Hypersensitivity of vagal pulmonary C-fibers is induced by hemorrhagic hypotension in anesthetized rats

2015 ◽  
Vol 192 ◽  
pp. 94
Author(s):  
Lu-Yuan Lee ◽  
Ruei-Lung Lin
Keyword(s):  
Hemorrhagic Hypotension ◽  
C Fibers ◽  
Anesthetized Rats

scholarly journals Hemorrhagic hypotension-induced hypersensitivity of vagal pulmonary C-fibers to chemical stimulation and lung inflation in anesthetized rats

2015 ◽  
Vol 308 (7) ◽  
pp. R605-R613 ◽  
Author(s):  
Ruei-Lung Lin ◽  
Yu-Jung Lin ◽  
Fadi Xu ◽  
Lu-Yuan Lee
Keyword(s):  
Lactic Acid ◽  
Systemic Arterial Pressure ◽  
The Body ◽  
Lung Inflation ◽  
Tissue Ischemia ◽  
Hemorrhagic Hypotension ◽  
C Fibers ◽  
Anesthetized Rats ◽  
C Fiber ◽  
Endogenous Release

This study was carried out to investigate whether hemorrhagic hypotension (HH) altered the sensitivity of vagal pulmonary C-fibers. The fiber activity (FA) of single vagal pulmonary C-fiber was continuously recorded in anesthetized rats before, during, and after HH was induced by bleeding from the femoral arterial catheter into a blood reservoir and lowering the mean systemic arterial pressure (MSAP) to ∼40 mmHg for 20 min. Our results showed the following. First, after MSAP reached a steady state of HH, the peak FA response to intravenous injection of capsaicin was elevated by approximately fivefold. The enhanced C-fiber sensitivity continued to increase during HH and sustained even after MSAP returned to baseline during the recovery, but slowly returned to control ∼20 min later. Second, responses of FA to intravenous injections of other chemical stimulants of pulmonary C-fibers (phenylbiguanide, lactic acid, and adenosine) and a constant-pressure lung hyperinflation were all significantly potentiated by HH. Third, infusion of sodium bicarbonate alleviated the systemic acidosis during HH, and it also attenuated, but did not completely prevent, the HH-induced C-fiber hypersensitivity. In conclusion, the pulmonary C-fiber sensitivity was elevated during HH, probably caused by the endogenous release of chemical substances (e.g., lactic acid) that were produced by tissue ischemia during HH. This enhanced C-fiber sensitivity may heighten the pulmonary protective reflexes mediated through these afferents (e.g., cough, J reflex) during hemorrhage when the body is more susceptible to other hazardous insults and pathophysiological stresses.

Role of pulmonary C fibers in adenosine-induced respiratory inhibition in anesthetized rats

1998 ◽  
Vol 84 (2) ◽  
pp. 417-424 ◽  
Author(s):  
Kevin Kwong ◽  
Ju-Lun Hong ◽  
Robert F. Morton ◽  
Lu-Yuan Lee
Keyword(s):  
Left Ventricular ◽  
Right Atrial ◽  
Dependent Manner ◽  
Sensory Afferents ◽  
C Fibers ◽  
Respiratory Inhibition ◽  
Anesthetized Rats ◽  
Long Latency ◽  
Therapeutic Doses

Kwong, Kevin, Ju-Lun Hong, Robert F. Morton, and Lu-Yuan Lee. Role of pulmonary C fibers in adenosine-induced respiratory inhibition in anesthetized rats. J. Appl. Physiol. 84(2): 417–424, 1998.—The clinical use of adenosine is commonly associated with pulmonary side effects, namely dyspnea, that suggest the possible involvement of bronchopulmonary sensory afferents. Our objective in this study was to characterize the effects of adenosine on breathing and to determine whether the vagal pulmonary afferents play a role in mediating these effects. We measured respiratory and cardiovascular changes in anesthetized, spontaneously breathing rats after bolus injections of adenosine at therapeutic doses. Right atrial injection of adenosine (0.04–0.6 mg/kg) elicits, in a dose-dependent manner, a pulmonary chemoreflex-like response consisting of a delayed apnea, bradycardia, and hypotension. In contrast, the classic capsaicin-elicited pulmonary chemoreflex occurs immediately after injection. Perineural capsaicin treatment of the cervical vagi blocked the adenosine-induced respiratory inhibition. Left ventricular administration of adenosine failed to elicit an apneic response. Pretreatment with the adenosine A1-receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine attenuated the adenosine-induced apnea. These results indicate that adenosine elicits a respiratory inhibition via stimulation of pulmonary C fibers and that activation of the A1-receptor is probably involved. It is unclear, however, what accounts for the exceedingly long latency in this response.

