Effect of verapamil on ventilation and chemical control of breathing in anesthetized rats

1985 ◽  
Vol 63 (12) ◽  
pp. 1608-1611 ◽  
Author(s):  
Richard W. Chapman
Keyword(s):  
Tidal Volume ◽  
Respiration Rate ◽  
Channel Blocker ◽  
Minute Volume ◽  
Respiratory Frequency ◽  
Deep Breathing ◽  
Ventilatory Responses ◽  
Anesthetized Rats ◽  
Dose Dependent Increase ◽  
Dose Dependent

The calcium channel blocker, verapamil (0.1–1.0 mg/kg, i.v.) was administered to anesthetized rats to determine its effects on ventilation and on ventilatory responses to hypoxia and CO2. Verapamil produced a dose-dependent increase in tidal volume (VT) and a decrease in respiration rate (f). The bradypnea due to verapamil was characterized by an increase in expiratory duration (TE) and no change of inspiratory duration (TI). Verapamil produced similar changes in VT and f in vagotomized rats. The increase in respiration rate and minute volume due to hypoxia were inhibited by verapamil (0.5 and 1.0 mg/kg) but the increase in tidal volume due to hypoxia was depressed only with the 1.0 mg/kg dose. On the other hand, the increase in VT due to breathing CO2 was not changed by verapamil (0.1–1.0 mg/kg), but depression of the respiratory frequency response to CO2 occurred with 1.0 mg/kg of verapamil. These results indicate that verapamil produced slow, deep breathing and these responses were not mediated by vagal mechanisms. Ventilatory responses to hypoxia were depressed by verapamil. However, since the calcium blocker demonstrated no effect on the VT-CO2 relationship, verapamil did not change ventilatory chemosensitivity to CO2. The data also suggest that mechanisms governing the control of respiratory frequency are more sensitive to verapamil than tidal volume responses.

Integration of chemoreceptor stimuli by caudal pontile and rostral medullary sites

1976 ◽  
Vol 41 (5) ◽  
pp. 612-622 ◽  
Author(s):  
W. M. St John ◽  
S. C. Wang
Keyword(s):  
Tidal Volume ◽  
Minute Volume ◽  
Respiratory Frequency ◽  
Primary Role ◽  
Frequency Responses ◽  
Radiofrequency Lesions ◽  
Pneumotaxic Center ◽  
Definition Of ◽  
Decerebrate Cats ◽  
Paco2 Level

Ventilatory regulation by pontile pneumotaxic and apneustic centers and by rostral medullary sites was evaluated in intercollicular decerebrate cats. Following pneumotaxic center ablation, PAco2 was significantly elevated.Moreover, in response to hypercapina or hypoxia, frequency responses were significantly diminished whereas tidal volume responses were unchanged or elevated. Interruption of apneustic center function by caudal pontile transection or radiofrequency lesions in the caudal pons and/or rostral medulla resulted in significant decreases of tidal volume responses and significant elevations of frequency responses to both hypercapnia and hypoxia. Neither minute volume responses nor the PAco2 level was altered. It is concluded that the apneustic center exercises a primary role in the brainstem definitionof tidal volume responses for both peripheral and central chemoreceptor afferent stimuli. The apneustic center is also considered to exert an impoetant function in the definition of respiratory frequency. A medially placed pathway in the rostral medulla is proposed to interconnect the apneustic center with the medullary respiratory nuclei.

Mechanism of ozone-induced tachypneic response to hypoxia and hypercapnia in conscious dogs

1980 ◽  
Vol 48 (1) ◽  
pp. 163-168 ◽  
Author(s):  
L. Y. Lee ◽  
T. D. Djokic ◽  
C. Dumont ◽  
P. D. Graf ◽  
J. A. Nadel
Keyword(s):  
Tidal Volume ◽  
Breathing Pattern ◽  
Atropine Sulfate ◽  
Minute Volume ◽  
Conscious Dogs ◽  
Ozone Exposure ◽  
Control Value ◽  
Ventilatory Responses ◽  
Vagal Blockade ◽  
The Relationship

