Ventral medullary extracellular fluid pH and blood flow during hypoxia

1982 ◽  
Vol 242 (3) ◽  
pp. R195-R198 ◽  
Author(s):  
W. F. Nolan ◽  
P. C. Houck ◽  
J. L. Thomas ◽  
D. G. Davies

Vascular responses of the ventral medulla and total brain to 30-60 min of isocapnic hypoxia (PaO2 = 32 +/- 2 Torr) were examined using radioactive microspheres in anesthetized, paralyzed, and artificially ventilated cats. Ventral medullary extracellular fluid (ECF) pH was measured using pH microelectrodes with tip diameters of 1-2 micrometers. Total brain blood flow (Q) increased significantly from a control value of 53 +/- 8 (mean +/- SE) to 160 +/- 42 ml.100 g-1.min-1 following 30-60 min of hypoxia. Ventral medullary Q increased from 28 +/- 5 to 97 +/- 20 ml.100 g-1.min-1 and ECF pH decreased by 0.15 +/- 0.06 pH U. Q responses are attributable to decreased vascular resistance as arterial pressure remained constant. The sensitivity of the ventral medullary vasculature to isocapnic hypoxia did not differ from that of the brain as a whole. The results show that under the conditions of our experiment, the ventral medullary vascular response to hypoxia is not sufficient to stabilize local ECF pH. The observation of simultaneously reduced pH and increased Q is consistent with a role for ECF H+ in mediating the cerebrovascular response to hypoxia.

1983 ◽  
Vol 244 (1) ◽  
pp. H142-H149 ◽  
Author(s):  
J. A. Orr ◽  
L. C. Wagerle ◽  
A. L. Kiorpes ◽  
H. W. Shirer ◽  
B. S. Friesen

This study determined whether blood flow through the internal carotid artery (ICA) could be used to sample total cerebral blood flow in the pony. To answer this question we considered both the anatomic arrangement of the ICA in cadavers and the relative distribution of ICA blood flow to cerebral and extracerebral tissue using radioactive microspheres. Acrylic corrosion casts of the ICA indicated that this vessel traveled directly to the base of the brain, contributing to the formation of the circle of Willis, and did not send any significant branches to other tissues. Two vessels (internal ethmoidal artery and internal ophthalamic artery) did arise anteriorly from the circle of Willis and were, therefore, indirectly supplied by the ICA. Injection of radioactive microspheres of 15 microns diameter indicated that blood flow to extracerebral structures supplied by the internal ethmoidal and internal ophthalamic arteries was less than 5% of total ICA blood flow. Increases in ICA blood flow as measured with an electromagnetic flowmeter during isocapnic hypoxia (arterial PO2 near 40 Torr) in the awake pony (n = 6) were compared with increases in total brain flow as measured with radioactive microspheres (n = 6). ICA blood flow increased 40% compared with a 38% increase in total brain blood flow as measured with microspheres. We conclude that the ICA supplies predominantly brain tissue (approximately 95%) and that changes in ICA blood flow are representative of changes in total brain blood flow in the awake pony.


1982 ◽  
Vol 53 (1) ◽  
pp. 247-252 ◽  
Author(s):  
W. P. Nolan ◽  
D. G. Davies

