Histamine and pulmonary responses to cigarette smoke in periphery of the lung

1982 ◽  
Vol 53 (3) ◽  
pp. 582-588 ◽  
Author(s):  
A. Gertner ◽  
B. Bromberger ◽  
R. Traystman ◽  
H. Menkes
Keyword(s):  
Cigarette Smoke ◽  
Fiber Optic ◽  
Local Responses ◽  
Before And After ◽  
Environmental Agents ◽  
Peripheral Airway ◽  
Anesthetized Dogs ◽  
Lung Periphery ◽  
Histamine Challenge

An animal model for studying responses of the lung periphery to controlled levels of environmental agents has been used to assess the role of histamine in pulmonary responses to cigarette smoke. A fiber-optic bronchoscope was wedged in a peripheral airway of anesthetized dogs. Measurements of collateral resistance (Rcoll) were used to monitor responses to histamine and cigarette smoke. Responses to an aerosol containing histamine (1.5 X 10(-4) mg) and cigarette smoke (420 ml) were measured before and after the administration of an aerosol containing 1.0 mg chlorpheniramine. Prior to the administration of chlorpheniramine, the histamine challenge produced a 75 +/- 26% increase in Rcoll and cigarette smoke produced a 74 +/- 26% increase. Following the administration of chlorpheniramine, the peak responses to histamine and cigarette smoke were reduced by 82 +/- 9 and 61 +/- 8%, respectively. Administration of the same dose of chlorpheniramine prior to challenge with methacholine did not reduce the response to that agent. These results indicate that acute local responses to cigarette smoke in the periphery of the lung are mediated in part through the release of histamine.

Evidence against local neural mechanism for intestinal postprandial hyperemia

1983 ◽  
Vol 245 (3) ◽  
pp. H437-H446 ◽  
Author(s):  
R. A. Nyhof ◽  
C. C. Chou
Keyword(s):  
Oxygen Consumption ◽  
Oleic Acid ◽  
Neural Mechanism ◽  
Jejunal Mucosa ◽  
Vasoactive Substances ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Postprandial Hyperemia

The role of local intestinal nerves in the nutrient-induced intestinal hyperemia was investigated in jejunal segments of anesthetized dogs by comparing the hyperemic effect of intraluminal glucose and oleic acid solutions before and after mucosal anesthesia and infusions of methysergide, hexamethonium, and tetrodotoxin. Methysergide, hexamethonium, and tetrodotoxin all failed to alter either the vascular or metabolic responses to luminal placement of glucose or oleic acid. The increases in blood flow and oxygen uptake produced by glucose or oleic acid, however, were blocked or attenuated after exposing the mucosa to dibucaine. The effect was norepinephrine due to an altered vascular response to vasoactive substances as dibucaine did not alter vascular responses to isoproterenol or norepinephrine. Dibucaine, however, inhibited active transport and increased passive transport of glucose across rat intestinal sacs in vitro. Oxygen consumption of the canine jejunal mucosa was also inhibited by dibucaine in vitro. It seems that inhibition of the nutrient-induced intestinal hyperemia by dibucaine is due, at least in part, to its effect on oxygen consumption and glucose transport of the mucosal epithelial cells. Nutrient-induced hyperemia appears not to be neurally mediated but more closely related to metabolism.

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.

Role of the descending pressor pathway in the conscious and pentobarbital-anesthetized dog

1978 ◽  
Vol 234 (2) ◽  
pp. H152-H156
Author(s):  
G. S. Geis ◽  
G. Barratt ◽  
R. D. Wurster
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Control ◽  
Conscious Dogs ◽  
Cardiovascular Parameters ◽  
Bilateral Carotid ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Conscious Animals

