Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans

Clar, Christine; Pedersen, Michala; Poulin, Marc J.; Tansley, John G.; Robbins, Peter A.

doi:10.1113/expphysiol.1997.sp004065

Cited by 5 publications

(4 citation statements)

References 21 publications

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“…Our control data showed an increase in heart rate over the 8 h of hypoxia. This is consistent with previous results in humans from our laboratory (Clar et al 1997b;Dorrington et al 1997) and with results from other laboratories in humans (Grover et al 1976;Hoon et al 1977) and sheep (Krasney et al 1984(Krasney et al , 1985. It is important to note the period over which this…”

Section: Effects On Heart Rate -Comparison With Other Studies In Humanssupporting

confidence: 93%

“…Consistent with our previous results (Clar et al 1997b), most of the observed increase in heart rate appears to be linked to an increase in G HR , with only a small, barely detectable effect on heart rate during acute hyperoxia. We are unaware of any other studies examining the heart rate response to prolonged hypoxia during muscarinic blockade.…”

Section: Figuresupporting

confidence: 92%

“…Firstly, we studied the effect of glycopyrrolate on AHVR and AHHR before and after the hypoxic exposure. Secondly, since part of the increment in V E and heart rate following exposure to hypoxia persists under conditions of acute hyperoxia (Clar et al 1997b;Tansley et al 1997), we investigated whether this component of the V E and heart rate response to hypoxia could be altered by glycopyrrolate.…”

mentioning

confidence: 99%

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Effects of 8 h of Isocapnic Hypoxia with and without Muscarinic Blockade on Ventilation and Heart Rate in Humans

Clar

Dorrington

Fatemian

et al. 2001

Experimental Physiology

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Ventilatory acclimatisation to hypoxia involves a slow and progressive rise in ventilation (V E ), starting within the first few hours of the onset of the exposure to hypoxia. This rise in V E is accompanied by an increase in the sensitivity of the peripheral chemoreflex to acute hypoxia (acute hypoxic ventilatory response, AHVR). The slow increase in V E causes a slow decrease in end-tidal P CO 2 (P ET,CO 2 ) and a progressive respiratory alkalosis. The mechanisms underlying the slow respiratory changes during the early stages of acclimatisation are not fully understood, but it has been established that the main stimulus pathway does not involve the fall in P CO 2 and rise in pH that normally accompany hypoxia; during isocapnic hypoxia, the progressive increase in V E is more pronounced than during poikilocapnic hypoxia, but the increase in AHVR is similar (Busch et al. 1985;Bisgard et al. 1986; Howard & Robbins, 1995a,b).One possibility is that slow changes in autonomic activity underlie part of these slow ventilatory changes. Both sympathetic and parasympathetic activity have been shown to change during exposure to hypoxia (Petersen et al. 1974;Somers et al. 1989), and carotid body activity can be changed both by efferent sympathetic and parasympathetic inputs (Goodman, 1973;O'Regan, 1981). In a previous study, we have investigated the influence of b-adrenergic blockade on the ventilatory response to 8 h of isocapnic hypoxia (Clar et al. 1997a). We found that neither the increase in V E observed during this period of hypoxia nor the increase in AHVR was altered by b-adrenergic blockade. As a logical next step we consider here the other division of the autonomic nervous system, namely the parasympathetic nervous system. Even though increases in V E in response to acute hypoxia have been shown to be unrelated to parasympathetic mechanisms (Koller et al. 1988;Akiyama et al. 1996), there has been evidence from animal studies that parasympathetic mechanisms may alter carotid body hypoxic sensitivity during prolonged hypoxia (Lahiri et al. 1983).In addition to the increase in V E during 8 h of hypoxia, there is also an increase in heart rate during this time. It is already recognised that the parasympathetic nervous system mediates most of the variation in heart rate in response to acute hypoxia (acute hypoxic heart rate response, AHHR) (Petersen et al. 1974), but it is not clear whether parasympathetic mechanisms play a role in the slow increase in heart rate over 8 h. We have shown in a previous study that b-adrenergic blockade could not abolish the increase in heart rate seen during an 8 h exposure to isocapnic hypoxia (Clar et al. 2000), and hence it is unlikely that this increase is related to sympathetic mechanisms. A second objective of this study was therefore to test whether or not slow increases in heart rate over 8 h of isocapnic hypoxia are mediated by a parasympathetic mechanism. This study examined the role of muscarinic parasympathetic mechanisms in generating the progressive increases in ventilation...

