Propranolol and the Ventilatory Response to Hypoxia and Hypercapnia in Normal Man

1978 ◽  
Vol 55 (5) ◽  
pp. 491-497 ◽  
Author(s):  
J. M. Patrick ◽  
Janice Tutty ◽  
S. B. Pearson
Keyword(s):  
Heart Rate ◽  
Chemical Control ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Control Of Breathing ◽  
Maximal Expiratory Flow ◽  
Progressive Exercise ◽  
Normal Man ◽  
Ventilatory Response To Hypoxia

1. The effect on respiration of a single dose of propranolol has been studied in normal subjects. 2. The degree of β-adrenoreceptor blockade was assessed in terms of the impaired heart-rate response to progressive exercise and the plasma propranolol concentration. 3. No effect of propranolol was demonstrated on either the ventilatory response to rebreathing CO2 in hyperoxia, or the response to progressive isocapnic hypoxia. Simple indices of maximal expiratory flow (FEV1.0% and PEFR) were also unchanged. 4. The absence of any effect of propranolol on the chemical control of breathing in man is discussed in relation to the conflicting literature.

scholarly journals Intravenous adenosine and dyspnea in humans

2005 ◽  
Vol 98 (1) ◽  
pp. 180-185 ◽  
Author(s):  
Nausherwan K. Burki ◽  
Wheeler J. Dale ◽  
Lu-Yuan Lee
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Peripheral Chemoreceptor ◽  
C Fibers ◽  
Group Data ◽  
Lung Resistance ◽  
Time Latency ◽  
Stimulation Of

Intravenous adenosine for the treatment of supraventricular tachycardia is reported to cause bronchospasm and dyspnea and to increase ventilation in humans, but these effects have not been systematically studied. We therefore compared the effects of 10 mg of intravenous adenosine with placebo in 21 normal subjects under normoxic conditions and evaluated the temporal sequence of the effects of adenosine on ventilation, dyspnea, and heart rate. The study was repeated in 11 of these subjects during hyperoxia. In all subjects, adenosine resulted in the development of dyspnea, assessed by handgrip dynamometry, without any significant change ( P > 0.1) in lung resistance as measured by the interrupter technique. There were significant increases ( P < 0.05) in ventilation and heart rate in response to adenosine. The dyspneic response occurred slightly before the ventilatory or heart rate responses in every subject, but the timing of the dyspneic, ventilatory, and heart rate responses was not significantly different when the group data were analyzed (18.9 ± 5.8, 20.3 ± 5.5, and 19.7 ± 4.5 s, respectively). During hyperoxia, adenosine resulted in similar effects, with no significant differences in the magnitude of the ventilatory response; however, compared with the normoxic state, the intensity of the dyspneic response was significantly ( P < 0.05) reduced, whereas the heart rate response increased significantly ( P < 0.05). These data indicate that intravenous adenosine-induced dyspnea is not associated with bronchospasm in normal subjects. The time latency of the response indicates that the dyspnea is probably not a consequence of peripheral chemoreceptor or brain stem respiratory center stimulation, suggesting that it is most likely secondary to stimulation of receptors in the lungs, most likely vagal C fibers.

Luft's syndrome: O2 cost of exercise and chemical control of breathing

1975 ◽  
Vol 39 (5) ◽  
pp. 857-859 ◽  
Author(s):  
N. H. Edelman ◽  
T. V. Santiago ◽  
H. L. Conn
Keyword(s):  
Chemical Control ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Control Of Breathing ◽  
O2 Consumption ◽  
Arterial Blood ◽  
Skeletal Muscle Mitochondria ◽  
Ventilatory Response To Co2

The oxygen cost of exercise and chemical control of breathing were studied in a subject with Luft's syndrome, a disorder in which skeletal muscle mitochondria have a high “resting” O2 consumption which is imcreased only slightly by stimulation with excess phosphate acceptor, but a normal P/O ratio. The O2 consumption was more than three times normal (1.05 1/min) at rest but could be doubled when stimulated by maximal exercise. The O2 cost of exercise was similar to that of normal subjects. At rest, arterial blood PCO2 and ventilatory response to CO2 were normal, while ventilatory response to hypoxia was four times the predicted value. The data 1) confirm, in vivo, the normal respiratory efficiency of skeletal muscles in this disorder; 2) suggest that in vitro estimates of the extent to which mitochondrial respiration can be stimulated may not correlate with in vivo determinations; and 3) suggests that hypermetabolism per se can cause the ventilatory adjustments which are associated with exercise in normal subjects.

