Reflex cardiorespiratory responses to pulmonary vascular congestion

1987 ◽  
Vol 62 (3) ◽  
pp. 870-879 ◽  
Author(s):  
W. B. Wead ◽  
S. S. Cassidy ◽  
J. R. Coast ◽  
H. K. Hagler ◽  
R. C. Reynolds
Keyword(s):  
Heart Rate ◽  
Left Lung ◽  
Systemic Arterial Pressure ◽  
Nerve Endings ◽  
Alveolar Wall ◽  
C Fibers ◽  
Vascular Congestion ◽  
Lung Expansion ◽  
Central Inspiratory Activity ◽  
Inspiratory Activity

The purpose of these studies was to determine the reflex responses of the cardiovascular system and central inspiratory activity caused by pulmonary vascular congestion. We used a canine preparation in which the left lung was isolated in situ and could be exposed to a variety of stimuli, including distension of the pulmonary capillaries with blood, without direct mechanical or chemical alterations on the circulation. We found that lung expansion to 30 cmH2O and stimulation of nerve endings of the left lung with capsaicin caused pronounced transient reflex bradycardia (-30 to -50 beats/min) and hypotension (-25 to -40 mmHg) and caused reflex cessation of inspiratory activity. Pressurizing the left pulmonary vessels by injecting blood in volumes sufficient to raise pulmonary transcapillary pressures to 30 mmHg caused no changes in heart rate, systemic arterial pressure, or inspiratory muscle activity. These results lead us to conclude that pulmonary vascular congestion does not stimulate pulmonary C-fibers or any other nerve endings to such a degree as to cause detectable changes in blood pressure, heart rate, or central inspiratory activity. Morphometric analysis revealed distended capillaries engorged with blood, but the alveolar wall surface area was not increased which raises the possibility that expansion of the alveolar membrane may be needed to mechanically initiate the C-fiber reflex.

Respiratory arrhythmias and airway CO2, lung receptors, and central inspiratory activity

1986 ◽  
Vol 60 (5) ◽  
pp. 1713-1721 ◽  
Author(s):  
R. L. Coon ◽  
E. J. Zuperku ◽  
J. P. Kampine
Keyword(s):  
Heart Rate ◽  
Cardiopulmonary Bypass ◽  
Breathing Frequency ◽  
Lung Inflation ◽  
Efferent Activity ◽  
Central Inspiratory Activity ◽  
Baroreceptor Stimulation ◽  
Inspiratory Activity ◽  
Lung Receptor

The purpose of this study was to determine whether hypocapnia affects heart rate secondary to an effect on pulmonary receptors. Dogs were anesthetized and placed on cardiopulmonary bypass. Interrelationships among airway CO2, central inspiratory activity, and lung receptor effects on respiratory-related heart rate changes (respiratory arrhythmias) were studied after vagal efferent activity was increased secondary to baroreceptor stimulation. Hypocapnia, isolated to the lungs, produced an increase in the magnitude of the respiratory arrhythmias observed. Two mechanisms may produce these results. Hypocapnia affects pulmonary receptors, which 1) reflexly alter heart rate and 2) modulate breathing frequency, thus altering the dynamics of the respiratory arrhythmias that were produced. The results also suggested that the reflex increase in heart rate in response to lung inflation and the Hering-Breuer expiratory-facilitatory reflex are either produced by different pulmonary receptors or by the same pulmonary receptors but may be mediated by different central mechanisms.

Inhibition of skeletal muscle activity by lung expansion in the dog

1987 ◽  
Vol 62 (5) ◽  
pp. 2058-2065 ◽  
Author(s):  
J. R. Coast ◽  
G. S. Thompson ◽  
S. S. Cassidy
Keyword(s):  
Skeletal Muscle ◽  
Muscle Activity ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Monosynaptic Reflex ◽  
Reflex Response ◽  
Lung Inflation ◽  
Knee Jerk ◽  
C Fibers ◽  
Lung Expansion

The ability of lung expansion to reflexly decrease skeletal muscle activity was tested in anesthetized dogs. In animals whose left lung was vascularly isolated but neurally intact, the left lung was inflated statically to 40 cmH2O pressure or cyclically with tidal volumes of 10, 20, or 30 ml/kg. Responses to these stimuli were compared with those of injecting 120 or 240 micrograms capsaicin into the left pulmonary artery. Skeletal muscle activity was assessed from the electromyogram (EMG) response of the left hindlimb muscles and from the monosynaptic reflex response to a periodic patellar tendon tap of the right leg (knee jerk). Static inflation and cyclic inflations above 10 ml/kg resulted in significant decreases in both EMG and knee jerk responses. The results indicate that lung expansion is capable of initiating a reflex decrease in skeletal muscle activity. Capsaicin injections caused responses that were similar to those caused by lung inflation, suggesting that at least part of this skeletal muscle reflex response to lung inflation can be attributed to the stimulation of pulmonary C-fibers that could be caused by stretch of the lung.