Resting cardiovascular parameters and the responses to bilateral carotid occlusions (BCO) were monitored in pentobarbital-anesthetized and conscious dogs before and after placing lesions in the dorsolateral funiculi at C7-C8 and after spinal transections at C7. Pre- and postlesion blood pressure (BP) and heart rate (HR) responses to exercise were also monitored. The lesions significantly attenuated the responses to BCO and decreased resting BP in anesthetized dogs. Yet neither resting HR in anesthetized or conscious dogs nor the resting BP in conscious dogs was affected by the lesions. Subsequent spinal transections significantly decreased resting HR and BP and the responses to BCO but did not affect the BP response to BCO in anesthetized dogs as compared with corresponding postlesion parameters. BP responses to exercise were significantly attenuated by the lesions, but HR responses were not affected. Since stimulation and BP studies indicated that the descending pressor pathway had been ablated, the data suggest that the pathway mediates BP and HR responses to BCO in pentobarbital-anesthetized and conscious dogs. It does not maintain resting HR in anesthetized or conscious animals, and the resting BP in conscious dogs. This pathway is important for BP responses to exercise but is not necessary for HR responses. Finally, other spinal pathways are involved in cardiovascular control.

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.

Role of tachykinins in ozone-induced airway hyperresponsiveness to cigarette smoke in guinea pigs

1997 ◽  
Vol 83 (3) ◽  
pp. 958-965 ◽  
Author(s):  
Zhong-Xin Wu ◽  
Robert F. Morton ◽  
Lu-Yuan Lee
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Airway Hyperresponsiveness ◽  
Lung Compliance ◽  
Smoke Inhalation ◽  
Before And After ◽  
Sham Exposure ◽  
Inhalation Challenge ◽  
Dynamic Lung Compliance

Wu, Zhong-Xin, Robert F. Morton, and Lu-Yuan Lee. Role of tachykinins in ozone-induced airway hyperresponsiveness to cigarette smoke in guinea pigs. J. Appl. Physiol. 83(3): 958–965, 1997.—Acute exposure to ozone (O3) induces airway hyperresponsiveness to various inhaled bronchoactive substances. Inhalation of cigarette smoke, a common inhaled irritant in humans, is known to evoke a transient bronchoconstrictive effect. To examine whether O3 increases airway responsiveness to cigarette smoke, effects of smoke inhalation challenge on total pulmonary resistance (Rl) and dynamic lung compliance (Cdyn) were compared before and after exposure to O3 (1.5 ppm, 1 h) in anesthetized guinea pigs. Before O3 exposure, inhalation of two breaths of cigarette smoke (7 ml) at a low concentration (33%) induced a mild and reproducible bronchoconstriction that slowly developed and reached its peak (ΔRl= 67 ± 19%, ΔCdyn = −29 ± 6%) after a delay of >1 min. After exposure to O3 the same cigarette smoke inhalation challenge evoked an intense bronchoconstriction that occurred more rapidly, reaching its peak (ΔRl = 620 ± 224%, ΔCdyn = −35 ± 7%) within 20 s, and was sustained for >2 min. By contrast, sham exposure to room air did not alter the bronchomotor response to cigarette smoke challenge. Pretreatment with CP-99994 and SR-48968, the selective antagonists of neurokinin type 1 and 2 receptors, respectively, completely blocked the enhanced responses of Rl and Cdyn to cigarette smoke challenge induced by O3. These results show that O3 exposure induces airway hyperresponsiveness to inhaled cigarette smoke and that the enhanced responses result primarily from the bronchoconstrictive effect of endogenous tachykinins.

Maintenance of renal autoregulation during infusion of aminophylline or adenosine

1985 ◽  
Vol 248 (3) ◽  
pp. F366-F373 ◽  
Author(s):  
A. J. Premen ◽  
J. E. Hall ◽  
H. L. Mizelle ◽  
J. E. Cornell
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Receptor Blockade ◽  
Renal Metabolism ◽  
Renal Autoregulation ◽  
Before And After ◽  
Anesthetized Dogs