Cerebrovascular responses to 30 min of isocapnic hypoxia [arterial O2 partial pressure (PaO2) = 33 +/- 1 Torr; means +/- SE] were examined in eight chloralose-urethan-anesthetized, paralyzed, and artificially ventilated New Zealand White rabbits. Cerebral blood flow (Q) was measured using the radioactive microsphere technique. Vascular resistance (R) was calculated from arterial pressure and Q. Brain extracellular fluid (ECF) pH was measured continuously in the same animals using pH microelectrodes (1- to 2-micrometers tip diameter) placed stereotaxically in the diencephalon. Diencephalon Q increased from 40 +/- 2 to 69 +/- 4 ml . 100 g-1 . min-1 (P less than 0.05) as R decreased (P less than 0.05) after 413;6 min of isocapnic hypoxia. Total brain Q and R changes resembled those of the diencephalon. The ECF pH of the diencephalon increased by 0.016 +/- 0.006 (P less than 0.05) after 1 min of isocapnic hypoxia and remained significantly elevated through the first 20 min of hypoxia. Ten minutes after the return of normoxia Q and R were at control levels, whereas diencephalon ECF pH was 0.043 +/- 0.006 below control (P less than 0.05). Five additional rabbits were prepared as described above then made hypocapnic [arterial CO2 partial pressure (PaCO2) = 21 +/- 0.3 Torr] for 18 min. Diencephalon and total brain Q and R remained at control levels through 12–14 min of hyperventilation, whereas diencephalon ECF pH was elevated by 0.03 +/- 0.006 (P less than 0.05). Hyperventilation was then continued with hypoxic gas to lower PaO2 to 35 +/- 4 Torr for 30 min. Both diencephalon and total brain R decreased (P less than 0.05), with no change in Q after 4–6 min of hypocapnic hypoxia. Diencephalon ECF pH was not significantly different from control throughout the hypocapnic-hypoxic period. We conclude that the early cerebral vasodilation during hypoxia is not mediated by increased brain ECF acidity.


1989 ◽  
Vol 257 (6) ◽  
pp. H1917-H1926 ◽  
Author(s):  
C. W. Leffler ◽  
D. W. Busija ◽  
R. Mirro ◽  
W. M. Armstead ◽  
D. G. Beasley

Brain circulation after 20 min of total brain ischemia was examined in unanesthetized newborn pigs. Except in the cerebrum, reactive hyperemia was observed throughout the brain, peaking by 5 min and subsiding by 20 min of reperfusion. Brain blood flow after 15 min of reperfusion matched the control. Blood flow to the cerebrum then decreased at 40 and 90 min reperfusion, while the rest of the brain was unaffected. Blood flow to the cerebrum returned to control by 24 h. Cerebral vascular resistance doubled by 15 min reperfusion, remained elevated at 90 min reperfusion, but returned to control by 24 h. Cerebral oxygen consumption followed a pattern similar to blood flow. Ninety minutes postischemia, hypercapnia-induced hyperemia was greatly attenuated in the cerebrum, reduced modestly in the diencephalon-mesencephalon, but unaffected in the rest of the brain. Thus 20 min of global brain ischemia in piglets does not produce reactive hyperemia in the cerebrum that is detectable at 5 min reperfusion but does in the remainder of the brain. Subsequent hemodynamic abnormalities apparently are confined to the cerebrum. Blood flow throughout the brain returns to normal by 24 h. Thus cerebral hemodynamic effects of total global ischemia are regionally dependent.


1989 ◽  
Vol 257 (1) ◽  
pp. H157-H161 ◽  
Author(s):  
F. M. Faraci ◽  
K. A. Kadel ◽  
D. D. Heistad

The goal of this study was to examine vascular responses of the dura mater. Microspheres were used to measure blood flow to the dura and brain in anesthetized dogs. Under control conditions, blood flow to the dura was 38 +/- 3 (SE) ml.min-1.100 g-1. Values for blood flow to the dura obtained with simultaneous injection of 15- and 50-microns microspheres were similar, which suggests that shunting of 15-microns spheres was minimal. Left atrial infusion of substance P (100 ng.kg-1.min-1) and serotonin (40 micrograms.kg-1.min-1), two agonists that have been reported to increase vascular permeability in the dura, increased blood flow to the dura two- to threefold. Adenosine (iv) produced vasodilatation in the dura. Adenosine and serotonin did not affect cerebral blood flow, but substance P increased blood flow to the brain by approximately 40%. Seizures, which produce pronounced dilatation of cerebral vessels despite activation of sympathetic nerves, produced vasoconstriction in the dura. Thus 1) the dura is perfused at a relatively high level of blood flow under normal conditions and is very responsive to vasoactive stimuli, and 2) substance P and serotonin, which have been implicated in the pathogenesis of vascular headache, produce pronounced vasodilator responses in the dura mater.


