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.

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.

Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man

1995 ◽  
Vol 133 (6) ◽  
pp. 723-728 ◽  
Author(s):  
Ettore C degli Uberti ◽  
Maria R Ambrosio ◽  
Marta Bondanelli ◽  
Giorgio Transforini ◽  
Alberto Valentini ◽  
...  
Keyword(s):  
Heart Rate ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Heart Rate Response ◽  
Statistical Significance ◽  
Inhibitory Effect ◽  
Amino Acid Residues ◽  
Nerve Activity ◽  
Receptor Stimulation

degli Uberti EC, Ambrosio MR, Bondanelli M, Trasforini G, Valentini A, Rossi R, Margutti A, Campo M. Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man. Eur J Endocrinol 1995;133:723–8. ISSN 0804–4643 Human galanin (hGAL) is a neuropeptide with 30 amino acid residues that has been found in the peripheral and central nervous system, where it often co-exists with catecholamines. In order to clarify the possible role of hGAL in the regulation of sympathoadrenomedullary function, the effect of a 60 min infusion of hGAL (80 pmol·kg−1 · min−1) on plasma epinephrine and norepinephrine responses to insulin-induced hypoglycemia in nine healthy subjects was investigated. Human GAL administration significantly reduced both the release of basal norepinephrine and the response to insulin-induced hypoglycemia, whereas it attenuated the epinephrine response by 26%, with the hGAL-induced decrease in epinephrine release failing to achieve statistical significance. Human GAL significantly increased the heart rate in resting conditions and clearly exaggerated the heart rate response to insulin-induced hypoglycemia, whereas it had no effect on the blood pressure. We conclude that GAL receptor stimulation exerts an inhibitory effect on basal and insulin-induced hypoglycemia-stimulated release of norepinephrine. These findings provide further evidence that GAL may modulate sympathetic nerve activity in man but that it does not play an important role in the regulation of adrenal medullary function. Ettore C degli Uberti, Chair of Endocrinology, University of Ferrara, Via Savonarola 9, I-44100 Ferrara, Italy

Causes of bradycardia with static respiratory hypoxia in athletes

2021 ◽  
Vol 11 (1) ◽  
pp. 30-36
Author(s):  
Yu. E. Vaguine
Keyword(s):  
Heart Rate ◽  
Standard Deviation ◽  
Arterial Oxygen Saturation ◽  
The Other ◽  
Arterial Oxygen ◽  
Breath Holding ◽  
Basketball Players ◽  
Heart Rate Monitor ◽  
Arterial Blood

According to some literature data, during voluntary long-term breath holding (BH), the heart rate (HR) increases, and according to others, it decreases.Objective: to determine the psychophysiological parameters that cause a change in HR during BH in athletes with different resistance to respiratory hypoxia.Materials and methods: HR at BH was studied in 14 beginner athletes, 15 basketball players and 12 swimmers-divers. Duration of BH was recorded. The HR was recorded on a heart rate monitor. After recording an electrocardiogram, the standard deviation of the duration of cardiac cycles was calculated. The arterial oxygen saturation was measured with a pulse oximeter. The statistically significant values of the correlation coefficient (r) were ≥0.33 with p < 0.05.Results: it was found that out of 41 sportsmen, HR increased by more than 5 % in 4, changed insignificantly in 7 and decreased by less than 5 % in 30. Beginner athletes had tachycardia, and BH was quickly interrupted by an imperative inhalation. The saturation of arterial blood with oxygen did not change and did not affect the change in HR. The decrease in heart rate in swimmers-divers in comparison with the other two groups of people examined was statistically significant (p < 0.05). The duration of BH had a direct correlation (r = 0.5) with bradycardia in these people. The duration of BH caused (r = 0.8) hypoxia, the value of which also directly influenced (r = 0.38) the severity of bradycardia. In addition, the decrease in HR depended on high HR (r = 0.36) and low HR variability (r = 0.38) before BH.Conclusion: tachycardia occurs in beginner athletes who experience discomfort with BH. Bradycardia occurs in sportsmen with a long-term BH setting without discomfort. Sympathicotonia in the prelaunch state predetermines the severity of bradycardia in BH. The duration of BH and the resulting hypoxia provide the occurrence of bradycardia.