Microvascular control in intestinal mucosa of normal and hemorrhaged rats

1975 ◽  
Vol 229 (5) ◽  
pp. 1159-1164 ◽  
Author(s):  
HG Bohlen ◽  
PM Hutchins ◽  
CE Rapela ◽  
HD Green
Keyword(s):  
Small Intestine ◽  
Intestinal Mucosa ◽  
Neural Activity ◽  
Resting State ◽  
Neural Control ◽  
Baroreceptor Reflex ◽  
Carotid Occlusion ◽  
Hemorrhagic Hypotension ◽  
Anesthetized Rats

The mucosal microcirculation in innervated and denervated small intestine was studied using anesthetized rats. Denervation did not cause significant (P greater than 0.05) diameter changes in the precapillary vasculature; however, venules did constrict significantly. These results indicate minimum neural control in the precapillary vasculature during the resting state. The innervated precapillary vasculature constricted during both the carotid occlusion reflex and hemorrhagic hypotension. The diameter of the denervated precapillary vasculature was unchanged during the carotid occlusion reflex and dilated during hemorrhage. The responses of innervated and denervated precapillary vasculatures were attributed to increased neural activity and autoregulatory mechanisms, respectively. Neither innervated nor denervated venules responded during the carotid occlusion reflex. During hemorrhage, however, innervated venules constricted and denervated vessels dilated. The vasoconstriction of the innervated vasculature during hemorrhage contributed to a stoppage of blood and epithelial detachment; these responses did not occur in the dilated, denervated vasculature. Therefore, neural vasoconstriction, qualitatively similar to that in normal animals during the baroreceptor reflex, is a contributing cause to the vascular and tissue impairment in the intestinal mucosa during hemorrhage.

Vagal C-fiber blockade abolishes sympathetic inhibition by atrial natriuretic factor

1988 ◽  
Vol 255 (1) ◽  
pp. R6-R13 ◽  
Author(s):  
H. D. Schultz ◽  
D. G. Gardner ◽  
C. F. Deschepper ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Atrial Natriuretic Factor ◽  
Splanchnic Nerve ◽  
Nerve Activity ◽  
Renal Nerve ◽  
C Fibers ◽  
Natriuretic Factor ◽  
Anesthetized Rats ◽  
Renal Nerve Activity ◽  
Afferent Vagal ◽  
Atrial Natriuretic

Administration of atrial natriuretic factor (ANF) to anesthetized rats decreases renal nerve activity (RNA), an effect prevented by vagotomy but not by atropine. We sought to determine whether afferent vagal C-fibers mediate the inhibition of sympathetic outflow. ANF (2.5 micrograms/kg iv) decreased mean arterial pressure (MAP) by 25 +/- 2 mmHg, RNA by 11 +/- 5%, and least splanchnic nerve activity (LSNA) by 10 +/- 4% in anesthetized rats with arterial baroreceptors intact, and by 40 +/- 3 mmHg, 28 +/- 7%, and 23 +/- 4%, respectively, in sinoaortic-denervated rats. Inhibition of RNA and LSNA by ANF was reduced slightly by cooling the vagi to 6 or 7 degrees C, a temperature at which conduction in A-fibers was blocked and that in C-fibers attenuated; inhibition was abolished when C-fibers were blocked by cooling to 0 degrees C. We conclude that the inhibition of RNA and LSNA by ANF was mediated by afferent vagal C-fibers. We also obtained evidence that the aortic nerves contribute to ANF-induced inhibition of RNA. Our results support the notion that ANF evokes a generalized decrease in sympathetic tone that contributes to the hypotension, cardiac inhibition, and natriuresis accompanying systemic administration of the peptide.

