Effects of potassium depletion on control of breathing in awake rats

1976 ◽  
Vol 231 (2) ◽  
pp. 588-592 ◽  
Author(s):  
EE Nattie ◽  
SM Tenney
Keyword(s):  
Breathing Pattern ◽  
Ventilatory Response ◽  
Inhibitory Effect ◽  
Catecholamine Metabolism ◽  
Membrane Excitability ◽  
Acid Base ◽  
Pneumotaxic Center ◽  
Low K ◽  
Base Data ◽  
K Depletion

Possible mechanisms for the variable ventilatory response to metabolic acid-base disturbances have been examined in normal and K-depleted rats. Ventilatory measurements are correlated with CSF acid-base data. The ratios VE/VO2 and 1/PaCO2 are utilized as indices of alveolar ventilation. The log of these indices correlates closely with CSF [H+] independent of [K+] except at very low CSF [H+] where the change in log 1/PaCO2 and log VE/VO2 per change in CSF [H+] is much diminished in low-K rats. This finding suggests the presence of an additional stimulus to breathing in the low-K rat opposing the inhibitory effect of low CSF [H+]. Otherwise the chemical control of ventilation appears to be normal. However, low-K rats always breath with a low-flight-Vt pattern and occasionally with abnormal rhythms. The similarity of the low K breathing pattern to that reported in awake animals with vagotomy and pneumotaxic center (PC) lesions suggests that the altered breathing pattern in depletion involves vagal and/or PC pathways. The similarity of the low-K breathing pattern to that observed with reserpine administration together with the known relationships of K and catecholamine metabolism lead to the speculation that K depletion alters breathing via an effect on central catecholamine metabolism. However, other mechanisms involving changes in membrane excitability and intracellular pH in K depletion might also be involved.

Ventilatory response to sustained hypoxia after pretreatment with aminophylline

1988 ◽  
Vol 64 (4) ◽  
pp. 1445-1450 ◽  
Author(s):  
P. A. Easton ◽  
N. R. Anthonisen
Keyword(s):  
Young Adults ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Inhibitory Effect ◽  
Significant Difference ◽  
Adult Humans ◽  
Intravenous Saline ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

During sustained hypoxia the decline in ventilation that occurs in normal adult humans may be related to central accumulation of a neurochemical with net inhibitory effect. Recent investigations have shown that the putative neurotransmitter adenosine can effect a prolonged respiratory inhibition. Therefore we evaluated the possible role of adenosine in the hypoxia ventilatory decline by employing aminophylline as an adenosine blocker. We evaluated the ventilatory response to 25 min of sustained hypoxia (80% arterial O2 saturation), in eight young adults after pretreatment with either intravenous saline or aminophylline. With a mean serum aminophylline level of 15.7 mg/l, over 25 min of sustained hypoxia, peak hypoxic ventilation decreased by only 12.8% compared with 24.8% with saline, a significant difference. However, the ventilatory decline during sustained hypoxia was not abolished by the aminophylline pretreatment. Unlike the usual tidal volume-dependent attenuation of hypoxic ventilation exhibited after saline, after aminophylline the ventilatory decline was achieved predominantly through alterations in respiratory timing. Thus aminophylline pretreatment did alleviate the hypoxic ventilatory decline, although the associated alterations in breathing pattern were uncharacteristic. We conclude that adenosine may play a contributing role in the hypoxic ventilatory decline.

Effects of hypoxia on ventilation during postnatal development in conscious kittens

1984 ◽  
Vol 56 (6) ◽  
pp. 1464-1471 ◽  
Author(s):  
M. Bonora ◽  
D. Marlot ◽  
H. Gautier ◽  
B. Duron
Keyword(s):  
Postnatal Development ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Inhibitory Effect ◽  
Respiratory Frequency ◽  
Excitatory Effect ◽  
States Of Consciousness ◽  
Adult Cats ◽  
Ventilatory Response To Hypoxia

Effects of steady-state hypoxia (inspired O2 fraction = 0.11) on ventilation and breathing pattern were studied during postnatal development in unanesthetized kittens. Studies were done from 2 days to 8 mo of age, every week during the first month and every month thereafter. During the first 2 months, states of consciousness were determined. In the first month, minute ventilation (VE) was depressed in hypoxia compared with control values in air, whereas in the older kittens VE was increased in hypoxia, as in adult cats. The inhibitory effect of hypoxia was observed in all three states of consciousness in 7- and 14-day-old kittens. In the 21- and 28-day-old kittens, VE could not be reliably related to the state of consciousness. In the 2-mo-old kittens, VE increased in all states. Tidal volume (VT) was markedly decreased in kittens up to 14 days of age, and respiratory frequency increased. In the 21- and 28-day-old kittens, changes in breathing pattern were variable. In the oldest, the increase of VE was mainly due to an increase of VT. We conclude that in unanesthetized kittens, the ventilatory response to hypoxia is mature at 2 mo of age. The hypoxic tachypnea observed at 7 and 14 days resembles that previously seen in adult carotid-denervated cats, and may be due to a low level of carotid chemoreceptor drive and to a central excitatory effect of hypoxia on respiratory frequency. The complex response observed during the first month of life must reflect the development of peripheral and central mechanisms and their interactions.

