Regulation of cerebral blood flow in the ovine fetus

1978 ◽  
Vol 235 (2) ◽  
pp. H162-H166 ◽  
Author(s):  
M. D. Jones ◽  
R. E. Sheldon ◽  
L. L. Peeters ◽  
E. L. Makowski ◽  
G. Meschia
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Content ◽  
Linear Regression Analysis ◽  
Multiple Linear Regression Analysis ◽  
Arterial Oxygen ◽  
Flow Measurements ◽  
Arterial Oxygen Content ◽  
Sagittal Sinus ◽  
Ovine Fetus

The effects on fetal cerebral blood flow (Qc) of changes in the carotid arterial and sagittal sinus venous PO2, PCO2, and oxygen content were studied in the chronically catheterized ovine fetus in utero at 130–140 days of gestation. Forty-seven measurements of Qc were made in 20 fetuses with radioactive microspheres. In 11 of these animals, 84 measurements of cerebral arteriovenous differences of oxygen content were performed, permitting an indirect measurement of cerebral blood flow (Qc*), assuming a constant cerebral metabolic rate. Arterial and, in 11 animals, sagittal sinus blood was withdrawn for analysis of PO2, PCO2, oxygen content, and pH at the time of the flow measurements. Preliminary analysis showed the best predictor of Qc and Qc* to be the reciprocal of the arterial oxygen content (1/CaO2). Multiple linear regression analysis combining the effects of 1/CaO2 with arterial PCO2 (PaCO2) gave the following equations: Qc = 458.8 (1/CaO2) + 2.68 PaCO2 - 107.93 (R2 = 0.68); Qc* = 435.54 (1CaO2) + 2.20 PaCO2 - 75.03 (R2 = 0.86). As a result of the hyperbolic relationship between Qc (and Qc*) and CaO2, changes in CaO2 at the low levels found during intrauterine life exert an important influence on the fetal cerebral circulation.

Oxygen delivery at high blood viscosity and decreased arterial oxygen content to brains of conscious rats

2001 ◽  
Vol 280 (6) ◽  
pp. H2591-H2597 ◽  
Author(s):  
A. Rebel ◽  
C. Lenz ◽  
H. Krieter ◽  
K. F. Waschke ◽  
K. Van Ackern ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Content ◽  
Blood Viscosity ◽  
Oxygen Delivery ◽  
Brain Structures ◽  
Arterial Oxygen ◽  
Cerebral Oxygen ◽  
Compensatory Mechanisms ◽  
Arterial Oxygen Content

We addressed the question to which extent cerebral blood flow (CBF) is maintained when, in addition to a high blood viscosity (Bvis) arterial oxygen content (CaO2 ) is gradually decreased. CaO2 was decreased by hemodilution to hematocrits (Hct) of 30, 22, 19, and 15% in two groups. One group received blood replacement (BR) only and served as the control. The second group received an additional high viscosity solution of polyvinylpyrrolidone (BR/PVP). Bvis was reduced in the BR group and was doubled in the BR/PVP. Despite different Bvis, CBF did not differ between BR and BR/PVP rats at Hct values of 30 and 22%, indicating a complete vascular compensation of the increased Bvis at decreased CaO2 . At an Hct of 19%, local cerebral blood flow (LCBF) in some brain structures was lower in BR/PVP rats than in BR rats. At the lowest Hct of 15%, LCBF of 15 brain structures and mean CBF were reduced in BR/PVP. The resulting decrease in cerebral oxygen delivery in the BR/PVP group indicates a global loss of vascular compensation. We concluded that vasodilating mechanisms compensated for Bvis increases thereby maintaining constant cerebral oxygen delivery. Compensatory mechanisms were exhausted at a Hct of 19% and lower as indicated by the reduction of CBF and cerebral oxygen delivery.

scholarly journals 1416 VISCOSITY REGULATES CEREBRAL BLOOD FLOW INDEPENDENTLY OF ARTERIAL OXYGEN CONTENT

1985 ◽  
Vol 19 (4) ◽  
pp. 346A-346A
Author(s):  
Mark L Hudak ◽  
Raymond C Koehler ◽  
Adam A Rosenberg ◽  
Richard J Traystman ◽  
M Douglas Jones
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Content ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content

Blood flow to fetal organs as a function of arterial oxygen content

1979 ◽  
Vol 135 (5) ◽  
pp. 637-646 ◽  
Author(s):  
Louis L.H. Peeters ◽  
Roger E. Sheldon ◽  
M. Douglas Jones ◽  
Edgar L. Makowski ◽  
Giacomo Meschia
Keyword(s):  
Blood Flow ◽  
Oxygen Content ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Fetal Organs

scholarly journals Effects of Hematocrit Variations on Cerebral Blood Flow and Oxygen Transport in Ischemic Cerebrovascular Disease

