Effects of hypercapnia and hypoxia on abdominal expiratory nerve activity

1983 ◽  
Vol 55 (5) ◽  
pp. 1614-1622 ◽  
Author(s):  
J. F. Ledlie ◽  
A. I. Pack ◽  
A. P. Fishman
Keyword(s):  
Mechanical Ventilation ◽  
Chest Wall ◽  
Neural Activity ◽  
Intravenous Infusion ◽  
Base Line ◽  
Medial Branch ◽  
Plateau Phase ◽  
Nerve Activity ◽  
Proprioceptive Inputs ◽  
Line Level

We examined the effects of progressive hypercapnia and hypoxia on the efferent neural activity in a whole abdominal expiratory nerve (medial branch of the cranial iliohypogastric nerve (L1) in anesthetized, paralyzed dogs. To eliminate effects of phasic lung and chest-wall movements on expiratory activity, studies were performed in the absence of breathing movements. Progressive hyperoxic hypercapnia and isocapnic hypoxia were produced in the paralyzed animals by allowing 3-5 min of apnea to follow mechanical ventilation with 100% O2 or 35% O2 in N2, respectively; during hypoxia, isocapnia was maintained by intravenous infusion of tris(hydroxymethyl)aminomethane buffer at a predetermined rate. To quantify abdominal expiratory activity, mean abdominal nerve activity in a nerve burst was computed by integrating the abdominal neurogram and dividing by the duration of the nerve burst. Hypercapnia and hypoxia both increased mean abdominal nerve activity and decreased expiratory duration. In contrast to the ramplike phrenic neurogram, the abdominal neurogram consisted of three phases: an initial rising phase, a plateau phase in which abdominal nerve activity was approximately constant, and a terminal declining phase in which the activity returned to the base-line level. The height of this plateau phase and the rates of rise and decline of abdominal nerve activity all increased with increasing hypercapnia and hypoxia. We conclude that, with proprioceptive inputs constant, both hypercapnia and hypoxia are excitatory to abdominal expiratory neural activity.

Ozone increases susceptibility to antigen inhalation in allergic dogs

1990 ◽  
Vol 68 (6) ◽  
pp. 2267-2273 ◽  
Author(s):  
M. Yanai ◽  
T. Ohrui ◽  
T. Aikawa ◽  
H. Okayama ◽  
K. Sekizawa ◽  
...  
Keyword(s):  
Intravenous Infusion ◽  
Airway Responsiveness ◽  
Base Line ◽  
Plasma Histamine ◽  
Respiratory Resistance ◽  
Histamine Concentration ◽  
Protein Nitrogen ◽  
Before And After ◽  
Plasma Histamine Concentration ◽  
Line Level

To determine whether O3 exposure increased airway responsiveness to antigen inhalation, we studied airway responsiveness to acetylcholine (ACh) and Ascaris suum antigen (AA) before and after O3 in dogs both sensitive and insensitive to AA. Airway responsiveness was assessed by determining the provocative concentration of ACh and AA aerosols that increased respiratory resistance (Rrs) to twice the base-line value. O3 (3 parts per million) increased airway responsiveness to ACh in dogs both sensitive and insensitive to AA, and it significantly decreased the ACh provocation concentration from 0.541 +/- 0.095 to 0.102 +/- 0.047 (SE) mg/ml (P less than 0.01; n = 10). AA aerosols, even at the highest concentration in combination with O3, did not increase Rrs in dogs insensitive to AA. However, O3 increased airway responsiveness to AA in AA-sensitive dogs and significantly decreased log AA provocation concentration from 2.34 +/- 0.22 to 0.50 +/- 0.17 (SE) log protein nitrogen units/ml (P less than 0.01; n = 7). O3-induced hyperresponsiveness to ACh returned to the base-line level within 2 wk, but hyperresponsiveness to AA continued for greater than 2 wk. The plasma histamine concentration after AA challenge was significantly higher after than before O3 (P less than 0.01). Intravenous infusion of OKY-046 (100 micrograms.kg-1.min-1), an inhibitor of thromboxane synthesis, inhibited the O3-induced increase in responsiveness to ACh, but it had no effects on the O3-induced increase in responsiveness to AA and the increase in the plasma histamine concentration. These results suggest that O3 increases susceptibility to the antigen in sensitized dogs via a different mechanism from that of O3-induced muscarinic hyperresponsiveness.