Cerebral blood flow, glucose use, and CSF ionic regulation in potassium-depleted rats

1988 ◽  
Vol 254 (2) ◽  
pp. H250-H257
Author(s):  
H. Schrock ◽  
W. Kuschinsky
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Local Cerebral Blood Flow ◽  
Arterial Pco2 ◽  
Average Decrease ◽  
K Concentration ◽  
Low K ◽  
The Brain ◽  
K Depletion

Rats were kept on a low-K+ diet for 25 or 70 days. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 31 different structures of the brain by means of the [14C]iodoantipyrine and [14C]2-deoxy-D-glucose method. After 25 and 70 days of K+ depletion LCBF was decreased significantly in 27 and 30 structures, respectively, the average decrease being 19 and 25%. In contrast, average LCGU was not changed. Cisternal cerebrospinal fluid (CSF) K+ concentration decreased significantly from 2.65 +/- 0.02 mM in controls to 2.55 +/- 0.02 mM and 2.47 +/- 0.02 mM in the two treated groups (P less than 0.01). CSF [HCO3-], pH, and PCO2 were increased in K+-depleted animals. These data show that K+ depletion induces an increase in CSF pH and a decrease in CSF K+ concentration, both of which cause a reduction in cerebral blood flow. The increased CSF PCO2 is secondary to the reduction of blood flow, since brain metabolism and arterial PCO2 remained constant.

Effects of hypoxia and hypercapnia on VT, f, and VI of nestling and adult bank swallows

1987 ◽  
Vol 253 (6) ◽  
pp. R854-R860 ◽  
Author(s):  
C. Colby ◽  
D. L. Kilgore ◽  
S. Howe
Keyword(s):  
Chronic Exposure ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Volume ◽  
Additive Effect ◽  
Riparia Riparia ◽  
Fractional Concentration ◽  
Ventilatory Response To Hypoxia

The effects of hypoxia, hypercapnia, and hypoxic hypercapnia on ventilation, and breathing pattern in adult and nestling bank swallows (Riparia riparia) were assessed. The CO2 threshold above which inhaled minute volume (VI) increased significantly in adults and nestlings was 0.045. At each level of fractional concentration of inspired CO2 (FICO2), ventilation in nestlings was lower than that in adults. At a FICO2 of 0.09, VI of adults increased by 284%, whereas VI in nestlings changed 238%. Adult bank swallows also showed a blunted ventilatory response to hypoxia, and the nestling's response was similar to other birds. Adults exhibited greater changes in VI at all levels of hypoxic hypercapnia compared with nestlings. Combined hypoxic and hypercapnic stimuli had an additive effect on ventilation in both groups. Chronic exposure of nestlings to the hypercapnia and hypoxia within burrows seems to significantly alter their ventilatory response to these respiratory stimuli.

Quality Control in the Astrup Method for Determining Acid-Base Parameters in Blood

1970 ◽  
Vol 16 (9) ◽  
pp. 789-791
Author(s):  
C D Russell ◽  
H-D Roeher
Keyword(s):  
Quality Control ◽  
Human Blood ◽  
Digital Computer ◽  
Acid Base ◽  
Base Parameters ◽  
Automatic Error ◽  
Base Data

Abstract We present a method for automatic error screening by digital computer of acid-base data obtained by the Astrup procedure. It is based on the detection of discrepancies between the slope of the line joining the high- and low-pCOCO2, measurements on the Astrup diagram and the known slope for human blood.

Effects of Chronic Acid-Base Changes on the Rebreathing Hypercapnic Ventilatory Response in Man

Respiration ◽  
1991 ◽  
Vol 58 (3-4) ◽  
pp. 181-185 ◽  
Author(s):  
Ami Oren ◽  
Brian J. Whipp ◽  
Karlman Wasserman
Keyword(s):  
Ventilatory Response ◽  
Acid Base ◽  
Hypercapnic Ventilatory Response

Breathing Pattern and Ventilatory Response to CO2during Exercise

1992 ◽  
Vol 13 (01) ◽  
pp. 1-5 ◽  
Author(s):  
J. Mercier ◽  
M. Ramonatxo ◽  
C. Préfaut
Keyword(s):  
Breathing Pattern ◽  
Ventilatory Response

An assessment of nasal functions in control of breathing

1988 ◽  
Vol 65 (4) ◽  
pp. 1520-1524 ◽  
Author(s):  
Y. Tanaka ◽  
T. Morikawa ◽  
Y. Honda
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Airway Resistance ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Control Of Breathing ◽  
Mouth Breathing ◽  
Occlusion Pressure ◽  
Ventilatory Responses ◽  
End Tidal

Breathing pattern and steady-state CO2 ventilatory response during mouth breathing were compared with those during nose breathing in nine healthy adults. In addition, the effect of warming and humidification of the inspired air on the ventilatory response was observed during breathing through a mouthpiece. We found the following. 1) Dead space and airway resistance were significantly greater during nose than during mouth breathing. 2) The slope of CO2 ventilatory responses did not differ appreciably during the two types of breathing, but CO2 occlusion pressure response was significantly enhanced during nose breathing. 3) Inhalation of warm and humid air through a mouthpiece significantly depressed CO2 ventilation and occlusion pressure responses. These results fit our observation that end-tidal PCO2 was significantly higher during nose than during mouth breathing. It is suggested that a loss of nasal functions, such as during nasal obstruction, may result in lowering of CO2, fostering apneic spells during sleep.

Sign in / Sign up

Export Citation Format

Share Document