1981 ◽  
Vol 1 (4) ◽  
pp. 413-417 ◽  
Author(s):  
Masahito Kusunoki ◽  
Kazufumi Kimura ◽  
Masaichi Nakamura ◽  
Yoshinari Isaka ◽  
Shotaro Yoneda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Disease ◽  
Oxygen Transport ◽  
Oxygen Delivery ◽  
Inverse Correlation ◽  
Arterial Oxygen ◽  
Brain Oxygenation ◽  
Arterial Oxygen Content ◽  
Ischemic Cerebrovascular Disease

The contribution of hematocrit (Ht) changes on cerebral blood flow (CBF) and brain oxygenation in ischemic cerebrovascular disease is still controversial. In the present study, effects of Ht variations on CBF and oxygen delivery were investigated in patients with ischemic cerebrovascular disease. CBF was measured by the Xe-133 intracarotid injection method in 27 patients, whose diagnoses included completed stroke, reversible ischemic neurological deficit, and transient ischemic attack. Ht values in the patients ranged from 31 to 53%. There was a significant inverse correlation between CBF and Ht in these Ht ranges. Oxygen delivery, i.e., the product of arterial oxygen content and CBF, increased with Ht elevation and reached the maximum level in the Ht range of 40–45% and then declined. The CBF-Ht and oxygen transport-Ht relations observed in our study were similar to those in the glass-tube model studies by other workers rather than to those in intact animal experiments. From these results, it is conceivable that in ischemic cerebrovascular disease, the vasomotor adjustment was impaired in such a manner that the relations among Ht, CBF, and oxygen delivery were different from those in healthy subjects. Further, an “optimal hematocrit” for brain oxygenation was also discussed.

Fetal sheep endocrine responses to sustained hypoxemic stress after chronic fetal placental embolization

1997 ◽  
Vol 272 (5) ◽  
pp. E817-E823 ◽  
Author(s):  
R. Gagnon ◽  
J. Murotsuki ◽  
J. R. Challis ◽  
L. Fraher ◽  
B. S. Richardson
Keyword(s):  
Blood Flow ◽  
Oxygen Content ◽  
Regional Distribution ◽  
Arterial Oxygen ◽  
Control Group ◽  
Fetal Sheep ◽  
Arterial Oxygen Content ◽  
Placental Blood ◽  
Chronic Hypoxemia ◽  
Placental Blood Flow

The purpose of this study was to determine the endocrine and circulatory responses of the ovine fetus, near term, to sustained hypoxemic stress superimposed on chronic hypoxemia. Fetal sheep were chronically embolized (n = 7) for 10 days between 0.84 and 0.91 of gestation via the descending aorta until arterial oxygen content was decreased by approximately 30%. Control animals (n = 8) received saline only. On experimental day 10, both groups were embolized over a 6-h period until fetal arterial pH decreased to approximately 7.00. Regional distribution of lower body blood flows was measured on day 10, before and at the end of acute embolization. On day 10, the chronically embolized group had lower arterial oxygen content (P < 0.05), Po2 (P < 0.01), and placental blood flow (P < 0.05) than controls and higher prostaglandin E2 (PGE2) and norepinephrine plasma concentrations (both P < 0.05). In response to a superimposed sustained hypoxemic stress, there was a twofold greater increase in PGE2 in the chronically embolized group than in the control group (P < 0.05). However, the increase in fetal plasma cortisol in response to superimposed hypoxemic stress was similar in both groups, despite significantly lower adrenocorticotropic hormone and adrenal cortex blood flow responses in the chronically hypoxemic group (both P < 0.05). We conclude that PGE2 response to a sustained superimposed reduction in placental blood flow, leading to metabolic acidosis, is enhanced under conditions of chronic hypoxemia and may play an important role for the maintenance of the fetal cortisol response to an episode of superimposed acute stress.