In seven studies on three dogs exercising on a treadmill (1.6 km/h), we studied the effect of ozone on ventilatory responses to hypercapnia and to hypoxia. After ozone exposure (0.67 +/- 0.02 ppm by vol; 2 h), the responses of minute volume of ventilation (VE) to progressive hypercapnia and hypoxia were not changed, but the breathing pattern in response to these stimuli changed. We analyzed the breathing pattern by plotting the relationship between VE and tidal volume (VT). During progressive hypercapnia, the slope of VE-VT relationship increased from a control value of 36.1 +/- 1.6 (mean +/- SE) to 93.5 +/- 8.9 min-1 after ozone (n = 7, P less than 0.005); during hypoxia, the slope increased from a control value of 46.1 +/- 8.6 to 142.7 +/- 18.3 min-1 after ozone (n = 6, P less than 0.005). The ozone-induced tachypneic responses to hypercapnia and hypoxia were not affected by inhalation of atropine sulfate or isoproterenol aerosols, but were completely abolished by bilateral vagal blockade. These findings indicate an effect of ozone on the vagal receptors located in the airways and lungs that causes reflex tachypnea during hypercapnia and hypoxia.

Restraining hamsters alters their breathing pattern

1991 ◽  
Vol 70 (3) ◽  
pp. 1271-1276 ◽  
Author(s):  
T. D. Sweeney ◽  
D. E. Leith ◽  
J. D. Brain
Keyword(s):  
Muscle Strength ◽  
Exercise Training ◽  
Tidal Volume ◽  
Adult Male ◽  
Breathing Pattern ◽  
Minute Volume ◽  
Respiratory Frequency ◽  
Prior Exercise ◽  
Sedentary Group ◽  
Inhaled Aerosols

Does the restraint required for head or nose-only exposure of rodents to inhaled aerosols or gases alter their breathing pattern? And does prior exercise training, which may increase muscle strength, affect this response to restraint? To answer those questions, we measured breathing pattern in 11 adult male hamsters while they were either 1) free to move in small cages or 2) closely restrained in head-out cones. The measurements were repeated after hamsters spent 6 wk either sedentary in standard cages or in cages with exercise wheels. Hamsters were placed in a plethysmograph to measure respiratory frequency (f) and tidal volume (VT). Their product is minute volume (V). When restrained, f and V were 1.9 and 1.7 times, respectively, greater than when hamsters were free, but VT did not change. After 6 wk, the sedentary group responded differently to restraint; f increased 3-fold, VT decreased by one-half, and V increased 1.6-fold. Exercised hamsters increased f 2.3-fold and decreased VT by one-third; V increased by 1.5-fold. In inhalation studies, changes in breathing pattern would significantly influence the amount of material inhaled, the fraction retained, and thus the amount and distribution of material deposited in the lungs.

Exotoxin A stimulates fluid reabsorption from distal airspaces of lung in anesthetized rats

1996 ◽  
Vol 270 (2) ◽  
pp. L232-L241 ◽  
Author(s):  
J. F. Pittet ◽  
S. Hashimoto ◽  
M. Pian ◽  
M. C. McElroy ◽  
G. Nitenberg ◽  
...  
Keyword(s):  
Fluid Transport ◽  
Exotoxin A ◽  
Lung Epithelium ◽  
Fluid Removal ◽  
Anesthetized Rats ◽  
Colony Forming Units ◽  
Adp Ribosyltransferase ◽  
Dose Dependent Increase ◽  
Dose Dependent

To determine whether exotoxin A may affect the transport of fluid across the lung epithelium, two isogenic strains of Pseudomonas aeruginosa PA103 (10(8) colony-forming units), one (PA103 tox omega) with a structural gene mutation in exotoxin A, were instilled into the distal airspaces of anesthetized rats. PA103 parental strain, but not its mutant, stimulated the removal of fluid from the distal airspaces of the lung. Instillation of exotoxin A alone caused a dose-dependent increase in the fluid transport across the lung epithelium. Instillation of amiloride (10(-3) M) with exotoxin A demonstrated that this effect partially depended on increased uptake of sodium across the lung epithelium. The absence of stimulation after instillation of an exotoxin A mutant (PE delta Glu553) without ADP-ribosyltransferase activity demonstrated that the effect of exotoxin A depended on its ADP-ribosyltransferase activity. Finally, the instillation of exotoxin A in rats depleted of macrophages indicated that the effect of exotoxin A was not secondary to the activation of alveolar macrophages by this toxin. In conclusion, these results indicate that the in vivo release of exotoxin A by live airspace P. aeruginosa directly stimulates the fluid removal from the airspaces by the lung epithelium. This may alter the volume or composition of airway secretions, and may contribute to the lung disease in patients infected with P. aeruginosa.

