventricular nucleus (PVN) lesion resulted in damage scores (0.33 +/- 0.17) that were significantly reduced compared with intact PVN and non-PVN-lesioned animals (P less than 0.01). These results indicate that the development of vagal stimulation-induced gastric damage requires the activation of both afferent and efferent vagal components and suggest further that such damage is dependent upon an intact PVN.


1993 ◽  
Vol 264 (5) ◽  
pp. G902-G909 ◽  
Author(s):  
G. R. Greenberg

Somatostatin-like immunoreactivity (SLI) released into the circulation after nutrients or secretagogues is heterogeneous. To determine whether similar neural pathways regulate secretion of SLI molecular forms, circulating somatostatin-28 (S-28) and somatostatin-14 (S-14) responses to ingestion of a solid meal, intraduodenal perfusion of a liquid defined formula meal, and intravenous infusion of cholecystokinin octapeptide (CCK-OP, 250 pmol.kg-1.h-1) were measured in four conscious dogs with and without cryogenic blockade of the cervical vagus nerves. SLI was separated by gel-filtration chromatography of extracted, acidified plasma and quantified by radioimmunoassay. Basal plasma concentrations of S-28 were 4.1 +/- 0.6 fmol/ml and of S-14 were 3.8 +/- 0.4 fmol/ml. Ingestion of the solid meal increased plasma SLI threefold, and elevations of S-28 and S-14 were equivalent. After the intraduodenal liquid meal or infusion of CCK-OP, plasma SLI rose twofold, but increments of S-28 exceeded S-14, comprising approximately 70% of SLI released. Vagal blockade by cooling reversibly inhibited both the S-28 and S-14 responses to the solid meal, intraduodenal liquid meal, and CCK-OP. In contrast, atropine (50 micrograms/kg iv), given after solid food, intraduodenal nutrients, and CCK-OP, suppressed S-28 but further increased S-14 responses. Atropine did not, however, alter the suppression of S-14 and S-28 by vagal cooling.(ABSTRACT TRUNCATED AT 250 WORDS)


1916 ◽  
Vol 24 (5) ◽  
pp. 605-619 ◽  
Author(s):  
G. Canby Robinson

The experiments that have been reported indicate that stimulation of either the right vagus or the left vagus nerve is equally effectual in blocking impulses from the auricles to the ventricles when auricular fibrillation is present. Stimulation of the left vagus nerve is as effectual in blocking impulses from the normally beating auricles as from the auricles when in a state of fibrillation, and the type of auricular activity has apparently no influence on the effect which stimulation of the left vagus has on auriculoventricular conduction.


1981 ◽  
Vol 241 (5) ◽  
pp. F502-F508 ◽  
Author(s):  
M. A. Knepper ◽  
M. B. Burg

To investigate whether mineralocorticoids affect the intrinsic capacity of the proximal tubule to absorb sodium and fluid, rabbits were chronically treated a number of ways to systematically vary plasma concentrations of mineralocorticoid hormones. The rate of fluid absorption and tubule dimensions were measured in superficial S2 segments from these rabbits. Chronic administration of deoxycorticosterone acetate (DOCA) was associated with a 67% increase in fluid absorption and a 29% increase in cell volume per unit tubule length. However, neither adrenalectomy nor low sodium diet significantly affected either fluid absorption or cell volume. Furthermore, marked dietary sodium restriction prevented the response to DOCA. We conclude that the DOCA-induced increases in fluid absorption and cell volume do not result from a direct stimulation of the proximal tubular cells by the steroid but more likely are responses to systemic effects of DOCA administration that are dependent on the level of sodium intake. Thus, we find no evidence for a direct mineralocorticoid stimulation of sodium and fluid transport by the S2 portion of the proximal tubule.


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