Effect of dexmedetomidine on cardiorespiratory regulation in spontaneously breathing adult rats

Purpose We examined the cardiorespiratory effect of dexmedetomidine, an α2- adrenoceptor/imidazoline 1 (I1) receptor agonist, in spontaneously breathing adult rats. Methods Male rats (226−301 g, n = 49) under isoflurane anesthesia had their tail vein cannulated for drug administration and their tail artery cannulated for analysis of mean arterial pressure (MAP), pulse rate (PR), and arterial blood gases (PaO2, PaCO2, pH). After recovery, one set of rats received normal saline for control recording and was then divided into three experimental groups, two receiving dexmedetomidine (5 or 50 μg·kg−1) and one receiving normal saline (n = 7 per group). Another set of rats was divided into four groups receiving dexmedetomidine (50 μg·kg−1) followed 5 min later by 0.5 or 1 mg∙kg−1 atipamezole (selective α2-adrenoceptor antagonist) or efaroxan (α2-adrenoceptor/I1 receptor antagonist) (n = 6 or 8 per group). Recordings were performed 15 min after normal saline or dexmedetomidine administration. Results Compared with normal saline, dexmedetomidine (5 and 50 μg·kg−1) decreased respiratory frequency (fR, p = 0.04 and < 0.01, respectively), PR (both p < 0.01), and PaO2 (p = 0.04 and < 0.01), and increased tidal volume (both p = 0.049). Dexmedetomidine at 5 μg·kg−1 did not significantly change minute ventilation (V′E) (p = 0.87) or MAP (p = 0.24), whereas dexmedetomidine at 50 μg·kg−1 significantly decreased V′E (p = 0.03) and increased MAP (p < 0.01). Only dexmedetomidine at 50 μg·kg−1 increased PaCO2 (p < 0.01). Dexmedetomidine (5 and 50 μg·kg−1) significantly increased blood glucose (p < 0.01), and dexmedetomidine at 50 μg·kg−1 increased hemoglobin (p = 0.04). Supplemental atipamezole or efaroxan administration similarly prevented the 50 μg·kg−1 dexmedetomidine-related cardiorespiratory changes. Principal conclusion These results suggest that dexmedetomidine-related hypoventilation and hypertension are observed simultaneously and occur predominantly through activation of α2-adrenoceptors, but not I1 receptors, in spontaneously breathing adult rats.

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Influence of airway resistance on hypoxia-induced periodic breathing

Journal of Applied Physiology ◽

10.1152/jappl.1992.72.6.2128 ◽

1992 ◽

Vol 72 (6) ◽

pp. 2128-2133 ◽

Cited By ~ 3

Author(s):

F. Series ◽

I. Series ◽

L. Atton ◽

A. Blouin

Keyword(s):

Minute Ventilation ◽

Upper Airway ◽

Blood Gases ◽

Random Order ◽

Periodic Breathing ◽

Arterial Blood Gases ◽

Arterial Blood ◽

Posthypoxic Period ◽

Index Value ◽

Spontaneously Breathing

We studied the effects of changing upper airway pressure on the variability of the dynamic response of ventilation to a hypoxic disturbance in 11 spontaneously breathing dogs. Supralaryngeal pressure, instantaneous inspiratory flow, end-expiratory lung volume, and the inspiratory and expiratory O2 and CO2 concentrations were continuously recorded at baseline and after a 1.5-min hypoxic stimulus (abrupt normoxic recovery). Arterial blood gases were obtained at baseline, at the end of the hypoxic period, and after 1 min of recovery. Airway resistances were modified during the recovery by changing the composition of the inspired gas (all with an inspiratory O2 fraction of 20.9%) among four different trials: two trials were realized with air (density 1.12 g/l), and the other two were with He or SF6 (respective density 0.42 and 4.20) in random order. There was no difference between baseline minute ventilation, arterial blood gases, and supralaryngeal resistance values preceding the trials. The hypoxemic and hypocapnic levels and the hypoxia-induced hyperventilation reached during the hypoxic tests were identical for the different hypoxic stimuli. The supralaryngeal resistance measured at peak flow was dramatically influenced by the composition of the inspired gas: 8.8 +/- 1.8 and 6.9 +/- 1.7 (SE) cmH2O.l-1.s with air, 7.2 +/- 2.2 with He, 21.9 +/- 5.5 with SF6 (P less than 0.05). Ventilatory fluctuations were consistently seen during the posthypoxic period. They were characterized by a strength index value (M) (Waggener et al. J. Appl. Physiol. 56: 576–581, 1984).(ABSTRACT TRUNCATED AT 250 WORDS)

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Respiratory syncytial virus infection in anesthetized weanling rather than adult rats prolongs the apneic responses to right atrial injection of capsaicin