Adenosine has been postulated to link control of glomerular filtration rate (GFR) and renal blood flow (RBF) with changes in renal metabolism. In the present study, we examined the role of adenosine in renal autoregulation by comparing the responses of normal anesthetized dogs to step decreases in renal artery pressure (RAP) to the response obtained after receptor blockade of adenosine with aminophylline or by flooding the kidney with exogenous adenosine. In six dogs at normal RAP, intrarenal infusion of aminophylline (10 mumol/min) did not alter renal hemodynamics. GFR and RBF were well autoregulated (greater than 90% of control) at RAP values equal to or greater than 85 mmHg before and after aminophylline. At RAP equal to 75 mmHg, GFR and RBF decreased by 27 +/- 10 and 20 +/- 8%, respectively, before aminophylline and by 25 +/- 7 and 13 +/- 6% after aminophylline. In a different group of six dogs, intrarenal infusion of adenosine (6 mumol/min) significantly increased RBF (32 +/- 9%) and decreased GFR (38 +/- 10%) at normal RAP. However, GFR and RBF were both well autoregulated (greater than 90% of control) at RAP values equal to or greater than 85 mmHg before and after adenosine. At RAP equal to 75 mmHg, GFR and RBF decreased by 10 +/- 5 and 7 +/- 3%, respectively, before adenosine and by 12 +/- 6 and 17 +/- 5% after adenosine. Neither aminophylline nor adenosine attenuated the elevations in plasma renin activity associated with reductions in RAP. These data fail to provide evidence that adenosine is an important factor in autoregulation of GFR and RBF during acute reductions in RAP within the autoregulatory range.

Renal effects of prostaglandin inhibition during increases in renal venous pressure

1991 ◽  
Vol 260 (4) ◽  
pp. F525-F529 ◽  
Author(s):  
M. J. Fiksen-Olsen ◽  
J. C. Romero
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Venous Pressure ◽  
Interstitial Pressure ◽  
Pentobarbital Sodium ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Pressure Changes

The role of prostaglandins (PGs) in mediating the hemodynamic and natriuretic responses to increases in renal interstitial pressure (RIP) induced by altering renal venous pressure (RVP) from control (3.6 +/- 0.6) to 15 and 30 mmHg was examined before and after PG inhibition in pentobarbital sodium-anesthetized dogs. These elevations of RVP resulted in RIP increasing from control (6 +/- 1) to 11 +/- 1 and 23 +/- 2 mmHg, respectively, without altering mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR). Sodium excretion increased only when RVP reached 30 mmHg. During the inhibition of PG synthesis, 15 mmHg RVP induced a 10% decrease in RBF, and 30 mmHg RVP induced a further 20% decrease in RBF and a 50% decrease in GFR. PG synthesis inhibition did not alter either the RIP or the sodium excretory response. In conclusion, the natriuresis associated with the RIP increases induced by increasing RVP appears to be independent of PG synthesis. PGs, however, appear to be important for the maintenance of RBF and GFR during increased RVP. These findings suggest that different mechanisms are involved in the hemodynamic and natriuretic responses to arterial vs. venous pressure changes.

Adenosine 5′-monophosphate challenge elicits a more peripheral airway response than methacholine challenge

2011 ◽  
Vol 110 (5) ◽  
pp. 1241-1247 ◽  
Author(s):  
Alain Michils ◽  
Yvon Elkrim ◽  
Amaryllis Haccuria ◽  
Alain Van Muylem
Keyword(s):  
Airway Hyperreactivity ◽  
Phase Iii ◽  
Ventilation Distribution ◽  
Methacholine Challenge ◽  
Single Breath ◽  
Before And After ◽  
Asthma Patients ◽  
Peripheral Airway ◽  
Airway Response ◽  
Lung Periphery