Pulmonary edema in dogs fails to cause reflex responses

1987 ◽  
Vol 252 (1) ◽  
pp. H89-H99
Author(s):  
W. B. Wead ◽  
S. S. Cassidy ◽  
R. C. Reynolds
Keyword(s):  
Pulmonary Edema ◽  
Left Lung ◽  
Cardiovascular Function ◽  
Cardiovascular Responses ◽  
Left Pulmonary Artery ◽  
Coagulation Necrosis ◽  
Pulmonary Vascular Permeability ◽  
Reflex Responses ◽  
C Fibers ◽  
Inspiratory Activity

Pulmonary edema has been proposed as a stimulus for pulmonary C-fibers. Stimulation of pulmonary C-fibers causes depression of cardiovascular function and either tachypnea or apnea. Our objective was to determine whether pulmonary edema, induced by either increasing pulmonary vascular permeability with alloxan or hydrostatic challenges, would elicit depression of cardiovascular function or changes in frequency of inspiratory activity. Utilizing a preparation in which the left pulmonary vessels and left airway were isolated, we monitored systemic blood pressure (BP), heart rate (HR), and diaphragm contractions (DC) in 13 anesthetized dogs. Injection of alloxan into the left pulmonary artery (LPA) produced transient decreases in HR, BP, and frequency of DC within 20 s of injection with no subsequent cardiorespiratory changes up to 5 min. These alloxan injections also caused coagulation necrosis. Generation of hydrostatic pulmonary edema in the left lung caused no changes in HR, BP, or in the frequency and amplitude of DC. We conclude that alloxan does stimulate reflex cardiorespiratory depression consistent with C-fiber stimulation, but these reflex responses are probably caused by alloxan's caustic effect and not by the resultant edema. We also conclude that pulmonary edema induced by increased hydrostatic pressure does not evoke any reflex cardiovascular responses or changes in frequency of inspiratory activity.

Nocturnal headache: systemic arterial pressure and heart rate during sleep

Cephalalgia ◽  
1983 ◽  
Vol 3 (1_suppl) ◽  
pp. 54-57 ◽  
Author(s):  
Fabio Cirignotta ◽  
Giorgio Coccagna ◽  
Tommaso Sacquegna ◽  
Emiliana Sforza ◽  
Giuseppe Lamontanara ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Rem Sleep ◽  
Continuous Monitoring ◽  
Systemic Arterial Pressure ◽  
Fréquence Cardiaque ◽  
The Awakening ◽  
Sono Stati ◽  
Autonomic Instability ◽  
Polygraphic Recording

In order to evaluate autonomic nervous system changes occurring before nocturnal headache attacks, we studied three subjects (one male, two females) suffering from chronic migraine. All three patients underwent a nocturnal polygraphic recording including continuous monitoring of systemic arterial pressure and heart rate. Two subjects showed increases and irregularities of arterial pressure before awakening with headache. These changes began during N–REM sleep and lasted during REM sleep preceding the awakening with headache. Heart rate did not change before the attacks. These findings do not support the hypothesis that autonomic instability during REM sleep represents the precipitating factor of the attacks. On a étudié avec des méthodes polygrafiques trois sujets (1 homme et deux femmes) souffrant d'hémicranie chronique avec des crises nocturnes. Chez deux malades les crises étaient précédées d'augmentation et d'irrégularité de la tension artérielle. Ces modifications commençaient pendant le sommeil N-REM et contineaient pendant le sommeil REM qui précédait le réveil avec hémicranie. La fréquence cardiaque n'a pas subi de modification avant les crises. Les résultats obtenus ne confirment l'hypothèse selon laquelle le facteur causant les crises est l'instabilité anticronique à la fase REM. Sono stati studiati con metodiche poligrafiche 3 soggetti (1 maschio e 2 femmine) affetti da emicrania cronica con attacchi notturni. In 2 di essi gli attacchi erano preceduti da incrementi ed irregolarità della pressione arteriosa. Tali modificazioni iniziavano durante il sonno N-REM e perduravano nel corso del sonno REM che precedeva il risveglio con cefalea. La frequenza cardiaca non si modificava prima dell'attacco. I risultati ottenuti non confermano l'ipotesi che il fattore precipitante gli attacchi emicranici sia l'instabilità anticronica della fase REM.

