Chronic hypoxia and the cerebral circulation

2006 ◽  
Vol 100 (2) ◽  
pp. 725-730 ◽  
Author(s):  
Kui Xu ◽  
Joseph C. LaManna

Exposure to mild hypoxia elicits a characteristic cerebrovascular response in mammals, including humans. Initially, cerebral blood flow (CBF) increases as much as twofold. The blood flow increase is blunted somewhat by a decreasing arterial Pco2 as a result of the hypoxia-induced hyperventilatory response. After a few days, CBF begins to fall back toward baseline levels as the blood oxygen-carrying capacity is increasing due to increasing hemoglobin concentration and packed red cell volume as a result of erythropoietin upregulation. By the end of 2 wk of hypoxic exposure, brain capillary density has increased with resultant decreased intercapillary distances. The relative time courses of these changes suggest that they are adjusted by different control signals and mechanisms. The CBF response appears linked to the blood oxygen-carrying capacity, whereas the hypoxia-induced brain angiogenesis appears to be in response to tissue hypoxia.

1977 ◽  
Vol 43 (5) ◽  
pp. 784-789 ◽  
Author(s):  
J. F. Borgia ◽  
S. M. Horvath

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.


2000 ◽  
Vol 20 (12) ◽  
pp. 1632-1635 ◽  
Author(s):  
Jeff F. Dunn ◽  
Oleg Grinberg ◽  
Marcie Roche ◽  
Casmiar I. Nwaigwe ◽  
Huagang G. Hou ◽  
...  

Factors regulating cerebral tissue Po2 (PtO2) are complex. With the increased use of clinical PtO2 monitors, it has become important to elucidate these mechanisms. The authors are investigating a new methodology (electron paramagnetic resonance oximetry) for use in monitoring cerebral PtO2 in awake animals over time courses of weeks. The authors used this to study cerebral PtO2 in rats during chronic acclimation to hypoxia predicting that such acclimation would cause an increase in PtO2 because of increases that occur in capillary density and oxygen carrying capacity. The average PtO2 between 7 and 21 days was increased by 228% over controls.


1990 ◽  
Vol 258 (5) ◽  
pp. F1432-F1437 ◽  
Author(s):  
K. U. Eckardt ◽  
J. Dittmer ◽  
R. Neumann ◽  
C. Bauer ◽  
A. Kurtz

Serum erythropoietin (EPO) levels in response to hypoxia are known to decline before an increase in blood oxygen carrying capacity. To define the possible mechanisms underlying this phenomenon, we have investigated 1) how renal EPO mRNA content and EPO production rate underlying the early kinetics of serum EPO levels change under different degrees of normobaric hypoxia, and 2) if a feedback inhibition of either EPO formation or EPO survival in the circulation exists by the hormone itself. We found that serum immunoreactive EPO levels in rats peaked after 12-h exposure to 7.5 or 9% oxygen (2,949 +/- 600 and 756 +/- 108 mU/ml, respectively, mean +/- SE) and declined to 29 and 64% of peak levels, respectively, after 36 h of hypoxia. EPO levels in response to 11.5% oxygen showed no consistent change between 12 (122 +/- 21 mU/ml, mean +/- SE) and 36 h (182 +/- 35 mU/ml) of hypoxia. The decline in EPO levels under severe hypoxia (7.5% O2) was paralleled by a marked reduction in renal EPO mRNA content, indicating that it was primarily a result of diminished hormone production. The observed reductions in serum EPO after 36 h corresponded to preceding declines of calculated EPO production rates from 163- to 62-fold (7.5% O2) and 36- to 25-fold (9% O2) basal values. Application of 50 IU recombinant human EPO to rats 12 h, 6 h, or immediately before hypoxic exposure to mimic the early increase in EPO levels did not affect endogenous EPO formation during a subsequent hypoxic exposure of 12 h.(ABSTRACT TRUNCATED AT 250 WORDS)


1964 ◽  
Vol 206 (4) ◽  
pp. 858-866 ◽  
Author(s):  
Wendell N. Stainsby ◽  
Arthur B. Otis

The effect of changes in blood flow and of blood oxygen tension on oxygen uptake of the in situ gastrocnemius-plantaris muscle group of the dog was examined. Oxygen uptake by resting muscle was not altered by changes in blood flow or blood oxygen tension except when these parameters were reduced below critical values. When the muscle group was contracting once per second, changes in blood oxygen tension were similarly without effect until a critically low value was reached. Although the contracting muscle used eight times as much oxygen per minute as resting muscle, the critical oxygen tension was lower than that for resting muscle. In an attempt to explain this observation the blood-tissue oxygen tension difference was estimated and used in the Krogh equation to calculate capillary density. The capillary density in contracting muscle was found to be much greater than in resting muscle and was about the same as the capillary density measured by others by histological techniques.


