scholarly journals THE CHANGE IN THE ARTERIAL OXYGEN AND CARBON DIOXIDE TENSION DURING VOLUNTARY HYPERVENTILATION AS A TEST OF LUNG FUNCTION

1954 ◽  
Vol 27 (6) ◽  
pp. 541-545
Author(s):  
Viking Olov Björk ◽  
Henry John Hilty
1995 ◽  
Vol 28 (4) ◽  
pp. 541 ◽  
Author(s):  
Yong Taek Nam ◽  
Sook Yeoung Lee ◽  
Jin Su Kim ◽  
Chae Hong Chung ◽  
Young Sun Seo

1980 ◽  
Vol 49 (1) ◽  
pp. 45-51 ◽  
Author(s):  
S. Lahiri ◽  
T. Nishino ◽  
A. Mokashi ◽  
E. Mulligan

Effects of dopamine and of a dopaminergic blocker, haloperidol, on the responses of carotid body chemoreceptors to hypoxia and hypercapnia were investigated in 16 anesthetized cats. Intravenous infusion of dopamine (10-20 micrograms.min-1) decreased carotid body chemoreceptor responses to hypoxia and hypercapnia. The effect was greater at higher levels of arterial oxygen and carbon dioxide tension (PaO2 and PaCO2) stimulus. Thus, the magnitude of the dopamine effect depended on the degree of both PO2- and PCO2-mediated excitation of the receptors. Haloperidol potentiated responses to both hypoxia and hypercapnia but apparently did not stimulate the receptors in the absence of these stimuli. Potentiation by haloperidol and inhibition by dopamine of excitatory effects due to PaO2 decrease and PaCO2 increase are complementary. The data suggest that chemoreception of dopamine, O2, and CO2 converge at some site in the carotid body. Persistence of hypoxic and hypercapnic responses, following dopamine-blocking doses of haloperidol, does not support the theory that regulation of dopamine release is responsible for O2 and CO2 chemoreception in carotid body of the cat.


Cardiology ◽  
1973 ◽  
Vol 58 (6) ◽  
pp. 335-346 ◽  
Author(s):  
C. Helmers ◽  
S. Hofvendahl ◽  
T. Lundman ◽  
L. Mogensen ◽  
O. Nyquist ◽  
...  

1997 ◽  
Vol 22 (3) ◽  
pp. 256-267 ◽  
Author(s):  
Deep Chatha ◽  
James Duffin

The pattern of breathing following a 10-breath voluntary hyperventilation period during hyperoxic rebreathing was compared to that without hyperventilation in 6 subjects (3 male and 3 female). The aim was to measure the posthyperventilation short-term potentiation of ventilation without changes in respiratory chemoreflex drives induced by the voluntary hyperventilation. Hyperoxia was used to reduce the peripheral chemoreflex drive, and rebreathing to prevent the decrease in arterial carbon dioxide tension normally produced by hyperventilation. There were significant differences between the male and female responses. However, in all subjects, ventilation and heart rate were increased during hyperventilation but end-tidal partial pressures of carbon dioxide and oxygen were unchanged. Following hyperventilation, ventilation immediately returned to the values observed when hyperventilation was omitted. Hyperventilation did not induce a short-term potentiation of ventilation under these conditions: changes in chemoreflex stimuli brought about by cardiovascular changes induced by hyperventilation may play a role in the short-term potentiation observed under other circumstances. Key words: rebreathing, hyperventilation, short-term potentiation


1979 ◽  
Vol 47 (4) ◽  
pp. 858-866 ◽  
Author(s):  
S. Lahiri ◽  
E. Mulligan ◽  
T. Nishino ◽  
A. Mokashi

Responses of aortic chemoreceptor afferents to a range of arterial carbon dioxide tension (Paco2) changes at various levels of arterial oxygen tension (Pao2) were investigated in 18 cats anesthetized with alpha-chloralose and maintained at 38 degrees C. Aortic chemoreceptor activity, end-tidal oxygen pressure, end-tidal carbon dioxide pressure, and arterial blood pressure were continuously monitored. Arterial blood gases were measured in steady states. Single or a few clearly identifiable afferents were studied during changes and steady states of Pao2 and Paco2. All the aortic chemoreceptor afferent discharge rates increased with Paco2 increases from hypercapnia (10–15 Torr) to normocapnia and moderate hypercapnia (30–50 Torr) and with Pao2 decreases from above 400 to 30 Torr. Hypoxia augmented the response to Paco2 most effectively in the range of 10–40 Torr. At any Pao2, the discharge rate reached a plateau with sufficient intensity of hypercapnia. The Paco2 stimulus threshold at a Pao2 of 440 Torr was about 15 Torr, and at a Pao2 of 60 Torr it was 10 Torr. In the transition from hypocapnia to hypercapnia, responses increased gradually, usually without an overshoot. The steady-state responses to Paco2 of the majority of aortic chemoreceptors resembled those of carotid chemoreceptors. The responses of both receptors can be attributed to the same basic type of mechanism.


