Cerebral blood flow is increased throughout 12 h of hypoxaemia in the mid-gestation ovine fetus

1995 ◽  
Vol 7 (3) ◽  
pp. 463 ◽  
Author(s):  
GJ McCrabb ◽  
R Harding
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Oxygen Delivery ◽  
Regional Cerebral Blood Flow ◽  
Cerebral Oxygen ◽  
Uterine Blood Flow ◽  
Regional Cerebral Blood ◽  
Ovine Fetus ◽  
Cerebral Vascular Resistance

The changes in regional cerebral blood flow (CBF) in response to prolonged hypoxaemia were measured using coloured microspheres in the 0.6-gestation ovine fetus (n = 5). Fetal hypoxaemia was induced for 12 h by reducing maternal uterine blood flow with an adjustable clamp. CBF (mL min-1 100 g-1) was increased (P < 0.05) from control values (38.7 +/- 3.5) to 105.6 +/- 5.6 at 6 h of hypoxaemia, and to 121.9 +/- 23.1 at 12 h of hypoxaemia. One hour after fetal hypoxaemia had ceased, CBF (54.0 +/- 3.3) had decreased (P < 0.05) towards control values indicating incomplete cardiovascular recovery. Cerebral vascular resistance at 6 h and 12 h of hypoxaemia was lower (P < 0.05) than control values, and returned to control values 1 h after fetal hypoxaemia had ceased. Cerebral oxygen delivery at 6 h and 12 h of hypoxaemia was not significantly different from control values, but was higher (P < 0.05) 1 h after hypoxaemia had ceased. It is concluded that CBF is sufficiently increased during prolonged hypoxaemia in the mid-gestation fetus to maintain cerebral oxygen delivery.

scholarly journals Interrelationships Among Regional Cerebral Blood Flow, Mean Transit Time, Vascular Volume and Cerebral Vascular Resistance

Stroke ◽  
1974 ◽  
Vol 5 (6) ◽  
pp. 719-724 ◽  
Author(s):  
YOSHIHIRO KURIYAMA ◽  
TAKASHI AOYAMA ◽  
KUNIHIKO TADA ◽  
SHOTARO YONEDA ◽  
TADAATSU NUKADA ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Transit Time ◽  
Regional Cerebral Blood Flow ◽  
Mean Transit Time ◽  
Regional Cerebral Blood ◽  
Vascular Volume ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Effect of Acetazolamide on Regional Cerebral Oxygen Saturation and Regional Cerebral Blood Flow

Stroke ◽  
1995 ◽  
Vol 26 (12) ◽  
pp. 2358-2360 ◽  
Author(s):  
Makio Kaminogo ◽  
Akio Ichikura ◽  
Shobu Shibata ◽  
Tamotsu Toba ◽  
Masahiro Yonekura
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Saturation ◽  
Regional Cerebral Blood Flow ◽  
Cerebral Oxygen Saturation ◽  
Cerebral Oxygen ◽  
Regional Cerebral Oxygen Saturation ◽  
Regional Cerebral Blood

scholarly journals Opioids and the Prostanoid System in the Control of Cerebral Blood Flow in Hypotensive Piglets

1991 ◽  
Vol 11 (3) ◽  
pp. 380-387 ◽  
Author(s):  
William M. Armstead ◽  
Robert Mirro ◽  
David W. Busija ◽  
Charles W. Leffler
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Brain Regions ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Consumption ◽  
Cerebral Vascular Resistance ◽  
Indomethacin Treatment ◽  
Cerebral Vascular

The interaction between opioid and prostanoid mechanisms in the control of cerebral hemodynamics was investigated in the conscious hypotensive piglet. Radiomicrospheres were used to determine regional cerebral blood flow (rCBF) in piglets pretreated with the opioid receptor antagonist, naloxone, or its vehicle, saline, during normotension, hypotension, and after the administration of indomethacin, a cyclooxygenase inhibitor, during hypotension. Hemorrhage (30 ml/kg) decreased systemic arterial pressure from 68 ± 12 to 40 ± 10 mm Hg but did not decrease blood flow to any brain region. Indomethacin treatment (5 mg/kg) of hypotensive piglets decreased blood flow to all brain regions within 20 min; this decrease in CBF resulted from increases in cerebral vascular resistance of 65 and 281% at 20 and 40 min after treatment, respectively. In hypotensive piglets, cerebral oxygen consumption was reduced from 2.62 ± 0.71 to 0.53 ± 0.27 ml 100g−1 min−1 and to 0.11 ± 0.04 ml 100 g−1 min−1 at 20 and 40 min following indomethacin, respectively. Treatment with naloxone (1 mg/kg) had no effect on rCBF, calculated cerebral vascular resistance, or cerebral oxygen consumption of normotensive or hypotensive piglets. However, decreases in CBF and oxygen consumption and increases in cerebral vascular resistance upon treatment of hypotensive piglets with indomethacin were attenuated in animals pretreated with naloxone. These data indicate that the removal of prostanoid modulation of an opioid-mediated constrictor influence on the cerebral circulation is a potential mechanism for the increase in cerebral vascular resistance that follows indomethacin treatment of hypotensive piglets.