Heliox increases quadriceps muscle oxygen delivery during exercise in COPD patients with and without dynamic hyperinflation

2012 ◽  
Vol 113 (7) ◽  
pp. 1012-1023 ◽  
Author(s):  
Zafeiris Louvaris ◽  
Spyros Zakynthinos ◽  
Andrea Aliverti ◽  
Helmut Habazettl ◽  
Maroula Vasilopoulou ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Content ◽  
Oxygen Delivery ◽  
Quadriceps Muscle ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Muscle Oxygen ◽  
Peripheral Muscle ◽  
Copd Patients ◽  
Gastric Pressure

Some reports suggest that heliox breathing during exercise may improve peripheral muscle oxygen availability in patients with chronic obstructive pulmonary disease (COPD). Besides COPD patients who dynamically hyperinflate during exercise (hyperinflators), there are patients who do not hyperinflate (non-hyperinflators). As heliox breathing may differently affect cardiac output in hyperinflators (by increasing preload and decreasing afterload of both ventricles) and non-hyperinflators (by increasing venous return) during exercise, it was reasoned that heliox administration would improve peripheral muscle oxygen delivery possibly by different mechanisms in those two COPD categories. Chest wall volume and respiratory muscle activity were determined during constant-load exercise at 75% peak capacity to exhaustion, while breathing room air or normoxic heliox in 17 COPD patients: 9 hyperinflators (forced expiratory volume in 1 s = 39 ± 5% predicted), and 8 non-hyperinflators (forced expiratory volume in 1 s = 48 ± 5% predicted). Quadriceps muscle blood flow was measured by near-infrared spectroscopy using indocyanine green dye. Hyperinflators and non-hyperinflators demonstrated comparable improvements in endurance time during heliox (231 ± 23 and 257 ± 28 s, respectively). At exhaustion in room air, expiratory muscle activity (expressed by peak-expiratory gastric pressure) was lower in hyperinflators than in non-hyperinflators. In hyperinflators, heliox reduced end-expiratory chest wall volume and diaphragmatic activity, and increased arterial oxygen content (by 17.8 ± 2.5 ml/l), whereas, in non-hyperinflators, heliox reduced peak-expiratory gastric pressure and increased systemic vascular conductance (by 11.0 ± 2.8 ml·min−1·mmHg−1). Quadriceps muscle blood flow and oxygen delivery significantly improved during heliox compared with room air by a comparable magnitude (in hyperinflators by 6.1 ± 1.3 ml·min−1·100 g−1 and 1.3 ± 0.3 ml O2·min−1·100 g−1, and in non-hyperinflators by 7.2 ± 1.6 ml·min−1·100 g−1 and 1.6 ± 0.3 ml O2·min−1·100 g−1, respectively). Despite similar increase in locomotor muscle oxygen delivery with heliox in both groups, the mechanisms of such improvements were different: 1) in hyperinflators, heliox increased arterial oxygen content and quadriceps blood flow at similar cardiac output, whereas 2) in non-hyperinflators, heliox improved central hemodynamics and increased systemic vascular conductance and quadriceps blood flow at similar arterial oxygen content.

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

2011 ◽  
Vol 300 (4) ◽  
pp. R931-R940 ◽  
Author(s):  
Roger G. Evans ◽  
Duncan Goddard ◽  
Gabriela A. Eppel ◽  
Paul M. O'Connor
Keyword(s):  
Blood Flow ◽  
Oxygen Content ◽  
Biceps Femoris ◽  
Oxygen Availability ◽  
Tissue Hypoxia ◽  
Arterial Oxygen ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Arterial Oxygen Content ◽  
Limited Oxygen

To better understand what makes the kidney susceptible to tissue hypoxia, we compared, in the rabbit kidney and hindlimb, the ability of feedback mechanisms governing oxygen consumption (V̇o2) and oxygen delivery (Do2) to attenuate tissue hypoxia during hypoxemia. In the kidney (cortex and medulla) and hindlimb (biceps femoris muscle), we determined responses of whole organ blood flow and V̇o2, and local perfusion and tissue Po2, to reductions in Do2 mediated by graded systemic hypoxemia. Progressive hypoxemia reduced tissue Po2 similarly in the renal cortex, renal medulla, and biceps femoris. Falls in tissue Po2 could be detected when arterial oxygen content was reduced by as little as 4–8%. V̇o2 remained stable during progressive hypoxemia, only tending to fall once arterial oxygen content was reduced by 55% for the kidney or 42% for the hindlimb. Even then, the fall in renal V̇o2 could be accounted for by reduced oxygen demand for sodium transport rather than limited oxygen availability. Hindlimb blood flow and local biceps femoris perfusion increased progressively during graded hypoxia. In contrast, neither total renal blood flow nor cortical or medullary perfusion was altered by hypoxemia. Our data suggest that the absence in the kidney of hyperemic responses to hypoxia, and the insensitivity of renal V̇o2 to limited oxygen availability, contribute to kidney hypoxia during hypoxemia. The susceptibility of the kidney to tissue hypoxia, even in relatively mild hypoxemia, may have important implications for the progression of kidney disease, particularly in patients at high altitude or with chronic obstructive pulmonary disease.

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