Journal of Applied Physiology ◽

10.1152/japplphysiol.01436.2006 ◽

2007 ◽

Vol 102 (6) ◽

pp. 2201-2206 ◽

Cited By ~ 12

Author(s):

Wenhong Peng ◽

Jianguo Zhuang ◽

Kevin S. Harrod ◽

Fadi Xu

Keyword(s):

Respiratory Syncytial Virus ◽

Blood Gases ◽

Respiratory Frequency ◽

Right Atrial ◽

Arterial Blood Gases ◽

Adult Rats ◽

Intranasal Inoculation ◽

Arterial Blood ◽

Rsv Infection ◽

Syncytial Virus

Apnea is a common complication in infants infected by respiratory syncytial virus (RSV). A recent study has shown that intranasal inoculation of RSV in conscious weanling rats strengthens the apneic responses to right atrial injection of capsaicin (CAP), leading to 66% mortality. The objectives of the present study were to determine 1) whether RSV infection changes baseline minute ventilation (V̇e) and arterial blood gases in anesthetized rats; 2) what the effects of RSV infection are on the respiratory responses to CAP; and 3) whether the RSV-strengthened apneic responses are age dependent. Our experiments were conducted in anesthetized and spontaneously breathing rats divided into four groups of weanling and adult rats that received either intranasal inoculation of RSV or virus-free medium. Two days after RSV infection (0.7 ml/kg), animal blood gases, baseline V̇e, and V̇e responses to right atrial injection of three doses of CAP (4, 16, and 64 μg/kg) were measured and compared among the four groups. Our results showed that RSV infection increased respiratory frequency (∼25%, P < 0.05) in weanling but not adult rats, with little effect on arterial blood gases. RSV infection amplified the apneic responses to CAP in weanling but not adult rats, characterized by increases in the initial (40%) and the longest apneic duration (650%), the number of apneic episodes (139%), and the total duration of apneas (60%). These amplifications led to 50% mortality ( P < 0.05). We conclude that RSV infection increases respiratory frequency and strengthens the apneic responses to CAP only in anesthetized weanling but not adult rats.

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Ventilatory responses of hamsters and rats to hypoxia and hypercapnia

Journal of Applied Physiology ◽

10.1152/jappl.1985.59.6.1955 ◽

1985 ◽

Vol 59 (6) ◽

pp. 1955-1960 ◽

Cited By ~ 41

Author(s):

B. R. Walker ◽

E. M. Adams ◽

N. F. Voelkel

Keyword(s):

Duty Cycle ◽

Minute Ventilation ◽

Natural Habitat ◽

Blood Gases ◽

Atmospheric Conditions ◽

Arterial Blood Gases ◽

Ventilatory Responses ◽

Arterial Blood ◽

Rat Experiments ◽

Fossorial Species

As a fossorial species the hamster differs in its natural habitat from the rat. Experiments were performed to determine possible differences between the ventilatory responses of awake hamsters and rats to acute exposure to hypoxic and hypercapnic environments. Ventilation was measured with the barometric method while the animals were conscious and unrestrained in a sealed plethysmograph. Tidal volume (VT), respiratory frequency (f), and inspiratory (TI) and expiratory (TE) time measurements were made while the animals breathed normoxic (30% O2), hypercapnic (5% CO2), or hypoxic (10% O2) gases. Arterial blood gases were also measured in both species while exposed to each of these atmospheric conditions. During inhalation of normoxic gas, the VT/100 g was greater and f was lower in the hamster than in the rat. Overall minute ventilation (VE/100 g) in the hamster was less than in the rat, which was reflected in the lower PO2 and higher PCO2 of the hamster arterial blood. When exposed to hypercapnia, the hamster increased VE/100 g solely through VT; however, the VE/100 g increase was significantly less than in the rat. In response to hypoxia, the hamster and rat increased VE/100 g by similar amounts; however, the hamster VE/100 g increase was through f alone, whereas the rat increased both VT/100 g and f. Mean airflow rates (VT/TI) were no different in the hamster or rat in each gas environment; therefore most of the ventilatory responses were the result of changes in TI and TE and respiratory duty cycle (TI/TT).