Baroreflex control of sympathetic outflow in pregnant rats: effects of captopril

1990 ◽  
Vol 258 (6) ◽  
pp. R1417-R1423 ◽  
Author(s):  
M. E. Crandall ◽  
C. M. Heesch
Keyword(s):  
Base Line ◽  
Operating Pressure ◽  
Sympathetic Outflow ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Pregnant Rats ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Near Term ◽  
Renal Sympathetic

Arterial baroreflex control of renal sympathetic nerve activity (RSNA) was compared in nonpregnant (NP) and near-term pregnant (P) chloralose-anesthetized rats. Baroreflex curves were obtained by recording reflex changes in RSNA (expressed as a percent of base line) due to increases and decreases in mean arterial pressure (MAP) [intravenous phenylephrine and nitroprusside (NTP)]. The slope, midpoint (EP50), and threshold pressures of the baroreflex curves were compared. Base-line MAP was significantly lower in the pregnant animals (P = 96 +/- 3 vs. NP = 113 +/- 5 mmHg). The baroreflex curves of pregnant animals also had significantly lower threshold (P = 95 +/- 3 vs. NP = 110 +/- 5 mmHg) and midpoint values (P = 105 +/- 4 vs. NP = 119 +/- 5 mmHg). The response to unloading the baroreceptors was attenuated in the pregnant animals as indicated by a decrease in slope of the NTP portion of the baroreflex curve (P = 0.95 +/- 0.17 vs. NP = 1.61 +/- 0.29% nerve activity/mmHg). Responses to blockade of angiotensin-converting enzyme with captopril (2 mg/kg iv) were also examined. There were no differences in EP50 or slope among the control, captopril, and recovery baroreflex curves within either the nonpregnant or pregnant animals. However, after captopril, MAP decreased to a greater extent in the pregnant rats, yet RSNA increased to the same level for the two groups. Thus pregnancy results in a leftward shift of the baroreflex function curve toward a lower operating pressure range. In addition, pregnant rats demonstrated an impaired ability to increase sympathetic outflow above base-line values in response to a hypotensive challenge.

Effects of hypercapnia and hypoxia on phrenic nerve activity and respiratory timing

1981 ◽  
Vol 51 (3) ◽  
pp. 732-738 ◽  
Author(s):  
J. F. Ledlie ◽  
S. G. Kelsen ◽  
N. S. Cherniack ◽  
A. P. Fishman
Keyword(s):  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Peak Height ◽  
Inspiratory Time ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Chemical Stimuli ◽  
Proprioceptive Inputs ◽  
Spontaneously Breathing ◽  
Respiratory Responses

In the spontaneously breathing animal, respiratory responses to chemical stimuli are influenced by phasic proprioceptive inputs from the thorax. We have compared the effects of hypercapnia and hypoxia on the level and timing of phrenic nerve activity while these phasic afferent signals were absent. Progressive hyperoxic hypercapnia and isocapnic hypoxia were produced in anesthetized paralyzed dogs by allowing 3–5 min of apnea to follow mechanical ventilation with 100% O2 or 35% O2 in N2, respectively; during hypoxia, isocapnia was maintained by intravenous infusion of tris(hydroxymethyl)aminomethane buffer. The peak height (P) of nerve bursts, inspiratory time (TI), and expiratory time (TE) were measured from the phrenic neurogram. With the vagi intact or severed, hypoxia decreased TI, whereas hypercapnia did not; both stimuli decreased TE. At the same minute phrenic activity (P x frequency), P, TI, and TE were all less during hypoxia than during hypercapnia. The decreases in TI and TE with hypoxia were significantly less after carotid sinus denervation. The results indicate that the patterns of phrenic nerve activity in response to hypoxia and hypercapnia are different: hypoxia has a greater effect on respiratory timing, whereas hypercapnia has a greater effect on peak phrenic nerve activity. The effect of hypoxia on respiratory timing is largely mediated by the peripheral chemoreceptors.

Neurotransmitters and biphasic respiratory response to hypoxia

1984 ◽  
Vol 57 (1) ◽  
pp. 213-222 ◽  
Author(s):  
W. A. Long ◽  
E. E. Lawson
Keyword(s):  
Phrenic Nerve ◽  
Initial Increase ◽  
Base Line ◽  
Respiratory Response ◽  
Biphasic Response ◽  
Controlled System ◽  
Initial Exposure ◽  
End Tidal ◽  
Line Level ◽  
End Tidal Co2

Recent work from this laboratory (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55:483–488, 1983) has shown that the biphasic respiratory response to hypoxia in piglets is due to changing central neural respiratory output. To test the hypothesis that either adenosine or opiatelike neurotransmitters mediate the failure to sustain hyperpnea in response to hypoxia, 12 piglets were studied ata mean age of 2.9 +/- 0.4 days (range 2–6 days). Animals were anesthetized, paralyzed, and ventilatedusing a servo-controlled system that maintained end-tidal CO2 constant. Electrical activity of the phrenic nerve was recorded as the index of breathing. An initial experimental trial of 6 min ventilation with 15% O2 was performed in all 12 piglets. Thereafter all 12 piglets were treated with aminophylline (n = 6), naloxone (n = 3), or naltrexone (n = 3) and again subjected to 15% O2. During initial exposure to hypoxia there was an initial increase in phrenic activity that was not sustained. During recovery ventilation with 100% O2, phrenic activity transiently declined below the base-line level and then gradually returned. Subsequent intravenous administration of aminophylline, naloxone, or naltrexone caused base-line phrenic activity to increase. Thereafter repeat exposures to 15% O2 were carried out. During these posttreatment trials of hypoxia, phrenic activity further increased, but the hyperventilation was again not sustained. These findings suggest it is unlikely that either adenosine or mu-endorphin neurotransmitters are the primary mediators of the biphasic response to hypoxia in newborns.