2000 ◽  
Vol 48 (4) ◽  
pp. 347 ◽  
Author(s):  
Cristina Davey ◽  
Alan Lill ◽  
John Baldwin

Parameters that influence blood oxygen carrying capacity (whole-blood haemoglobin content, haematocrit and red blood cell count) were measured in samples of 30 breeding, adult short-tailed shearwaters (Puffinus tenuirostris) on Phillip Island, Victoria at seven key stages of their reproductive cycle. The aim of the investigation was to determine whether variation in blood oxygen carrying capacity during the birds’ 7-month breeding cycle was correlated with variation in the energy demands they experienced or was an incidental by-product of other physiological changes. All the blood parameters varied significantly during breeding, but the pattern of variation was only partly correlated with the likely pattern of changing energy demand imposed on parents by their schedule of breeding activities. The main trend conceivably related to energy demand was that significantly higher values were recorded for these blood parameters during the nestling stage than earlier in the breeding cycle. This could have reflected the high costs of the very long foraging trips undertaken by parents feeding nestlings, but it could also have occurred in preparation for the long migration undertaken soon after breeding finished. It involved an ~10% increase in blood oxygen carrying capacity above the lowest mean value recorded during the breeding cycle and so other mechanisms must also be employed to achieve the increase in aerobic metabolism likely to be required at this stage. The lack of adjustment of blood oxygen carrying capacity to energy demand early in the breeding cycle suggests that either oxygen delivery was not a rate-limiting process for aerobic metabolism at that time or that delivery was enhanced through other mechanisms. At egg laying, females had a lower haematocrit and erythrocyte count than males, which could be attributable to either estrogenic suppression of erythropoiesis or an increase in osmotic pressure of the blood associated with yolk synthesis. Immature, non-breeding birds attending the colony were of similar mass to adults, but did not show the increase in the parameters determining blood oxygen carrying capacity that occurred in adults later in the breeding cycle. Factors other than changing energy requirements (dehydration, burrow hypoxia and differential responsiveness to capture stress) that might have influenced the pattern of variation in blood oxygen carrying capacity of adults during breeding are discussed.


1967 ◽  
Vol 24 (11) ◽  
pp. 2267-2281 ◽  
Author(s):  
Mary Anne DeWilde ◽  
A. H. Houston

The blood oxygen capacity of the rainbow trout has been investigated as a function of thermal acclimation in terms of erythrocyte abundance, packed cell volume, hemoglobin concentrations, and mean erythrocytic volume and hemoglobin content. Fish at the lower acclimation temperatures employed (3, 7 C) were characterized by relatively low erythrocyte counts, hematocrits, and hemoglobin levels. Mean erythrocyte volumes tended to be relatively high, whereas mean erythrocytic hemoglobin content was somewhat below that typical of the higher temperature groups. In general, animals held at intermediate temperatures (11, 14, 17 C) showed significant increases in oxygen-carrying capacity by comparison with cold-acclimated fish. Finally trout at 21 C typically had larger numbers of somewhat smaller red cells, more hemoglobin, and higher levels of hemoglobin per erythrocyte than either the low- or intermediate-temperature fish. Significant differences were observed between summer and fall–winter series of trout, particularly with respect to hemoglobin levels. The results are discussed in relation to the general problem of respiratory thermoadaptation.


1988 ◽  
Vol 33 (4) ◽  
pp. 298-299 ◽  
Author(s):  
A.R. Turner ◽  
G.D.O. Lowe ◽  
C.D. Forbes ◽  
J. G. Pollock

Patients with intermittent claudication frequently have high-normal levels of haematocrit and hence blood viscosity, which may contribute to decreased calf blood flow on exercise, and hence to the symptom of claudication. Reduction in haematocrit and viscosity by serial venesection in eight patients with stable claudication and high-normal haematocrit (mean 0.50) was performed, and the effects on claudication, calf blood flow, and calf oxygen delivery were studied. Following reduction in haematocrit to low-normal levels (mean 0.44), resting calf blood flow was unchanged; peak flow after ischaemic exercise increased slightly (+17%), but peak oxygen delivery (peak flow × haemoglobin concentration) was unchanged. Hence any increase in calf blood flow in the symptomatic leg is balanced by a decrease in oxygen-carrying capacity after venesection. No increase in claudication time would therefore be expected, and none was observed in the present study.


1992 ◽  
Vol 13 (10) ◽  
pp. 379-380
Author(s):  
William B. Strong

What is the likely pathophysiology of this event? What are the more common complications of hypoxemia in the older infant and young child? This clinical scenario is uncommon, but it represents one of the two feared central nervous system complications of cyanotic congenital heart disease, (ie, cerebrovascular accident and brain abscess). A uniform response to hypoxemia of cardiac etiology is the production of erythropoietin to produce more red blood cells. This is a compensatory mechanism to maintain oxygen delivery to the peripheral tissues. Normally, hemoglobin is about 96% saturated with oxygen. Therefore, the oxygen-carrying capacity of blood with a normal hemoglobin concentration of 15 g/dL is approximately 20.3 mL of oxygen per 100 mL of blood (ie, 15 g of hemoglobin x 1.35 mL of O2 per g of hemoglobin = 20.3). The oxygen content of blood equals the oxygen-carrying capacity multiplied by the oxygen saturation. At a normal oxygen saturation of 96%, the O2 content of arterial blood (Hgb 15 g/dL) equals 19.5 mL/dL (96% x 20.3 mm3/dL) or 195 mL per liter of cardiac output. The arterial O2 content of this child, assuming an average arterial saturation of 85%, will be 11.1 mL/dL. Therefore, every liter (10 dL) of cardiac output will carry 111 mL of O2 or 84 mL of O2 less than the child with a 15 g/dL hemoglobin level.


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