Cerebral Blood Flow Does Not Adapt to Sustained Hypoxia

Krasney, J. A.; Jensen, Johannes Rude; Lassen, Niels A.

doi:10.1038/jcbfm.1990.133

Cited by 26 publications

(23 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lassen and coworkers 3,4 have suggested that in newcomers to higher altitude, the occurrence of high-altitude cerebral edema (HACE), a potentially lethal manifestation of acute mountain sickness (AMS), resulted from a disturbed CA, combined with an elevated pressure in the cerebral microcirculation. Other investigators [5][6][7] have repeatedly supported this hypothesis. On the contrary, it is commonly assumed that Sherpas, who are high-altitude natives of Tibetan ancestry, have an intact autoregulatory response to blood-pressure variations, as a hallmark of a healthy cerebral vasculature.…”

mentioning

confidence: 84%

Cerebral Autoregulation in Subjects Adapted and Not Adapted to High Altitude

Jansen

Krins

Basnyat

et al. 2000

Stroke

View full text Add to dashboard Cite

Background and Purpose-Impaired cerebral autoregulation (CA) from high-altitude hypoxia may cause high-altitude cerebral edema in newcomers to a higher altitude. Furthermore, it is assumed that high-altitude natives have preserved CA. However, cerebral autoregulation has not been studied at altitude. Methods-We studied CA in 10 subjects at sea level and in 9 Sherpas and 10 newcomers at an altitude of 4243 m by evaluating the effect of an increase of mean arterial blood pressure (MABP) with phenylephrine infusion on the blood flow velocity in the middle cerebral artery (Vmca), using transcranial Doppler. Theoretically, no change of Vmca in response to an increase in MABP would imply perfect autoregulation. Complete loss of autoregulation is present if Vmca changes proportionally with changes of MABP. Results-In the sea-level group, at a relative MABP increase of 23Ϯ4% during phenylephrine infusion, relative Vmca did not change essentially from baseline Vmca (2Ϯ7%, Pϭ0.36), which indicated intact autoregulation. In the Sherpa group, at a relative MABP increase of 29Ϯ7%, there was a uniform and significant increase of Vmca of 24Ϯ9% (PϽ0.0001) from baseline Vmca, which indicated loss of autoregulation. The newcomers showed large variations of Vmca in response to a relative MABP increase of 21Ϯ6%. Five subjects showed increases of Vmca of 22% to 35%, and 2 subjects showed decreases of Vmca of 21% and 23%. Conclusions-All Sherpas and the majority of the newcomers showed impaired CA. It indicates that an intact autoregulatory response to changes in blood pressure is probably not a hallmark of the normal human cerebral vasculature at altitude and that impaired CA does not play a major role in the occurrence of cerebral edema in newcomers to the altitude.

show abstract

mentioning

confidence: 84%

Cerebral Autoregulation in Subjects Adapted and Not Adapted to High Altitude

Jansen

Krins

Basnyat

et al. 2000

Stroke

View full text Add to dashboard Cite

show abstract

“…In a review of the above and other studies, Krasney and colleagues (Krasney et al 1990) concluded that CBF does not adapt to sustained hypoxia. Primarily this conclusion was drawn from the absence of any progressive change in CBF during sustained isocapnic hypoxia in sheep.…”

Section: Figurementioning

confidence: 98%

“…The present study supports this conclusion with data derived from human subjects. Krasney et al (1990) concluded that the apparent adaptation observed with chronic poikilocapnic exposure to hypoxia was due to other factors, including the progressive fall in P ET,CO 2 . Our data support this view.…”

Section: Figurementioning

confidence: 99%

“…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). …”

mentioning

confidence: 99%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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...

show abstract

“…The impact of chronic hypoxia on cerebral blood flow (CBF) has been studied in healthy subjects and animals [10]. Only a few studies have been performed on patients with chronic hypoxia caused by lung diseases [11, 12, 13].…”

Section: Introductionmentioning

confidence: 99%

Effect of Long-Term Oxygen Therapy on Cognitive and Neurological Dysfunction in Chronic Obstructive Pulmonary Disease

Hjalmarsen¹,

Waterloo

Dahl

et al. 1999

Eur Neurol

View full text Add to dashboard Cite

The aim of this study was to assess effect of long-term oxygen therapy (LTOT) on the function of central and autonomic nervous system in patients with hypoxaemic chronic obstructive pulmonary disease (COPD). A battery of neuropsychological tests was used together with the Short Test of Mental Status in addition to transcranial Doppler ultrasonography, and five cardiovascular tests as well as a questionnaire on autonomic function. Ten COPD patients, 4 males and 6 females, with a mean age of 65.9 ± 7.3 (SD) years, were studied at the beginning and after 3 months of LTOT. At start PaO₂ was 6.7 ± 1.1 kPa without oxygen and 9.9 ± 1.5 kPa after 3 months with oxygen. Our results demonstrate that neuropsychological function, cerebral blood flow velocity and autonomic function were positively influenced after 3 months of LTOT although the changes did not reach statistical significance. The COPD patients were cognitively impaired as compared to age-matched healthy controls. Our findings were consistent with the previous notion of improvement of hypoxic cognitive dysfunction by LTOT.

show abstract

Cerebral Blood Flow Does Not Adapt to Sustained Hypoxia

Cited by 26 publications

References 17 publications

Cerebral Autoregulation in Subjects Adapted and Not Adapted to High Altitude

Cerebral Autoregulation in Subjects Adapted and Not Adapted to High Altitude

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

Effect of Long-Term Oxygen Therapy on Cognitive and Neurological Dysfunction in Chronic Obstructive Pulmonary Disease

Contact Info

Product

Resources

About