1994 ◽  
Vol 267 (2) ◽  
pp. R590-R595 ◽  
Author(s):  
G. E. Nilsson ◽  
P. Hylland ◽  
C. O. Lofman

The crucian carp (Carassius carassius) has the rare ability to survive prolonged anoxia, indicating an extraordinary capacity for glycolytic ATP production, especially in a highly energy-consuming organ like the brain. For the brain to be able to increase its glycolytic flux during anoxia and profit from the large liver glycogen store, an increased glucose delivery from the blood would be expected. Nevertheless, the effect of anoxia on brain blood flow in crucian carp has never been studied previously. We have used epireflection microscopy to directly observe and measure blood flow rate on the brain surface (optic lobes) during normoxia and anoxia in crucian carp. We have also examined the possibility that adenosine participates in the regulation of brain blood flow rate in crucian carp. The results showed a 2.16-fold increase in brain blood flow rate during anoxia. A similar increase was seen after topical application of adenosine during normoxia, while adenosine was without effect during anoxia. Moreover, superfusing the brain with the adenosine receptor blocker aminophylline inhibited the effect of anoxia on brain blood flow rate, clearly suggesting a mediatory role of adenosine in the anoxia-induced increase in brain blood flow rate.


2021 ◽  
Author(s):  
Kristina E. Almby ◽  
Martin H. Lundqvist ◽  
Niclas Abrahamsson ◽  
Sofia Kvernby ◽  
Markus Fahlström ◽  
...  

While Roux-en-Y Gastric Bypass (RYGB) surgery in obese individuals typically improves glycemic control and prevents diabetes, it also frequently causes hypoglycemia. Previous work showed attenuated counter-regulatory responses following RYGB. The underlying mechanisms as well as the clinical consequences are unclear. <p>In this study, 11 non-diabetic subjects with severe obesity were investigated pre- and post-RYGB during hyperinsulinemic hypoglycemic clamps. Assessments were made of hormones, cognitive function, cerebral blood flow by arterial spin labeling, brain glucose metabolism by FDG PET and activation of brain networks by functional MRI. Post- vs pre-surgery, we found a general increase of cerebral blood flow but a decrease of total brain FDG uptake during normoglycemia. During hypoglycemia, there was a marked increase in total brain FDG uptake and this was similar for post- and pre-surgery, whereas hypothalamic FDG uptake was reduced. During hypoglycemia, attenuated responses of counterregulatory hormones and improvements in cognitive function were seen post-surgery. In early hypoglycemia, there was increased activation post- vs pre-surgery of neural networks in CNS regions implicated in glucose regulation such as the thalamus and hypothalamus. The results suggest adaptive responses of the brain that contribute to lowering of glycemia following RYGB, and the underlying mechanisms should be further elucidated.</p>


1987 ◽  
Vol 96 (4) ◽  
pp. 341-348 ◽  
Author(s):  
Daniel Zaluzec ◽  
Joseph Ramzy ◽  
Robert Wotring ◽  
Lincoln Gray

Chickens were injected with 9-micron-diameter radioactive microspheres. Cochleas were removed through the external auditory meatus, and the positions of all embedded microspheres were drawn under camera-lucida. Constant measurements of arterial pressures and postinjection blood-gas determinations confirmed that injections were made into normal circulatory systems. The averaged estimate of cochlear blood flow in chickens is 0.75 μl/min. Variability in these data from chickens is similar to that reported from mammals. A potentially important but puzzling observation is an inverse relationship between blood flow to the cochlea and to the brain. The ease of cochlear extraction makes chickens ideal models for study of cochlear blood flow.