Abstract 4023: Aspirin “Resistance”: Role of Pre-existent Platelet Reactivity and Correlation Between Tests

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Andrew L Frelinger ◽  
Youfu Li ◽  
Matthew D Linden ◽  
Inge Tarnow ◽  
Marc R Barnard ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Normal Subjects ◽  
Aspirin Resistance ◽  
The Other ◽  
List Type ◽  
Platelet Function Test ◽  
Function Test

Background: Aspirin “resistance” (i.e. hyporesponsiveness to aspirin in a platelet function test) has been widely reported, but the underlying mechanism is unclear. We examined the role of pre-existent platelet hyperreactivity in aspirin “resistance”. We also determined the correlation between aspirin resistance defined by serum thromboxane (TX) B 2 (the most specific test of aspirin’s effect) and other assays of platelet function. Methods: Platelet function measured before and after aspirin 81 mg daily for 7 days was analyzed by Spearman’s rank correlation. Normal subjects (n=165) were studied because virtually all clinically relevant patients are already taking aspirin. An additional advantage of the use of normal subjects is that the platelet response to stimuli is not influenced (with resultant increased scatter of the data) by an underlying disease, e.g. coronary artery disease, which causes platelet hyperreactivity. Results: The proportion of the post-aspirin platelet function predicted by the pre-aspirin platelet function was 28.3 ± 7.5% (mean ± asymptotic standard error) for serum TXB 2 , 39.3 ± 6.8% for urinary 11-dehydro TXB 2 , 4.4 ± 7.7% for arachidonic acid-induced platelet aggregation, 40.4 ± 7.1% for ADP-induced platelet aggregation, 26.3 ± 9.2% for the VerifyNow Aspirin Assay®, and 45.0 ± 10.9% for the TEG® PlateletMapping ™ System with arachidonic acid. Spearman rank order correlations were highly significant for comparisons between assays when both pre-aspirin and post-aspirin results were included in the analysis. However, residual serum TXB 2 levels post-aspirin treatment were not significantly associated with post-treatment results of any of the other assays. Platelet count correlated with pre-aspirin serum TXB 2 and VerifyNow Aspirin Assay, but not with any post-aspirin platelet function test. Conclusions: Aspirin “resistance” (i.e. hyporesponsiveness to aspirin in a laboratory test) is in part unrelated to aspirin but is the result of underlying platelet hyperreactivity prior to the institution of aspirin therapy. Individuals identified as aspirin “resistant” defined by serum TXB 2 are not the same individuals identified by the other tests.

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 SINGLE BREATH DIFFUSING CAPACITY AND THE PERMEABILITY OF THE LUNGS OF NORMAL MAN

1963 ◽  
Vol 41 (1) ◽  
pp. 1283-1292
Author(s):  
Edith Rosenberg
Keyword(s):  
Molecular Sieve ◽  
The Other ◽  
Breath Holding ◽  
Diffusing Capacity ◽  
Alveolar Volume ◽  
Lung Volumes ◽  
Test Gas ◽  
Single Breath ◽  
Normal Man ◽  
Molecular Sieve Column

The single breath diffusing capacity for CO, DL, and the permeability of the lungs, K, were measured in six male and two female medical students at various lung volumes. The subjects rested 15 minutes before each test and the expired alveolar volume as well as breath-holding time and inspired volume were recorded on a spirogram. The test gas used consisted of 0.3% CO, 0.3% SF6, 20% O2, and the balance N2. The sample of alveolar gas expired after breath-holding was analyzed for CO and SF6 on a vapor fractometer using a 2-meter molecular sieve column. DL varied with the surface area of the subjects as well as with the alveolar volume at which the test was performed. K, on the other hand, was independent of the size of the subjects and decreased towards a constant value as lung volume became large. K should, therefore, be more reproducible than DL. The average permeability of the eight subjects used in this study was 0.0715 ml CO per second per ml of alveolar volume. In every experiment, alveolar volumes were also calculated from the SF6 dilution. These values, VD, were compared to alveolar volumes calculated from the maximum lung volumes, VA. For the males there was no measurable difference between alveolar volumes calculated by these two methods when 2 liters or more of test gas were inspired. It is suggested that the replacement of the measurement of DL in pulmonary function laboratories by an evaluation of K and VD may transform the single breath diffusing capacity test into a useful diagnostic tool.