Role of NO in goat basal cerebral circulation and after vasodilatation to hypercapnia or brief ischemias

1993 ◽  
Vol 265 (6) ◽  
pp. R1410-R1415 ◽  
Author(s):  
G. Dieguez ◽  
J. L. Garcia ◽  
N. Fernandez ◽  
A. L. Garcia-Villalon ◽  
L. Monge ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Methyl Ester ◽  
Cerebral Circulation ◽  
Systemic Arterial Pressure ◽  
Nitric Oxide Production ◽  
Hemodynamic Effects ◽  
Arterial Pco2 ◽  
Different Levels

The role of nitric oxide (NO) in the cerebral circulation under basal conditions and after vasodilatation to hypercapnia or reactive hyperemias was studied in 17 anesthetized goats. The intravenous administration of NG-nitro-L-arginine methyl ester (L-NAME, 3-4 or 8-10 mg/kg), an inhibitor of nitric oxide production, reduced middle cerebral artery (MCA) flow (electromagnetically measured) by 19 and 30% and increased systemic arterial pressure by 21 and 26%, respectively, whereas heart rate did not significantly change; MCA resistance increased by 48 and 86%, respectively. These hemodynamic effects were reversed by L-arginine (200-300 mg/kg iv; 5 goats). Different levels of hypercapnia (PCO2 of 30-35, 40-45, and 55-65 mmHg) (12 goats) produced arterial PCO2-dependent increases in MCA flow that were similar under control and L-NAME treatment. Graded cerebral hyperemia occurred after 5, 10, and 20 s of MCA occlusion in 5 goats, but its magnitude was decreased during L-NAME treatment. It suggests that, in the cerebral circulation, nitric oxide 1) produces a basal vasodilator tone and 2) is probably not involved in the vasodilatation to hypercapnia but may mediate hyperemic responses after short brain ischemias.

Stimulation of vagal C-fibers alters timing and distribution of respiratory motor output in cats

1989 ◽  
Vol 67 (6) ◽  
pp. 2249-2256 ◽  
Author(s):  
H. R. Holmes ◽  
J. E. Remmers
Keyword(s):  
Vagus Nerve ◽  
Recurrent Laryngeal Nerve ◽  
Breathing Pattern ◽  
Laryngeal Nerve ◽  
C Fibers ◽  
Vascular Congestion ◽  
Vagal Afferent ◽  
Posterior Cricoarytenoid ◽  
The Right ◽  
Decerebrate Cats

Pulmonary vascular congestion or pulmonary embolism in humans produces shallow tachypnea, and indirect experimental evidence suggests that this characteristic breathing pattern may result from activation of vagal unmyelinated afferents from the lung. We have investigated, in decerebrate cats, reflex changes in breathing pattern and in the activation of the diaphragm, posterior cricoarytenoid, and thyroarytenoid muscles caused by activating C-fiber afferents in the vagus nerve. The right vagus nerve was sectioned distal to the origin of the recurrent laryngeal nerve, eliminating vagal afferent traffic although preserving motor innervation of the larynx on that side. The left cervical vagus was stimulated electrically, and efferent activation of the laryngeal muscles was avoided by cutting the left recurrent laryngeal nerve. Transmission to the brain of vagal afferent traffic resulting from this stimulation was controlled by graded cold block of the nerve cranial to the site of application of the stimulus. Activation of C-fibers, when A-fibers were blocked, significantly decreased respiratory period and amplitude of diaphragm inspiratory burst. In addition, this selective activation of vagal C-fibers augmented postinspiratory activity of the diaphragm and recruited phasic expiratory bursts in the thyroarytenoid. We conclude that, in unanesthetized decerebrate cats, afferent traffic of vagal C-fibers initiates a pontomedullary reflex that increases respiratory frequency, decreases tidal volume, and augments braking of expiratory airflow.

scholarly journals Ruptured Hydatid Cyst with an Unusual Presentation

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Deepak Puri ◽  
Amit Kumar Mandal ◽  
Harinder Pal Kaur ◽  
Tek Singh Mahant
Keyword(s):  
Hydatid Cyst ◽  
Bronchopleural Fistula ◽  
Left Lung ◽  
Young Male ◽  
Uneventful Recovery ◽  
Pleural Thickening ◽  
Peripheral Hospital ◽  
Lung Expansion ◽  
Probable Site ◽  
Pulmonary Hydatid Cyst

Ruptured pulmonary hydatid cyst may sometimes cause complications like empyema, bronchopleural fistula, and collapsed lung. These complications may mislead the diagnosis and treatment if prior evidence of cyst has not been documented before rupture. We present a case of a young male who presented with complete collapse of left lung with pyopneumothorax and bronchopleural fistula which was misdiagnosed as pulmonary tuberculosis. He was referred to us from peripheral hospital for pneumonectomy when his condition did not improve after six months of antitubercular chemotherapy and intercostals drainage. On investigation, CT scan revealed significant pleural thickening and massive pneumothorax restricting lung expansion. Decortication of thickened parietal and visceral pleura revealed a ruptured hydatid endocyst, and repair of leaking bronchial openings in floor of probable site of rupture in left upper lobe helped in the complete expansion of the collapsed lung followed by uneventful recovery.