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Response of newborn lambs to CO-induced hypoxia

Journal of Applied Physiology ◽

10.1152/jappl.1988.64.5.1870 ◽

1988 ◽

Vol 64 (5) ◽

pp. 1870-1877 ◽

Cited By ~ 6

Author(s):

M. A. Bureau ◽

J. L. Carroll ◽

E. Canet

Keyword(s):

Minute Ventilation ◽

Blood Gases ◽

Periodic Breathing ◽

Respiratory Frequency ◽

Gas Mixture ◽

Arterial Blood Gases ◽

Small Shift ◽

Arterial Blood ◽

The Right ◽

Very High

This study was undertaken to measure the neonate's response to CO-induced hypoxia in the first 10 days of life. CO breathing was used to induce hypoxia because CO causes tissue hypoxia with no or minimal chemoreceptor stimulation. An inspired gas mixture of 0.25 to 0.5% CO in air was used to raise the blood carboxyhemoglobin (HbCO) progressively from 0 to 60% over approximately 20 min. The study, conducted in awake conscious lambs aged 2 and 10 days, consisted in measuring the response of ventilation and the change in arterial blood gases during the rise of HbCO. The results showed that the 2- and 10-day-old lambs tolerated very high HbCO levels without an increase in minute ventilation (VE) and without metabolic acidosis. At both ages, HbCO caused no VE change until HbCO levels rose to between 45 and 50% after which the VE change was exponential in some animals but minimal in others. The VE change was brought about by a rise in tidal volume and respiratory frequency. During the period of maturation from 2 to 10 days, there was a small shift to the right in the VE-HbCO response. In the 10-day-old lambs the VE response to high HbCO was greater than that of the 2-day-olds because of the lambs' higher respiratory frequency response. Six of the 10-day-old lambs but only two of the 2-day-old lambs showed a hypoxic tachypnea to HbCO of 55–65%. None of the lambs developed periodic breathing, dysrhythmic breathing, or recurrent apneas with an HbCO level as high as 60%.(ABSTRACT TRUNCATED AT 250 WORDS)

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Arterial blood gases in conscious rats exposed to hypoxia, hypercapnia, or both

Journal of Applied Physiology ◽

10.1152/jappl.1975.38.4.581 ◽

1975 ◽

Vol 38 (4) ◽

pp. 581-587 ◽

Cited By ~ 63

Author(s):

W. E. Pepelko ◽

G. A. Dixon

Keyword(s):

Control Period ◽

Blood Gases ◽

Barometric Pressure ◽

Male Rats ◽

Arterial Blood Gases ◽

Blood Samples ◽

Air Breathing ◽

Breathing Control ◽

Arterial Blood ◽

Caudal Artery

Adult male rats were anesthetized and catheters were implanted in the caudal artery. Soon after recovery from short-lasting anesthesia, a total of 20 groups of six each were individually exposed to five different oxygen levels varying from 21.0 to 9.0% combined with four CO2 levels ranging from 0 to 12.9% at a mean barometric pressure of 744 Torr. Arterial blood samples were collected and analyzed for pH, Po2, and Pco2 before and near the end of 20-min exposures. During an air-breathing control period, pH averaged 7.466 plus or minus 0.020 SD, Paco2 41.2 plus or minus 1.9 Torr and Pao2 91.8 plus or minus 3.5 Torr. During hypoxia, Pao2 levels were similar to that of acutely hypoxic humans. Rats apparently differ from man in that blood buffering is greater, resulting in a higher pH during air breathing and a smaller [H-+] increase with increasing Paco2. Differences between arterial and inspired CO2 were about 10 Torr at 60 and 90 Torr Plco2 and were not influenced by Plo2.

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Effect of Endotracheal Suction with and Without Instillation of Normal Saline on Oxygenation, Hemodynamic and Arterial Blood Gases in Adult Mechanically Ventilated Patients

IOSR Journal of Nursing and health Science ◽

10.9790/1959-0602073744 ◽

2017 ◽

Vol 06 (02) ◽

pp. 37-44

Author(s):

Dr. Mervat A. Ghaleb ◽

Dr. Hatem O. Qutub ◽

Zainab Ali Al-Awami

Keyword(s):

Normal Saline ◽

Blood Gases ◽

Arterial Blood Gases ◽

Mechanically Ventilated ◽

Mechanically Ventilated Patients ◽

Endotracheal Suction ◽

Arterial Blood ◽

Ventilated Patients

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Changes in Lung Surfactant Proteins in Rats With Lipopolysaccharide--Induced Fever

Physiological Research ◽

10.33549/physiolres.932928 ◽

2014 ◽

pp. S619-S628

Author(s):

M. KOLOMAZNIK ◽

I. ZILA ◽

J. KOPINCOVA ◽

D. MOKRA ◽

A. CALKOVSKA

Keyword(s):