Perfusion ◽  
1998 ◽  
Vol 13 (2) ◽  
pp. 105-109 ◽  
Author(s):  
Lise Schlünzen ◽  
Jens Pedersen ◽  
Kirsten Hjortholm ◽  
Ole K Hansen ◽  
Emmy Ditlevsen

The effect of modified ultrafiltration (MUF) after cardiopulmonary bypass for paediatric cardiac surgery was evaluated in 138 children with moderate to severe congenital heart disease. The median age was 0.4 years (0 days to 6.5 years), and the weight 5.3 kg (2.2-20 kg). The operation was discontinued in six cases, three because of technical problems and three because of unstable circulation. One-hundred-and-thirty-four patients were ultrafiltrated for a median of 12 min (2-27 min) with an ultrafiltrate of median 44 ml/kg (6-118 ml/kg). Haematocrit was significantly increased from 28% (20-39%) to 36% (26-51%) and systolic arterial pressure from 56 mmHg (30-85 mmHg) to 74.0 mmHg (32-118 mmHg). Furthermore arterial oxygenation was significantly increased from 30.8 kPa (4.8-70.4 kPa) to 34.1 kPa (4.9-80.6 kPa), and arterial carbon dioxide tension from 4.8 kPa (3.1-7.3 kPa) to 5.1 kPa (3.1-7.6 kPa). Heart rate was significantly reduced from 145 beats/min (92-201 beats/min) to 136 beats/min (88-200 beats/min). There were no significant differences in central venous pressure, left atrial pressure and base excess before and after MUF. MUF increases systolic blood pressure, haematocrit, arterial oxygen and carbon dioxide tension coming off bypass in paediatric cardiac surgery and reduces heart rate and postoperative fluid overload.


1962 ◽  
Vol 17 (6) ◽  
pp. 933-937 ◽  
Author(s):  
M. McGregor ◽  
R. E. Donevan ◽  
N. M. Anderson

The effect of changes in ventilation and carbon dioxide tension on cardiac output was studied in seven normal human subjects in the supine posture using a dye dilution method. Voluntary hyperventilation of room air with resultant hypocapnia invariably produced an increase in cardiac output (mean, 38 ml blood/ liter increase in ventilation). Voluntary hyperventilation with maintenance of CO2 tension at near normal levels resulted in a smaller increase in cardiac output (mean, 15 ml/liter). Hyperventilation produced by the inhalation of 8.4% CO2 produced no change in cardiac output within the first 2 min but an increase thereafter. The response of the cardiac output to hyperventilation is thus largely determined by the carbon dioxide content of the inspirate. The manner in which this takes place is uncertain. The higher cardiac output response at 2 min with hypocapnia may be partly the result of respiratory alkalosis. It might also be related to the increase in respiratory mechanical work per liter ventilation associated with the fall in CO2. The reason for the late rise of cardiac output with hypercapnia is unknown. Submitted on May 14, 1962


CHEST Journal ◽  
2005 ◽  
Vol 128 (3) ◽  
pp. 1291-1296 ◽  
Author(s):  
Oliver Senn ◽  
Christian F. Clarenbach ◽  
Vladimir Kaplan ◽  
Marco Maggiorini ◽  
Konrad E. Bloch

PEDIATRICS ◽  
1968 ◽  
Vol 41 (6) ◽  
pp. 1063-1073
Author(s):  
George Russell ◽  
Ernest K. Cotton

Following the rapid intravenous injection of sodium bicarbonate in 19 infants suffering from the respiratory distress syndrome of the newborn (RDS), arterial oxygen tension, arterial oxygen saturation and base excess rose, while arterial carbon dioxide tension and hydrogen ion concentration fell. Effective pulmonary blood flow rose, and right-to-left shunting diminished. Following the administration of increased oxygen to 6 infants with less severe RDS, there was a rise in arterial oxygen tension and a fall in arterial carbon dioxide tension. It is suggested that the changes which occur after both forms of therapy are due to a decrease of pulmonary vascular resistance, reduced right-to-left shunt, and improved pulmonary capillary perfusion.


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