Central nervous system control of cardiorespiratory nasopharyngeal reflexes in the rabbit

1975 ◽  
Vol 228 (2) ◽  
pp. 404-409 ◽  
Author(s):  
S White ◽  
RJ McRitchie ◽  
PI Korner
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Carotid Sinus ◽  
Cerebral Hemispheres ◽  
System Control ◽  
Controlled Ventilation ◽  
Cardiovascular Reflex ◽  
Respiratory Reflex ◽  
Central Nervous System Control

The role of different central nervous regions in the reflex apnea, bradycardia, and mesenteric vasoconstriction evoked by nasopharyngeal stimulation with cigarette smoke was examined in unanesthetized shamoperated, thalamic, and pontine rabbits with intact and sectioned carotid sinus and aortic nerves (CS and AN). Apnea occurred in all preparations. In pontine animals with intact CS and AN, the heart rate response was reduced but not the mesenteric vasoconstriction. The role of suprabulbar and bulbospinal regions became more apparent when individual components of the input profile were examined in animals with controlled ventilation. The bradycardia and mesenteric vasoconstriction evoked by apnea without smoke, but not by smoke without apnea, were reduced in pontine animals. Prior section of the CS and AN attenuated the response in all neural preparations but to the least extent when cerebral hemispheres were intact. The data indicate that the respiratory reflex is predominantly integrated at bulbospinal sites, but the cardiovascular reflex is integrated at both bulbospinal and suprabulbar sites, or is integrated at bulbospinal and modulated from suprabulbar sites.

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.

scholarly journals THE ROLE OF β, α1 AND α2-ADRENO RECEPTORS IN THE REGULATION OF THE HEART RATE OF LABORATORY ANIMALS EXPOSED TO VARIOUS MODES OF MOTOR ACTIVITY

2021 ◽  
Vol 248 (4) ◽  
pp. 291-296
Author(s):  
A.V. Shigapova ◽  
◽  
I.Kh. Vakhitov ◽  
R.S. Safin ◽  
I.R. Ibatullin ◽  
...  
Keyword(s):  
Heart Rate ◽  
Motor Activity ◽  
Heart Rate Response ◽  
Laboratory Animals ◽  
Initial Reaction ◽  
Muscle Training ◽  
Pronounced Decrease ◽  
Motor Mode ◽  
First Time

For the first time, studies were conducted to study the features of the heart rate response of laboratory animals exposed to various modes of motor activity when administered with β, α1 and α2-blockers. It was found that in all the experimental groups of animals studied, a decrease in the heart rate response was observed in the first week after the introduction of β, α1 and α2-adreno blockers. It was revealed that the initial reaction of the heart rate on the introduction of β, α1 and α2-blockers depends on the level of motor activity of laboratory animals. It was found that the most pronounced decrease in the heart rate response to the introduction of different subtypes of adreno-blockers is observed in the group of animals with limited motor activity. At the same time, the smallest decrease in the heart rate response occurs in the group of animals subject to enhanced motor mode. It was revealed that in the group of experimental animals, during further muscle training, by the end of the fourth week, there was a less pronounced decrease in the heart rate response to the administration of β, α1 and α2-adreno blockers. It was found that in a group of animals subject to a regime of limited motor activity, by the end of the fourth week of hypokinesia, the most pronounced decrease in the heart rate response to the introduction of β, α1-targeted blockers occurs.

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