Angiotensin II acutely attenuates range of arterial baroreflex control of renal sympathetic nerve activity

2000 ◽  
Vol 279 (4) ◽  
pp. H1804-H1812 ◽  
Author(s):  
Max G. Sanderford ◽  
Vernon S. Bishop
Keyword(s):  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Renal Sympathetic

Acutely increasing peripheral angiotensin II (ANG II) reduces the maximum renal sympathetic nerve activity (RSNA) observed at low mean arterial blood pressures (MAPs). We postulated that this observation could be explained by the action of ANG II to acutely increase arterial blood pressure or increase circulating arginine vasopressin (AVP). Sustained increases in MAP and increases in circulating AVP have previously been shown to attenuate maximum RSNA at low MAP. In conscious rabbits pretreated with an AVP V1 receptor antagonist, we compared the effect of a 5-min intravenous infusion of ANG II (10 and 20 ng · kg−1 · min−1) on the relationship between MAP and RSNA when the acute pressor action of ANG II was left unopposed with that when the acute pressor action of ANG II was opposed by a simultaneous infusion of sodium nitroprusside (SNP). Intravenous infusion of ANG II resulted in a dose-related attenuation of the maximum RSNA observed at low MAP. When the acute pressor action of ANG II was prevented by SNP, maximum RSNA at low MAP was attenuated, similar to that observed when ANG II acutely increased MAP. In contrast, intravertebral infusion of ANG II attenuated maximum RSNA at low MAP significantly more than when administered intravenously. The results of this study suggest that ANG II may act within the central nervous system to acutely attenuate the maximum RSNA observed at low MAP.

In vivo regional diaphragm function in dogs

1989 ◽  
Vol 67 (2) ◽  
pp. 655-662 ◽  
Author(s):  
J. Sprung ◽  
C. Deschamps ◽  
R. D. Hubmayr ◽  
B. J. Walters ◽  
J. R. Rodarte
Keyword(s):  
Mechanical Ventilation ◽  
Chest Wall ◽  
Spontaneous Breathing ◽  
Considerable Variability ◽  
Diaphragm Function ◽  
Left Hemidiaphragm ◽  
Anesthetized Dogs ◽  
Abdominal Surface ◽  
Crural Diaphragm

A biplane videofluorographic system was used to track the position of metallic markers affixed to the abdominal surface of the left hemidiaphragm in supine anesthetized dogs. Regional shortening was determined from intermarker distances of rows of markers placed along muscle bundles in the ventral, middle, and dorsal regions of the costal diaphragm and of one row on the crural diaphragm. Considerable variability of regional shortening was seen in a given row, which was reproducible on repeat study in individual dogs but which differed between mechanical ventilation and spontaneous breathing. There were no consistent patterns among dogs. Regional shortening obtained from the change in length of rows extending from chest wall to central tendon showed no consistent differences among dogs during spontaneous breathing. At equal tidal volumes, all regions (except the ventral costal diaphragm) shortened more during spontaneous breathing than during mechanical ventilation.

Rapid up- and down-regulation of pheromone signalling due to trail crowding in the ant Lasius niger

Behaviour ◽  
2014 ◽  
Vol 151 (5) ◽  
pp. 669-682 ◽  
Author(s):  
Tomer J. Czaczkes ◽  
Christoph Grüter ◽  
Francis L.W. Ratnieks
Keyword(s):  
Cuticular Hydrocarbons ◽  
Social Insects ◽  
Glass Beads ◽  
Lasius Niger ◽  
Base Line ◽  
Baseline Levels ◽  
Line Level ◽  
Pheromone Signalling ◽  
Repeat Visits ◽  
Pheromone Trail

Social insects often respond to signals and cues from nest-mates, and these responses may include changes in the information they, in turn, transmit. During foraging, Lasius niger deposits a pheromone trail to recruit nestmates, and ants that experience trail crowding deposit pheromone less often. Less studied, however, is the time taken for signalling to revert to baseline levels after conditions have returned to baseline levels. In this paper we study the behaviour of L. niger foragers on a trail in which crowding is simulated by using dummy ants — black glass beads coated in nestmate cuticular hydrocarbons. Ants were allowed to make four repeat visits to a feeder with dummy ants, and thus crowding, being present on the trail on all visits (CCCC), none (UUUU) or only the first two (CCUU). If dummy ants were always present (CCCC), pheromone deposition probability was low in the first two visits (54% of ants deposited pheromone) and remained low in visits 3 and 4 (51%). If dummy ants were never present (UUUU) pheromone deposition probability was high in the first two visits (93%) and remained high in visits 3 and 4 (83%). If dummy ants were present on the first two visits but removed on the second two visits (CCUU) pheromone deposition probability was low in the first two visits (61%) but rose in the second two visits (69%). This demonstrates that even after pheromone deposition has been down-regulated due to crowding in the first two visits, it is rapidly up-regulated when crowding is reduced, although it does not immediately return to the base line level.

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