Minute Ventilation ◽

Lung Surfactant ◽

Intraperitoneal Administration ◽

Blood Gases ◽

The Body ◽

Surfactant Proteins ◽

Control Group ◽

Adult Rats ◽

Arterial Blood ◽

Specific Proteins

The study was designed to prove the hypothesis that lipopolysaccharide (LPS)-induced fever elicits the changes in surfactant specific proteins, potentially related to thermal tachypnea. In adult rats fever was induced by intraperitoneal administration of LPS at a dose 100 µg/kg of body weight; control group received saline. Respiratory parameters, arterial blood gases and pH and colonic body temperature (BT) were recorded. Five hours later, surfactant proteins (SP) A, B, C and D were evaluated in bronchoalveolar lavage fluid (BALF) and lung tissue (LT). LPS evoked monophasic thermic response (at 300 min 38.7±0.2 vs. 36.4±0.3 °C, P0.05) and an increase in minute ventilation due to changes in breathing rate and tidal volume. LPS-instilled animals had higher levels of SP-A and SP-D in LT (P0.05 and 0.01), and higher SP-D in BALF (P0.01) than controls. SP-B increased in LT and SP-C in BALF of animals with LPS (both P0.05 vs. controls). The changes in all surfactant specific proteins are present in LPS-induced fever. Alterations of proteins related to local immune mechanisms (SP-A, SP-D) are probably a part of general inflammatory response to pyrogen. Changes in proteins related to surface activity (SP-B and SP-C) might reflect the effort of the body to stabilize the lungs in thermal challenge.

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Brain ECF pH and central chemical control of ventilation during anoxia in turtles

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.252.5.r848 ◽

1987 ◽

Vol 252 (5) ◽

pp. R848-R852 ◽

Cited By ~ 1

Author(s):

D. G. Davies ◽

J. A. Sexton

Keyword(s):

Ventilatory Response ◽

Minute Ventilation ◽

Control Period ◽

Extracellular Fluid ◽

Blood Gases ◽

Breathing Frequency ◽

Arterial Blood Gases ◽

Brain Extracellular Fluid ◽

Arterial Blood

The role of changes in brain extracellular fluid [H+] in the control of breathing during anoxia was studied in unanesthetized turtles, Chrysemys scripta. Ventilation, [minute ventilation (VE), tidal volume (VT), and breathing frequency (f)], cerebral extracellular fluid (ECF) pH, and arterial blood gases were measured at 25 degrees C during a 30-min control period (room air), 30 min of anoxia (100% N2 breathing), and 60 min of recovery (room air). ECF pH was measured in the cerebral cortex with a glass microelectrode (1-2 micron tip diam). Large changes in ventilation, ECF [H+], and arterial blood gases were observed. The predominant ventilatory response was an increase in f with a slight increase in VT. A correlation was observed between ECF [H+] and f, which suggested that central chemoreceptor stimulation was involved in the ventilatory response.

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Ventilatory and metabolic adaptations to walking and cycling in patients with COPD

Journal of Applied Physiology ◽

10.1152/jappl.2000.88.5.1715 ◽

2000 ◽

Vol 88 (5) ◽

pp. 1715-1720 ◽

Cited By ~ 112

Author(s):

Paolo Palange ◽

Silvia Forte ◽

Paolo Onorati ◽

Felice Manfredi ◽

Pietro Serra ◽

...

Keyword(s):

Minute Ventilation ◽

Venous Blood ◽

Blood Gases ◽

Peak Exercise ◽

Chronic Obstructive ◽

Arterial Blood Gases ◽

Physiological Dead Space ◽

Arterial Blood ◽

Ergometer Exercise ◽

Walking Capacity

To test the hypothesis that in chronic obstructive pulmonary disease (COPD) patients the ventilatory and metabolic requirements during cycling and walking exercise are different, paralleling the level of breathlessness, we studied nine patients with moderate to severe, stable COPD. Each subject underwent two exercise protocols: a 1-min incremental cycle ergometer exercise (C) and a “shuttle” walking test (W). Oxygen uptake (V˙o 2), CO2output (V˙co 2), minute ventilation (V˙e), and heart rate (HR) were measured with a portable telemetric system. Venous blood lactates were monitored. Measurements of arterial blood gases and pH were obtained in seven patients. Physiological dead space-tidal volume ratio (Vd/Vt) was computed. At peak exercise, W vs. CV˙o 2,V˙e, and HR values were similar, whereasV˙co 2 (848 ± 69 vs. 1,225 ± 45 ml/min; P < 0.001) and lactate (1.5 ± 0.2 vs. 4.1 ± 0.2 meq/l; P < 0.001) were lower, ΔV˙e/ΔV˙co 2(35.7 ± 1.7 vs. 25.9 ± 1.3; P < 0.001) and ΔHR/ΔV˙o 2values (51 ± 3 vs. 40 ± 4; P < 0.05) were significantly higher. Analyses of arterial blood gases at peak exercise revealed higher Vd/Vt and lower arterial partial pressure of oxygen values for W compared with C. In COPD, reduced walking capacity is associated with an excessively high ventilatory demand. Decreased pulmonary gas exchange efficiency and arterial hypoxemia are likely to be responsible for the observed findings.

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