Role of the carotid bodies in the heart rate response to breath holding in man

1976 ◽  
Vol 41 (3) ◽  
pp. 336-340 ◽  
Author(s):  
P. M. Gross ◽  
B. J. Whipp ◽  
J. T. Davidson ◽  
S. N. Koyal ◽  
K. Wasserman
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Normal Subjects ◽  
The Other ◽  
Breath Holding ◽  
Asthmatic Patients ◽  
Carotid Bodies ◽  
Normal Man

To investigate the role of the carotid bodies in regulating the bradycardia of breath holding in man, we studied heart rate (HR) responses to prolonged breath holding (BH) in five asymptomatic asthmatic patients whose carotid bodies had been resected (CBR). Seven normal subjects served as controls. BH experiments were randomly initiated with single breaths of 100%, 21%,or 12% 92. During BH with 21% O2, normal subjects displayed the typical bradycardia; this response, however, was attenuated with the other O2 concentrations. In contrast, the CBR subjects manifested BH tachycardia which was inversely proportional to the O2 tension. HR increased in be CBR group by 5%, 31%, and 45% during BH with 100%, 21%, and 12% O2, respectively. These results demonstrate that the bradycardia of BH in normal man is under the influence of the carotid bodies. During BH and in the absence of carotid bodies, an O2 tension-dependent tachycardia is unveiled.

Comparison of phenylephrine bolus and infusion methods in baroreflex measurements

1990 ◽  
Vol 69 (3) ◽  
pp. 962-967 ◽  
Author(s):  
J. T. Sullebarger ◽  
C. S. Liang ◽  
P. D. Woolf ◽  
A. E. Willick ◽  
J. F. Richeson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Heart Rate Response ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Systolic Arterial Pressure ◽  
Normal Subjects ◽  
Vagus Nerves ◽  
Baroreflex Control

Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

The effect of Airway Anaesthesia on the Control of Breathing and the Sensation of Breathlessness in Man

1985 ◽  
Vol 68 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
S. A. Shea ◽  
C. Knott ◽  
A. Guz
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Cough Reflex ◽  
Before And After ◽  
Median Diameter ◽  
Receptor Block ◽  
Normal Man ◽  
End Tidal ◽  
Ventilatory Response To Co2

1. The effect on ventilation of airway anaesthesia, produced by the inhalation of a 5% bupivacaine aerosol (aerodynamic mass median diameter = 4.77 μm), was studied in 12 normal subjects. 2. The dose and distribution of the aerosol were determined from lung scans after the addition to bupivacaine of 99mTc. Bupivacaine labelled in this way was deposited primarily in the central airways. The effectiveness and duration of airway anaesthesia were assessed by the absence of the cough reflex to the inhalation of three breaths of a 5% citric acid aerosol. Airway anaesthesia always lasted more than 20 min. 3. Resting ventilation was measured, by respiratory inductance plethysmography, before and after inhalation of saline and bupivacaine aerosols. The ventilatory response to maximal incremental exercise and, separately, to CO2 inhalation was studied after the inhalation of saline and bupivacaine aerosols. Breathlessness was quantified by using a visual analogue scale (VAS) during a study and by questioning on its completion. 4. At rest, airway anaesthesia had no effect on mean tidal volume (VT), inspiratory time (Ti), expiratory time (Te) or end-tidal Pco2, although the variability of tidal volume was increased. On exercise, slower deeper breathing was produced and breathlessness was reduced. The ventilatory response to CO2 was increased. 5. The results suggest that stretch receptors in the airways modulate the pattern of breathing in normal man when ventilation is stimulated by exercise; their activation may also be involved in the genesis of the associated breathlessness. 6. A hypothesis in terms of a differential airway/alveolar receptor block, is proposed to explain the exaggerated ventilatory response to CO2.