scholarly journals A hemodynamic model to predict regional cerebral blood flow and blood flow reserve in patients with carotid stenosis

2020 ◽  
Author(s):  
joseph p archie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Carotid Stenosis ◽  
Vascular Resistance ◽  
Regional Cerebral Blood Flow ◽  
Patient Specific ◽  
Regional Cerebral Blood ◽  
Flow Curves ◽  
Flow Reserve

Joseph P Archie Jr, PhD, MD Abstract Purpose. Patients with 50% or greater diameter stenosis are at risk for ischemic stroke due to embolization and/or reduced cerebral blood flow. The hemodynamics of progressive carotid stenosis on cerebral blood flow and blood flow reserve has not been adequately measured or predicted. This information is needed for stroke risk stratification in patients with carotid stenosis. The aim of this hemodynamic model study is to predict the contribution of carotid and collateral blood flows to regional cerebral blood flow and cerebral blood flow reserve in patients with moderate to severe carotid stenosis. Methods. A one-dimensional three-parameter fluid mechanics model for the carotid, collateral and brain vascular systems is used to predict regional cerebral blood flow and blood flow reserve as a function of percent diameter carotid stenosis. The model is based on the principal of conservation of energy as employed by Bernoulli to describe fluid flow on a streamline. When applied to the human cerebrovascular system there are three vascular resistance components; carotid, collateral and brain. Carotid artery vascular resistance is assumed to be a function of fractional percent carotid artery area stenosis. This is not a complex modern computational fluid mechanics study. The model blood flow algebraic equations have simple solutions, one of which gives patient specific collateral resistance values. The solutions are given as patient specific cerebral blood flows and flow reserve as a function of percent diameter stenosis. Established normal clinical values of regional cerebral blood flow, cerebral blood flow auto-regulation and the lower threshold of cerebral perfusion pressure for cerebral auto-regulation are used. Carotid vascular resistance is assumed to be proportional to percent area carotid stenosis. Theoretical solutions use mean systemic arterial pressure of 100mmHg and key clinical values of patient collateral vascular resistance. Clinical solutions use patient measured systemic arterial pressures and carotid stump pressures. The solutions are given as patient specific cerebral blood flow and reserve cerebral blood flow curves over the range of diameter carotid stenosis. Results. Normal regional cerebral blood flow of 50ml/min/100g is predicted to be maintained up to 65% diameter carotid stenosis as reserve blood flow is reduced. With further progression of carotid stenosis to occlusion approximately half of patients are predicted to develop some reduction in cerebral blood flow. However, only about 20% of patients have a decrease in cerebral blood flow below the 30ml/min/100g threshold for cerebral ischemic symptoms. Approximately 10% of patients are predicted to develop regional cerebral blood flow less than the 18ml/min/100g threshold for irreversible ischemic injury. The model predicts critical carotid artery stenosis to be between 65% and 71% diameter depending on mean systemic arterial pressure. With higher degrees of stenosis carotid artery blood flow cannot maintain normal cerebral flow without the contribution of collateral flow. The predicted magnitude of carotid energy dissipation between 60% and 90% stenosis is consistent with observed cervical bruit intensity. Predicted patient specific cerebral blood flow reserve is adequate to prevent significant cerebral ischemia in the majority of patients. Conclusions. Patient specific collateral vascular resistance blood flow curves predict regional cerebral blood flow and blood flow reserve as a function of the degree of diameter carotid artery stenosis. The carotid component of cerebral blood flow is predicted to maintain normal cerebral blood flow up to a critical carotid diameter stenosis of 65% to 71%. Collateral blood flow is necessary to maintain normal cerebral flow at higher degrees of carotid stenosis. The clinical model predicts that many patients do not have sufficient collateral flow to prevent a decrease in cerebral flow should carotid stenosis progress to high grade or occlusion. However, only about 10% of patients are predicted to develop irreversible regional cerebral ischemic injury. Estimated carotid stenosis energy dissipation magnitudes agree with observed cervical bruit intensity. Correlation of predicted cerebral reserve blood flow curves with clinically measured cerebrovascular reactivity/reserve has the potential to predict the probability of future cerebral ischemia in asymptomatic patients with 60% to 80% stenosis.

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