1989 ◽  
Vol 66 (6) ◽  
pp. 2827-2832 ◽  
Author(s):  
J. M. Goplerud ◽  
L. C. Wagerle ◽  
M. Delivoria-Papadopoulos

The hemodynamic response during and after acute asphyxia was studied in 14 newborn piglets. An apnea-like asphyxial insult was produced in paralyzed mechanically ventilated piglets by discontinuing ventilation until the piglets became bradycardic (heart rate less than 80 beats/min). Seven piglets had organ blood flow measured by microspheres at control, during asphyxia (PO2 = 16 +/- 11 Torr, pH = 7.31 +/- 0.07, PCO2 = 47 +/- 9 Torr), and during recovery from asphyxia. During acute asphyxia, rapid organ blood flow redistribution occurred, producing decreased renal and skeletal muscle blood flow, while coronary blood flow increased. Although total brain blood flow changed little during asphyxia, regional cerebral blood flow (rCBF) analysis revealed significant nonhomogeneous blood flow distribution within the brain during asphyxia, with decreases to the cerebral gray and white matter and the choroid plexus, whereas brain stem structures had increased flow. During recovery with reventilation, total brain blood flow increased 24% above control, with a more uniform distribution and increased flow to all brain regions. The time course of rCBF changes during acute asphyxia was then determined in seven additional piglets with CBF measurements made sequentially at 30–60 s, 60–120 s, and 120–180 s of asphyxia. The vasoconstriction seen in cortical structures, concurrent with the reduction in skeletal and kidney blood flow, known to be sympathetically mediated, suggest a selective reflex effect in this brain region. The more gradual and progressive vasodilation in brain stem regions during asphyxia is consistent with chemical control. These findings demonstrate significant regional heterogeneity in CBF regulation in newborn piglets.


1984 ◽  
Vol 57 (6) ◽  
pp. 1803-1808 ◽  
Author(s):  
J. A. Neubauer ◽  
N. H. Edelman

In seven unanesthetized cats, radiolabeled microspheres were used to determine regional brain blood flow (rBBF) to the medulla-pons (M-P), midbrain-thalamus (M-T), cerebellum (Cb), and cortex (Cx) during three conditions: 1) control [arterial O2 tension (PaO2) = 81 Torr, arterial CO2 tension (PaCO2) = 26 Torr]; 2) hypocapnic hypoxia (PaO2 = 39 Torr, PaCO2 = 22 Torr); and 3) isocapnic hypoxia (PaO2 = 47 Torr, PaCO2 = 26 Torr). Hypoxia increased blood flow significantly more in the caudal brain stem (M-P) than in the Cx (P less than 0.05) during both hypocapnic hypoxia (M-P/Cx: +33/ +17 ml X min-1 X 100 g-1) and isocapnic hypoxia (M-P/Cx: +13/ -2 ml X min-1 X 100 g-1). Since sympathetic innervation is greater anatomically to rostral than to caudal vessels, we examined the rBBF response to hypocapnic hypoxia in seven additional cats after unilateral superior cervical gangliectomy. All seven cats had a reduction in the cortical-to-caudal brain stem trend on the denervated side of the brain (M-P/Cx: +27/+28 ml X min-1 X 100 g-1) compared with the intact side of the brain (M-P/Cx: +34/+24 ml X min-1 X 100 g-1) owing to both increases in Cx and decreases in M-P flows. We conclude that in unanesthetized cats hypoxia causes a greater increase in the caudal brain stem compared with cortical blood flow, and this differential response is related to modulation by the sympathetic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 61 (1) ◽  
pp. 87-90 ◽  
Author(s):  
D. G. Davies ◽  
W. F. Nolan ◽  
J. A. Sexton

Ventral medullary blood flow was measured in 33 chloralose-urethan anesthetized cats during 60 min of isocapnia-hypoxia, mild hypocapnia-hypoxia, or severe hypocapnia-hypoxia. In an additional group of six animals we measured ventral medullary extracellular fluid (ECF) pH during mild hypocapnia-hypoxia. The increase in blood flow during hypoxia was reduced by mild hypocapnia and eliminated by severe hypocapnia. With the exception of an initial decrease in ECF [H+], which occurred during the first 10 min of mild hypocapnia-hypoxia, ECF [H+] increased progressively throughout the exposure and recovery periods and was significantly elevated from the control value by the first 10 min of the recovery period. The results suggest that hypocapnia affects the hypoxic cerebrovascular response of the ventral medulla and that this phenomenon could affect the regulation of ventral medullary ECF [H+].


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