Depression of hypoxic ventilatory response in humans by somatostatin

1988 ◽  
Vol 65 (3) ◽  
pp. 1050-1054 ◽  
Author(s):  
R. B. Filuk ◽  
D. J. Berezanski ◽  
N. R. Anthonisen
Keyword(s):  
Intravenous Infusion ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Small Decrease ◽  
Hypoxic Ventilatory Response ◽  
Arterial O2 Saturation ◽  
Ventilatory Response To Hypoxia

In nine normal subjects we measured the ventilatory response to isocapnic hypoxia with and without an intravenous infusion of 1 mg of somatostatin. Arterial O2 saturation was rapidly lowered to 80 +/- 2% in 2 min and maintained for 30 min. During control experiments, ventilation increased immediately (3-5 min) and then declined so that at 25 min of hypoxia ventilation was little above that in room air. Somatostatin was associated with a small decrease in ventilation while the subjects breathed room air. With hypoxia there was no immediate increase in ventilation for the group as a whole, although an increase was observed in one subject. With somatostatin, after 25 min of hypoxia, mean ventilation was lower than at any other time in the study; as hypoxia was discontinued ventilation increased slightly. Somatostatin causes profound depression of the ventilatory response to hypoxia by a mechanism that is not known but may be central. With somatostatin hypoxia of 25-min duration tends to depress ventilation.

Effect of resistive loading on ventilatory response to hypoxia

1975 ◽  
Vol 38 (6) ◽  
pp. 965-968 ◽  
Author(s):  
A. S. Rebuck ◽  
E. F. Juniper
Keyword(s):  
Response Curve ◽  
Mechanical Load ◽  
Ventilatory Response ◽  
Arterial Oxygen Saturation ◽  
Normal Subjects ◽  
Arterial Oxygen ◽  
Resistive Load ◽  
O2 Concentration ◽  
Resistive Loading ◽  
Ventilatory Response To Hypoxia

Ventilatory responses to hypoxia, with and without an inspiratory resistive load, were measured in eight normal subjects, using a rebreathing technique. During the studies, the end-tidal P-CO2 was kept constant at mixed venous level (Pv-CO2) by drawing expired gas through a variable CO2-absorbing bypass. The initial bag O2 concentration was 24% and rebreathing was continued until the O2 concentration in the bag fell to 6% or the subject's arterial oxygen saturation (Sa-O2), monitored continuously by ear oximetry, fell to 70%. Studies with and without the load were performed in a formally randomized order for each subject. Linear regressions for rise in ventilation against fall in Sa-O2 were calculated. The range of unloaded responses was 0.78–3.59 1/min per 1% fall in Sa-O2 and loaded responses 0.37–1.68 1/min per 1% fall in Sa-O2. In each subject, the slope of the response curve during loading fell by an almost constant fraction of the unloaded response, such that the ratio of loaded to unloaded slope in all subjects ranged from 0.41 to 0.48. However, the extrapolated intercept of the response curve on the Sa-O2 axis did not alter significantly indicating that the P-CO2 did not alter between experiments. These results suggest that the change in ventilatory response to hypoxia during inspiratory resistive loading is related to the mechanical load applied, with the loaded slope being directly proportional to the unloaded one.

Effects of GABA receptor blockage on the respiratory response to hypoxia in sedated newborn piglets

1994 ◽  
Vol 77 (2) ◽  
pp. 1006-1010 ◽  
Author(s):  
J. Huang ◽  
C. Suguihara ◽  
D. Hehre ◽  
J. Lin ◽  
E. Bancalari
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Oxygen Consumption ◽  
Ventilatory Response ◽  
Receptor Blocker ◽  
Newborn Piglets ◽  
Arterial Blood ◽  
Ventilatory Response To Hypoxia