Adenosine 5′-monophosphate (AMP) and methacholine are commonly used to assess airway hyperreactivity. However, it is not fully known whether the site of airway constriction primarily involved during challenges with either agent is similar. Using a ventilation distribution test, we investigated whether the constriction induced by each agent involves the lung periphery in a similar fashion. Ventilation distribution was evaluated by the phase III slope (S) of the single-breath washout, using gases with different diffusivities like helium (He) and hexafluorosulfur (SF6). A greater postchallenge increase in SHe reflects alterations at the level of terminal and respiratory bronchioles, while a greater increase in SSF6 reflects alterations in alveolar ducts, increases to an equal extent reflecting alterations in more proximal airways where gas transport is still convective for both gases. SSF6 and SHe were measured in 15 asthma patients before and after airway challenges (20% forced expired volume in 1-s fall) with AMP and methacholine. SHe increased to a greater extent than SSF6 after AMP challenge (5.7 vs. 3.7%/l; P = 0.002), with both slopes increasing to an equal extent after methacholine challenge (3.1%/l; P = 0.959). The larger increase in SHe following AMP challenge suggests distal ventilation impairment up to the level of terminal and respiratory bronchioles. With methacholine, the similar increases in SHe and SSF6 suggest a less distal impairment. AMP, therefore, seems to affect more extensively the very peripheral airways, whereas methacholine seems to have an effect on less distal airways.

Response of collateral channels to histamine: lack of vagal effect

1981 ◽  
Vol 51 (5) ◽  
pp. 1314-1319 ◽  
Author(s):  
J. Kaplan ◽  
G. C. Smaldone ◽  
H. A. Menkes ◽  
D. L. Swift ◽  
R. J. Traystman
Keyword(s):  
Base Line ◽  
Flexible Fiber ◽  
Before And After ◽  
Cervical Vagotomy ◽  
A New Technique ◽  
Alpha Chloralose ◽  
Histamine Challenge ◽  
Line Resistance ◽  
Reproducible Manner

A new technique using a monodispersed aerosol of histamine delivered to sublobar bronchi through a flexible fiber-optic bronchoscope was used to study the role of the vagus nerve and the effect of anesthesia in the response of collateral channels to exogenous histamine. Studies were performed in paralyzed dogs anesthetized with pentobarbital sodium or alpha-chloralose. Challenges with histamine aerosol were delivered to separate bronchi in each animal before and after bilateral cervical vagotomy. Resistance through collateral channels increased in a reproducible manner following histamine challenge. Vagotomy resulted in no significant change in base-line resistance through collateral channels. The response of collateral channels to exogenous histamine aerosol was not significantly affected by vagotomy or the type of anesthesia used. We conclude that vagal reflexes do not play a significant role in the response of collateral channels to exogenous histamine.

Cigarette smoke-induced bronchoconstriction in dogs: vagal and extravagal mechanisms

1984 ◽  
Vol 57 (4) ◽  
pp. 1261-1270 ◽  
Author(s):  
J. Hartiala ◽  
C. Mapp ◽  
R. A. Mitchell ◽  
R. L. Shields ◽  
W. M. Gold
Keyword(s):  
Smooth Muscle ◽  
Cigarette Smoke ◽  
Airway Smooth Muscle ◽  
Airway Pressure ◽  
Muscle Tone ◽  
Motor Nerve ◽  
Respiratory Center ◽  
Airway Response ◽  
Anesthetized Dogs

We reassessed the severity of cigarette smoke-induced bronchoconstriction and the mechanisms involved in anesthetized dogs. To evaluate the severity of smoke-induced bronchoconstriction, we measured airway pressure and airflow resistance (Rrs, forced oscillation method). We studied the mechanisms in other dogs by measuring airway pressure, central airway smooth muscle tone in tracheal segments in situ, and respiratory center drive by monitoring phrenic motor nerve output, including the role of vagal and extravagal nerves vs. the role of blood-borne materials during inhalation of cigarette smoke. Rrs increased more than fourfold with smoke from one cigarette delivered in two tidal volumes. About half the airway response was due to local effects of smoke in the lungs. The remainder was due to stimulation of the respiratory center, which activated vagal motor efferents to the airway smooth muscle. Of this central stimulation, about half was due to blood-borne materials and the rest to vagal pulmonary afferents from the lungs. We conclude that inhalation of cigarette smoke in dogs causes severe bronchoconstriction which is mediated mainly by extravagal mechanisms.

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