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Section: Effects On Heart Rate -Comparison With Other Studies In Humanssupporting

confidence: 93%

Section: Figuresupporting

confidence: 92%

mentioning

confidence: 99%

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Effects of 8 h of Isocapnic Hypoxia with and without Muscarinic Blockade on Ventilation and Heart Rate in Humans

Clar

Dorrington

Fatemian

et al. 2001

Experimental Physiology

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“…A possible explanation for this difference is that the subjects were exposed to a greater degree of hypoxia in the previous studies compared with the present one. Two studies of isocapnic hypoxia of shorter duration (up to 8 h) in humans failed to find any evidence of adaptation of the CBF over the time course of the exposure (Jensen et al 1992;Clar et al 1997), which is a result in keeping with the present study.…”

Section: Hypoxic Exposure and Comparisons With Previous Studies Of Cbfsupporting

confidence: 88%

Changes in Cerebral Blood Flow During and After 48 H of Both Isocapnic and Poikilocapnic Hypoxia in Humans

Poulin

Fatemian

Tansley

et al. 2002

Experimental Physiology

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Numerous investigations have been carried out over many decades to gain a better understanding of the adaptations that occur during the process of acclimatization to the hypoxia of altitude. These studies have included descriptions of the changes in cerebral blood flow (CBF) during acclimatization, which are of some importance because of the potential role that changes in CBF may have in the aetiology of diseases such as acute mountain sickness and high altitude cerebral oedema.On exposure to the hypoxia of high altitude (altitude, 3810-4300 m; arterial PJ (P a,J ), ~43-45 Torr), there is an initial increase in CBF, which then slowly declines towards pre-hypoxic levels (Severinghaus et al. 1966;Huang et al. 1987). However, understanding the origin of these changes is complicated by the fact that the cerebral circulation is exposed to the competing influences of arterial hypoxia, which tends to cause vasodilatation, and arterial hypocapnia, which tends to cause vasoconstriction. Furthermore, these stimuli are not constant over time, because ventilatory acclimatization to hypoxia progressively increases the degree of hypocapnia and reduces the degree of hypoxia. In a set of experimental studies in sheep, Krasney and colleagues (Krasney et al. 1984(Krasney et al. , 1985(Krasney et al. , 1986) have attempted to separate the effects of hypoxia from those of hypocapnia by studying isocapnic hypoxia (where they added CO 2 to the inspired gas of the animal during hypoxia in order to prevent the arterial hypocapnia that normally results from the increase in pulmonary ventilation). They concluded that the adaptation of CBF back towards pre-hypoxic levels in poikilocapnic hypoxia was not a primary adaptation of the response of CBF to hypoxia, but was due to other factors, including the associated hypocapnia (Krasney et al. 1990).The broad aim of the present study was to undertake an investigation in human volunteers that was related to the work of Krasney and colleagues in sheep. In particular, we wished to study a sustained (48 h) period of constant hypoxia (regulated in the face of changing pulmonary During acclimatization to the hypoxia of altitude, the cerebral circulation is exposed to arterial hypoxia and hypocapnia, two stimuli with opposing influences on cerebral blood flow (CBF). In order to understand the resultant changes in CBF, this study examined the responses of CBF during a period of constant mild hypoxia both with and without concomitant regulation of arterial P CO 2 . Nine subjects were each exposed to two protocols in a purpose-built chamber: (1) 48 h of isocapnic hypoxia (Protocol I), where end-tidal PJ (P ET, J) was held at 60 Torr and end-tidal P CO 2 (P ET,CO 2 ) at the subject's resting value prior to experimentation; and (2) 48 h of poikilocapnic hypoxia (Protocol P), where P ET, J was held at 60 Torr and P ET,CO 2 was uncontrolled. Transcranial Doppler ultrasound was used to assess CBF. At 24 h intervals during and after the hypoxic exposure CBF was measured and the sensitivity of CBF to acute var...

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Ventilatory Effects of 8 Hours of Isocapnic Hypoxia with and Without ß;-Blockade

Clar

Dorrington

Robbins

1998

Advances in Experimental Medicine and Biology

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Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans

Cited by 5 publications

References 21 publications

Effects of 8 h of Isocapnic Hypoxia with and without Muscarinic Blockade on Ventilation and Heart Rate in Humans

Effects of 8 h of Isocapnic Hypoxia with and without Muscarinic Blockade on Ventilation and Heart Rate in Humans

Changes in Cerebral Blood Flow During and After 48 H of Both Isocapnic and Poikilocapnic Hypoxia in Humans

Ventilatory Effects of 8 Hours of Isocapnic Hypoxia with and Without ß;-Blockade

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