Brain gamma-aminobutyric acid (GABA) levels increase during hypoxia, which may modulate the ventilatory response to hypoxia. To test the possibility that the depressed neonatal ventilatory response to hypoxia may be related to increased central nervous system GABA activity, 26 sedated spontaneously breathing newborn piglets (age 5 +/- 1 day, wt 1.7 +/- 0.4 kg) were studied. Minute ventilation (VE), oxygen consumption, heart rate, arterial blood pressure, and arterial blood gases were measured in room air and after 1, 5, and 10 min of hypoxia (inspired O2 fraction 0.10) before drug intervention. Immediately after these measurements, an infusion of saline or the GABA alpha-receptor blocker (bicuculline, 0.3 mg/kg iv) or beta-receptor blocker (CGP-35348, 100–300 mg/kg iv) was administered while animals were hypoxic. All measurements were repeated at 1, 5, and 10 min after initiation of the drug infusion. Basal VE was similar among groups. During hypoxia, VE increased significantly in the animals that received either a GABA alpha- or beta-receptor blocker but not in those receiving saline. Changes in arterial Po2, oxygen consumption, heart rate, and arterial blood pressure were similar among groups before and after saline or GABA antagonist infusion. These results suggest that the decrease in ventilation during the biphasic ventilatory response to hypoxia in the neonatal piglet is in part mediated through the depressant effect of GABA on the central nervous system.

Cardiorespiratory responses following isoproterenol injection in rabbits

1979 ◽  
Vol 47 (2) ◽  
pp. 352-359 ◽  
Author(s):  
R. Winn ◽  
J. R. Hildebrandt ◽  
J. Hildebrandt
Keyword(s):  
Heart Rate ◽  
Carotid Artery ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Vena Cava ◽  
Direct Stimulation ◽  
Carotid Bodies ◽  
Receptor Sites ◽  
The Common ◽  
Stimulation Of

Receptor sites for the ventilatory response to isoproterenol were investigated in anesthetized rabbits with bolus injections in the common carotid artery (ia) and in the vena cava (iv). The delay from injection to the increase in ventilation (TVE) was significantly shorter following ia (1.5 s) compared to iv injections (about 5 s). The delay to the increase in heart rate (THR) was significantly shorter after iv (about 4.5 s) than after ia injections (12.5 s). When isoproterenol and NaCN injections were compared, there was no difference in TVE. Following carotid body resection, the VE response to isoproterenol was greatly reduced after iv and ia injections; however, THR was unaffected. In intact animals breathing 100% O2 the VE response to isoproterenol was significantly reduced with no change in TVE or in the heart rate response. We conclude that the ventilatory increase following the injection of isoproterenol is due primarily to direct stimulation of the carotid bodies.

Depressed ventilatory response to hypoxia in hypothermic newborn piglets: role of glutamate

1998 ◽  
Vol 84 (3) ◽  
pp. 830-836 ◽  
Author(s):  
Annette McCormick ◽  
Cleide Suguihara ◽  
Jian Huang ◽  
Carlos Devia ◽  
Dorothy Hehre ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Nucleus Tractus Solitarius ◽  
Ventilatory Response ◽  
Blood Gases ◽  
Arterial Blood ◽  
Significant Linear Correlation ◽  
The Central Nervous System ◽  
Ventilatory Response To Hypoxia

To evaluate whether changes in extracellular glutamate (Glu) levels in the central nervous system could explain the depressed hypoxic ventilatory response in hypothermic neonates, 12 anesthetized, paralyzed, and mechanically ventilated piglets <7 days old were studied. The Glu levels in the nucleus tractus solitarius obtained by microdialysis, minute phrenic output (MPO), O2 consumption, arterial blood pressure, heart rate, and arterial blood gases were measured in room air and during 15 min of isocapnic hypoxia (inspired O2 fraction = 0.10) at brain temperatures of 39.0 ± 0.5°C [normothermia (NT)] and 35.0 ± 0.5°C [hypothermia (HT)]. During NT, MPO increased significantly during hypoxia and remained above baseline. However, during HT, there was a marked decrease in MPO during hypoxia (NT vs. HT, P < 0.03). Glu levels increased significantly in hypoxia during NT; however, this increase was eliminated during HT ( P < 0.02). A significant linear correlation was observed between the changes in MPO and Glu levels during hypoxia ( r = 0.61, P < 0.0001). Changes in pH, arterial[Formula: see text], O2 consumption, arterial blood pressure, and heart rate during hypoxia were not different between the NT and HT groups. These results suggest that the depressed ventilatory response to hypoxia observed during HT is centrally mediated and in part related to a decrease in Glu concentration in the nucleus tractus solitarius.

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