Exercise responses following ozone exposure

1975 ◽  
Vol 38 (6) ◽  
pp. 996-1001 ◽  
Author(s):  
L. J. Folinsbee ◽  
F. Silverman ◽  
R. J. Shephard
Keyword(s):  
Aerobic Power ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Minute Volume ◽  
Respiratory Frequency ◽  
Ozone Exposure ◽  
Major Response ◽  
Ergometer Test ◽  
Response To Exercise ◽  
Dose Dependent

We have tested the response of 28 subjects to a three-stage ergometer test, with loads adjusted to 45, 60, and 75% of maximum aerobic power following ozone exposure. The subjects were exposed to one of 0.37, 0.50, or 0.75 ppm O3 for 2 h either at rest (R) or while exercising intermittently (IE) (15 min rest alternated with 15 min exercise at approximately 50 W. sufficient to increase VE by a factor of 2.5). Also, all subjects completed a mock exposure VE, respiratory frequency (fR), mixed expired PO2 and PCO2, and electrocardiogram were monitored continuously during the exercise test. Neither submaximal exercise oxygen consumption nor minute ventilation was significantly altered following any level of ozone exposure. The major response noted was an increase in respiratory frequency during exercise following ozone exposure. The increase in fR was closely correlated with the total dose of ozone (r = 0.98) and was accompanied by a decrease in tidal volume (r = 0.91) so that minute volume was unchanged. It is concluded that through its irritant properties, ozone modifies the normal ventilatory response to exercise, and that this effect is dose dependent.

Role of the carotid bodies in chemosensory ventilatory responses in the anesthetized mouse

2004 ◽  
Vol 97 (4) ◽  
pp. 1401-1407 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Mieczyslaw Pokorski ◽  
Ikuo Homma
Keyword(s):  
Tidal Volume ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Whole Body ◽  
Sudden Increase ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Before And After ◽  
Carotid Body Denervation

We examined the effects of carotid body denervation on ventilatory responses to normoxia (21% O2 in N2 for 240 s), hypoxic hypoxia (10 and 15% O2 in N2 for 90 and 120 s, respectively), and hyperoxic hypercapnia (5% CO2 in O2 for 240 s) in the spontaneously breathing urethane-anesthetized mouse. Respiratory measurements were made with a whole body, single-chamber plethysmograph before and after cutting both carotid sinus nerves. Baseline measurements in air showed that carotid body denervation was accompanied by lower minute ventilation with a reduction in respiratory frequency. On the basis of measurements with an open-circuit system, no significant differences in O2 consumption or CO2 production before and after chemodenervation were found. During both levels of hypoxia, animals with intact sinus nerves had increased respiratory frequency, tidal volume, and minute ventilation; however, after chemodenervation, animals experienced a drop in respiratory frequency and ventilatory depression. Tidal volume responses during 15% hypoxia were similar before and after carotid body denervation; during 10% hypoxia in chemodenervated animals, there was a sudden increase in tidal volume with an increase in the rate of inspiration, suggesting that gasping occurred. During hyperoxic hypercapnia, ventilatory responses were lower with a smaller tidal volume after chemodenervation than before. We conclude that the carotid bodies are essential for maintaining ventilation during eupnea, hypoxia, and hypercapnia in the anesthetized mouse.

Vagal control of respiratory pattern during hyperpnea in domestic fowl

1984 ◽  
Vol 56 (6) ◽  
pp. 1650-1654 ◽  
Author(s):  
M. Gleeson ◽  
J. H. Brackenbury
Keyword(s):  
Body Temperature ◽  
Tidal Volume ◽  
Domestic Fowl ◽  
Ventilatory Response ◽  
Normal Animal ◽  
Minute Volume ◽  
Respiratory Frequency ◽  
Respiratory Pattern ◽  
Varied Pattern ◽  
Before And After

Minute volume, tidal volume, and respiratory frequency were measured during hyperpnea induced by exercise, increased body temperature, and CO2 inhalation. Ventilatory characteristics were compared before and after the vagus nerve had been blocked. In normal birds exercise produced increases in both tidal volume and respiratory frequency; hyperthermia produced a typical thermal polypnea consisting of greatly increased respiratory frequency and reduced tidal volume; CO2 inhalation produced increases in tidal volume and respiratory frequency when the birds were euthermic but a slowing of respiratory rate when the birds were hyperthermic. After vagal block these pronounced differences in the pattern of ventilatory response to the various respiratory stimuli were abolished. Instead there was a uniform ventilatory response to all three stimuli consisting mainly of increases in tidal volume combined with small increases in respiratory frequency. It is concluded that in the normal animal control of the varied pattern of ventilatory response to different respiratory stimuli is dependent on vagal fiber activity.