Effect on the Cushing response of different rates of expansion of a supratentorial mass

1978 ◽  
Vol 49 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Abdul Hamid Zidan ◽  
John P. Girvin
Keyword(s):  
Heart Rate ◽  
Full Range ◽  
Blood Gases ◽  
Systemic Arterial Pressure ◽  
Critical Volume ◽  
Experimental Conditions ◽  
Content Type ◽  
Cerebral Dysfunction ◽  
Cushing Response ◽  
Supratentorial Mass

✓ The effects on the three components (respiration, blood pressure, and heart rate) of the Cushing response (CR) were studied in cats by the continuous expansion of a supratentorial balloon. The rate of expansion was varied over the range of 0.006 to 0.6 ml/min, during which systemic arterial pressure, heart rate, respiratory rate, and blood gases were monitored. For the different rates the time the CR took to develop, and the balloon volume required for that development were measured. The final volume (“critical volume”) for eliciting the CR was more or less constant over the full range of rates of infusion (balloon expansion), a fact that supports the Monro-Kellie doctrine. This constancy of critical volume (CCV) gives rise to a highly statistically significant relationship between the rate of infusion and the latency to the production of the CR, and it is described by a power curve. Thus the development of cerebral dysfunction under these experimental conditions is independent of the rate of expansion and only dependent upon this critical volume. Exceptions to this concept of a critical volume, at the extreme of rates of expansion of lesions in patients, are predicted.

Temperature and CO2 effect on phrenic activity and tracheal occlusion pressure

1977 ◽  
Vol 43 (3) ◽  
pp. 449-454 ◽  
Author(s):  
T. Trippenbach ◽  
J. Milic-Emili
Keyword(s):  
Body Temperature ◽  
Moving Average ◽  
Similar Increase ◽  
Occlusion Pressure ◽  
Tracheal Occlusion ◽  
Pentobarbital Sodium ◽  
Central Inspiratory Activity ◽  
Similar Index ◽  
Inspiratory Activity ◽  
Breathing Room

The present investigation was undertaken to study the interaction of CO2 and body temperature on phrenic activity (moving average) and tracheal occlusion pressure. Studies were performed on spontaneously ventilated cats anesthetized with pentobarbital sodium at different body temperatures (32–41 degrees C) while breathing room air, 2 and 4% CO2 in 50% O2. At any given chemical drive, increased body temperature caused a similar increase in rate of phrenic activity and tracheal occlusion pressure, while their peak values remained virtually unchanged. At any given body temperature, increased chemical drive caused an increase in both rate of rise and peak values of phrenic activity and tracheal occlusion pressure. These results confirm previous findings that body temperature affects the rate of rise of the central inspiratory activity (CIA), but not the inspiratory “off-switch” threshold, while CO2 increases both the rate of rise of CIA and off-switch threshold. In addition the results indicate that tracheal occlusion pressure provides a similar index of CIA as “integrated” phrenic activity.

Compensation to exsanguination hypotension in healthy conscious dogs

1963 ◽  
Vol 205 (5) ◽  
pp. 1000-1004 ◽  
Author(s):  
Robert F. Rushmer ◽  
Nolan Watson ◽  
Donald Harding ◽  
Donald Baker
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Human Subjects ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Series Of Experiments ◽  
The Mean ◽  
The Right

In some earlier studies on exsanguination hypotension in conscious dogs, reduction in systemic arterial pressure to shock levels was accompanied by a transient tachycardia during the removal of blood, but the heart rate returned to level, at or near control values during extended periods with the mean arterial pressure between 40 and 60 mm Hg. This observation stimulated a series of experiments on five healthy conscious dogs in which transient hypotension was induced by withdrawing blood from the region of the right atrium to determine which mechanisms were dominant in the compensatory reaction. A surprising degree of variability in response was encountered, such that tachycardia was the main response on some occasions, increased peripheral resistance on others, and in still others, several mechanisms appeared to play a role. Similar variability in the response to exsanguination have been reported in human subjects. These observations suggest that the baroceptor reflexes are not simple servo controls and their role in everyday cardiovascular responses should be re-examined.

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