Abstract:
:In summary, we can come to a number of meaningful conclusions regarding chronic exposure to hypobaric hypoxia in rats (refer to Figure 1). First, despite an increased hematocrit, and thus increased oxygen carrying capacity, regional cerebral blood flow is elevated after 4 weeks of chronic hypobaric hypoxia. This elevation in blood flow occurs even though the rat hyperventilates to lower than normal arterial CO2 content which would ordinarily decrease cerebral blood flow. Second, although blood flow is increased in both chronic and acute hypoxia, the increases can not be through similar mechanisms since in the acute hypoxic condition there is also an increase in local blood volume that is absent in the chronic response. Third, the effect of chronic hypoxic exposure on cerebral blood flow persists for at least 4 hours after the animal is returned to normobaric normoxia. Fourth, sometime between 4 and 24 hours of recovery is necessary to reverse the effect of chronic hypoxia on cerebral blood flow. One day after having been returned to normobaric normoxia cerebral blood flow had returned to control. On the other hand, hematocrit was still elevated in these rats. Thus, the change in hematocrit does not seem to be associated in any mechanistic manner with the blood flow response.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
LaManna JC,McCracken KA,Strohl KPdoi
10.1007/978-1-4684-5643-1_52subject
Has Abstractpub_date
1989-01-01 00:00:00pages
471-7eissn
0065-2598issn
2214-8019journal_volume
248pub_type
杂志文章abstract::This is the first publication using a fiber optic "optode" and a luminescence based pO2 detection method for assessing neural tissue oxygenation. The system was used to simultaneously monitor pO2 in tissue (PtO2) and venous blood (PvO2) during normoxia, hyperoxia and hypoxia. PaO2 was varied by changing inspired oxyge...
journal_title:Advances in experimental medicine and biology
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