Awake baboon's ventilatory response to venous and inhaled CO2 loading

1975 ◽  
Vol 39 (3) ◽  
pp. 417-422 ◽  
Author(s):  
S. M. Lewis
Keyword(s):  
Steady State ◽  
Tidal Volume ◽  
Ventilatory Response ◽  
Venous Blood ◽  
Minute Volume ◽  
Arteriovenous Shunt ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Change In Mean

Steady-state ventilatory responses to CO2 in trained awake baboons were studied to determine the response to a venous CO2 load. CO2 was loaded either directly into the venous blood through an arteriovenous shunt or by addition to the inhaled air. The two modes of loading were adjusted to produce the same increase in minute volume. Minute volume, tidal volume respiratory frequency, end-tidal PCO2, PaCO2, and pHa were measured. PaCO2 and PETCO2 increased the same amount during the two modes of CO2 loading; thus, the response to changes in arterial PCO2, deltaVE/deltaPaCO2, was the same. I conclude that the ventilatory response to venous CO2 loading occurs only through the change in mean arterial PCO2 and thus it is unlikely that there are any important venous CO2 receptors.

Control of ventilation in running birds: effects of hypoxia, hyperoxia, and CO2

1982 ◽  
Vol 53 (6) ◽  
pp. 1397-1404 ◽  
Author(s):  
J. H. Brackenbury ◽  
M. Gleeson ◽  
P. Avery
Keyword(s):  
Tidal Volume ◽  
Domestic Fowl ◽  
Ventilatory Response ◽  
Minute Volume ◽  
Respiratory Frequency ◽  
Gas Composition ◽  
Control Of Ventilation ◽  
Hypercapnic Response ◽  
Severe Tissue ◽  
Rest And Exercise

Minute volume (V), tidal volume (VT), respiratory frequency (f), venous lactate, and clavicular air sac gas composition were measured in domestic fowl at rest and during exercise, breathing hypoxic, hyperoxic, or hypercapnic gas. Hyperoxia produced no significant change in ventilation, CO2 inhalation produced increases in V and VT, but the changes in f appeared to be related to the stage of exercise at which CO2 was administered. The sensitivity of the hypercapnic response was similar in resting and exercising birds. Compared with the effects of CO2, hypoxia elicited only a weak ventilatory response in rest and exercise conditions despite severe tissue anaerobiosis.

Diaphragmatic and ventilatory responses to alveolar hypoxia and hypercapnia in conscious kittens

1992 ◽  
Vol 72 (1) ◽  
pp. 203-210 ◽  
Author(s):  
M. Bonora ◽  
M. Boule ◽  
H. Gautier
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Central Mechanism ◽  
Respiratory Frequency ◽  
Emg Activity ◽  
Phasic Change ◽  
Ventilatory Responses ◽  
Alveolar Hypoxia ◽  
The Difference

Ventilation and electromyographic (EMG) activity of the diaphragm were recorded in unanesthetized kittens 2 and 10 wk of age during normoxia, hypercapnia (2 and 4% CO2), and hypoxia (12 and 10% O2). We measured integrated diaphragmatic EMG activity at end inspiration (DIAI) and end expiration (DIAE); the difference (DIAI-E), which represents the phasic change of the diaphragmatic activity, was considered responsible for a given tidal volume (VT). During hypercapnia, the 2-wk-old kittens increased minute ventilation (V) by increases in both VT and respiratory frequency (f), whereas the 10-wk-old kittens increased V primarily by an increase in VT. At both ages, DIAI and DIAI-E increased during hypercapnia, whereas DIAE did not change significantly. During hypoxia, in the young kittens, V and VT decreased while f increased markedly; in the older kittens, V, VT, and f did not change significantly. In kittens of both ages, DIAI increased during hypoxia; because diaphragmatic activity persisted into expiration, DIAE also increased. DIAI-E, as well as VT, was decreased in the young kittens, whereas in the older ones DIAI-E was slightly increased despite an unchanged VT. Finally, the ventilatory and diaphragmatic response to hypoxia changes with maturation in contrast to the response to hypercapnia. It is concluded that 1) the hypoxia-induced reduction of VT may result from prolongation of diaphragmatic activity into expiration, inasmuch as it induces a reduction of the phasic change of the diaphragmatic activity, and 2) because DIAI-E indirectly reflects central inspiratory output, a central mechanism should be involved in the reduced VT and V in response to hypoxia in newborns.

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