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

2003 ◽  
Vol 94 (5) ◽  
pp. 1987-1998 ◽  
Author(s):  
Ting Ruan ◽  
Ching-Yin Ho ◽  
Yu Ru Kou
Keyword(s):  
Initial Response ◽  
Oxygen Species ◽  
C Fibers ◽  
Anesthetized Rats ◽  
Afferent Vagal ◽  
Vagal Cooling ◽  
Saline Vehicle ◽  
Respiratory Reflexes ◽  
Stimulation Of ◽  
Do So

We investigated the afferent vagal pathways mediating respiratory reflexes evoked by reactive oxygen species (ROS) in the lungs of anesthetized rats. Spontaneous inhalation of 0.2% aerosolized H2O2 acutely evoked initial bradypnea followed by delayed tachypnea, which was frequently mixed with delayed augmented inspiration. The initial response was abolished after perivagal capsaicin treatment (PCT), but was prolonged during vagal cooling (VC) to 7°C; PCT and VC are known to differentially block the conduction of unmyelinated C and myelinated fibers, respectively. The delayed responses were eliminated during VC but emerged earlier after PCT. Vagotomy, catalase (an antioxidant for H2O2), dimethylthiourea (an antioxidant for · OH), or deferoxamine (an antioxidant for · OH) largely or totally suppressed these reflexive responses, whereas sham nerve treatment, heat-inactivated catalase, saline vehicle, or iron-saturated deferoxamine failed to do so. These results suggest that 1) the H2O2-evoked initial and delayed airway reflexes are antagonistic and may result from stimulation of lung C fibers and rapidly adapting receptors, respectively, and 2) the reflex effects of H2O2 are, in part, due to the action of · OH on these afferents.

scholarly journals Adrenal and renal sympathetic nerve responses to acute hemorrhagic hypotension in anesthetized rats

1988 ◽  
Vol 46 ◽  
pp. 126
Author(s):  
Hiroko Togashi ◽  
Mitsuhiro Yoshioka ◽  
Machiko Matsumoto ◽  
Masahiro Tochihara ◽  
Hideya Saito
Keyword(s):  
Sympathetic Nerve ◽  
Hemorrhagic Hypotension ◽  
Renal Sympathetic Nerve ◽  
Anesthetized Rats ◽  
Renal Sympathetic

Pulmonary chemoreflexes elicited by intravenous injection of lactic acid in anesthetized rats

1996 ◽  
Vol 81 (6) ◽  
pp. 2349-2357 ◽  
Author(s):  
Lu-Yuan Lee ◽  
Robert F. Morton ◽  
Jan M. Lundberg
Keyword(s):  
Lactic Acid ◽  
Intravenous Injection ◽  
Inhibitory Effect ◽  
Electrophysiological Recording ◽  
Vagus Nerves ◽  
C Fibers ◽  
Anesthetized Rats ◽  
C Fiber ◽  
Intense Burst ◽  
Carotid Body Chemoreceptors

Lee, Lu-Yuan, Robert F. Morton, and Jan M. Lundberg.Pulmonary chemoreflexes elicited by intravenous injection of lactic acid in anesthetized rats. J. Appl. Physiol. 81(6): 2349–2357, 1996.—Experiments were carried out to characterize the cardiorespiratory reflex responses to intravenous injection of lactic acid and to determine the involvement of vagal bronchopulmonary C-fiber afferents in eliciting these responses in anesthetized rats. Bolus injection of lactic acid (0.2 mmol/kg iv) immediately elicited apnea, bradycardia, and hypotension, which were then followed by a sustained hyperpnea. The immediate apneic and bradycardiac responses to lactic acid were completely abolished by bilateral vagotomy and were absent when the same dose of lactic acid was injected into the left ventricle. The subsequent hyperpneic response was substantially attenuated by denervation of carotid body chemoreceptors. After a perineural capsaicin treatment of both vagus nerves to block the conduction of C fibers, lactic acid no longer evoked the immediate apnea and bradycardia, whereas the hyperpneic response became more pronounced and sustained, presumably because of the removal of the inhibitory effect on breathing mediated by pulmonary C-fiber activation. Single-unit electrophysiological recording showed that intravenous injection of lactic acid consistently evoked an abrupt and intense burst of discharge from the vagal C-fiber afferent endings in the lungs. In conclusion, the cardiorespiratory depressor responses induced by lactic acid are predominantly elicited by activation of vagal pulmonary C fibers.

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