Brain adenosine concentration during hypoxia in rats

1981 ◽  
Vol 241 (2) ◽  
pp. H235-H242 ◽  
Author(s):  
H. R. Winn ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Partial Pressure ◽  
Brain Tissue ◽  
Co2 Partial Pressure ◽  
Adenosine Concentration ◽  
Subsequent Measurement ◽  
Sustained Hypoxia ◽  
In Situ Technique

We analyzed brain tissue for adenosine and its metabolites, inosine and hypoxanthine, in rats during acute (30 s) hypoxia and during sustained (5 min) hypoxia and hypocarbia. Within 30 s of the onset of hypoxia, adenosine levels were increased from 0.34 +/- 0.08 (SE) to 1.65 +/- 0.33 nmol/g (P less than 0.005), paralleling temporally the changes in cerebral blood flow. During sustained hypoxia and hypocarbia, brain tissue was sampled by a fast (freeze-blow) or slow (in situ) freezing method. With the freeze-blow technique, adenosine concentrations remained stable between arterial partial pressure of O2 (PaO2) greater than 200 and 100 mmHg, doubled at PaO2 = 50 mmHg, and increased sevenfold (P less than 0.005) when PaO2 reached 30 mmHg. No increases in adenosine or its metabolites were noted with the in situ technique. During hypocarbia (arterial CO2 partial pressure less than 20 mmHg), adenosine concentrations increased with both sampling techniques. Freezing times in brain were measured during in situ freezing and were increased during hypoxia and decreased during hypocarbia. In conclusion, 1) adenosine concentrations in brain are increased during hypoxia, and 2) the in situ technique in rat does not appear to be optimal for sampling brain tissue for subsequent measurement of adenosine under conditions where cerebral blood flow is increased.

Effects on cerebral blood flow of position changes, hyperoxia, CO2 partial pressure variations and the Valsalva manoeuvre

2020 ◽  
Vol 38 (1) ◽  
pp. 49-57
Author(s):  
Javier Tercero ◽  
Isabel Gracia ◽  
Paola Hurtado ◽  
Nicolás de Riva ◽  
Enrique Carrero ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Partial Pressure ◽  
Valsalva Manoeuvre ◽  
Co2 Partial Pressure

Relationship between adenosine concentration and oxygen supply in rat brain

1975 ◽  
Vol 228 (6) ◽  
pp. 1896-1902 ◽  
Author(s):  
R Rubio ◽  
RM Berne ◽  
EL Bockman ◽  
RR CURNISH
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Regulation ◽  
Oxygen Supply ◽  
Normal Brain ◽  
Experimental Conditions ◽  
Adenosine Concentration ◽  
The Brain ◽  
Camp Formation

Since adenosine is present in normal brain tissue and cerebrosipinal fluid and since it dilates the pial vessels, it is possible that adenosine, in addition to H-+, is also a mediator of the metabolic regulation of cerebral blood flow. Evidence supporting this hypothesis was obtained under various experimental conditions characterized by achange in brain oxygen supply. The brain was frozen in situ by means of a small bonerongeur precooled in liquid N2 and the tissue was processed for adenosine determination (nmol/g of tissue). Electrical stimulation of the cortex at 0, 15, 30, and 45 Hz yielded adenosine levels of 5.4 plus or minus 0.7, 10.5 plus or minus 1.7, 13.0 plusor minus 1.2, and 9.0 plus or minus 2.1 nmol/g. Arterial pressures of 87, 60, and 40mmHg gave adenosine levels of 7.5 plus or minus 0.76, 13 plus or minus 2.6, and 26.6plus or minus 3.3, respectively. Ventilation with 29.7, 20, 10.7, and5.5% O2 significantly increased the adenosine levels to 9.4 plus or minus 3.0, 6.4 plus or minus 1.2, 30.0 plus or minus 9.3, and 63.3 plus or minus 18.2 nmol/g, respectively. Hyperventilation significantly increased adenosine form 6.7 plus or minus 1.0 to 11.8 plus or minus 1.4 nmol/g. This increased adenosine level was reduced by additionof CO2 to the ventilating gas mixture. Lactate, the main H-+ donor, pyruvate, and cAMP changed in a fashion parallel to adenosine. However, cAMP showedonly a small increase in adenosine. These findings are in accordance with the concept that adenosine and H-+ may act synergistally to regulate cerebral blood flow and that endogenous adenosine may exert a small effect on cAMP formation.

scholarly journals Local Cerebral Blood Flow and Glucose Consumption of Rats with Experimental Gliomas

1982 ◽  
Vol 2 (1) ◽  
pp. 25-32 ◽  
Author(s):  
K.-A. Hossmann ◽  
I. Niebuhr ◽  
M. Tamura
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Tumors ◽  
Brain Tissue ◽  
Glucose Utilization ◽  
Cell Clone ◽  
Tumor Development ◽  
Glucose Consumption ◽  
Contralateral Side ◽  
Opposite Hemisphere

Experimental brain tumors were produced in rats by intracerebral implantation of a neoplastic glial cell clone. Within 2–6 weeks, spherical brain tumors developed at the implantation site with a mean diameter of 6 mm. Local blood flow and local glucose utilization were measured under light barbiturate anesthesia by quantitative autoradiography in the tumor and peritumoral brain tissue. In solid parts of the tumor, blood flow was 57.8 ± 2.0 ml/100 g/min (mean ± SE), and glucose utilization was 87.2 ± 5.8 μmol/100 g/min, respectively. In necrotic regions, flow and glucose utilization were zero. In peritumoral brain tissue of the ipsilateral hemisphere blood flow was reduced by 13–23%, as compared to homologous regions of the opposite side, the greatest decrease being recorded in the ipsilateral thalamus. Flow in the opposite hemisphere was of the same order of magnitude as in normal control rats. Glucose consumption, in contrast, was distinctly reduced in both hemispheres: in the cortex and putamen, it was 40–50% lower than in normal controls. The following conclusions are drawn: (1) during tumor development the high glucose consumption in the tumor tissue is not coupled to an equal increase in blood flow; (2) peritumoral cerebral blood flow decreases on the ipsilateral but not on the contralateral side, and (3) the metabolic rate of glucose is distinctly inhibited in both hemispheres of tumor-bearing animals. The dissociation between blood flow and metabolism suggests that metabolic inhibition is not the consequence of a diaschitic depression of functional activity.

No effect of brain blood flow on ventilatory depression during sustained hypoxia

1989 ◽  
Vol 66 (4) ◽  
pp. 1674-1678 ◽  
Author(s):  
A. Suzuki ◽  
M. Nishimura ◽  
H. Yamamoto ◽  
K. Miyamoto ◽  
F. Kishi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brain Tissue ◽  
Initial Phase ◽  
Intermediate Phase ◽  
Minute Ventilation ◽  
Brain Blood Flow ◽  
Final Phase ◽  
Venous Pco2 ◽  
Tissue Pco2 ◽  
Sustained Hypoxia

Minute ventilation (VE) during sustained hypoxia is not constant but begins to decline within 10–25 min in adult humans. The decrease in brain tissue PCO2 may be related to this decline in VE, because hypoxia causes an increase in brain blood flow, thus resulting in enhanced clearance of CO2 from the brain tissue. To examine the validity of this hypothesis, we measured VE and arterial and internal jugular venous blood gases simultaneously and repeatedly in 15 healthy male volunteers during progressive and subsequent sustained isocapnic hypoxia (arterial PO2 = 45 Torr) for 20 min. It was assumed that jugular venous PCO2 was an index of brain tissue PCO2. Mean VE declined significantly from the initial (16.5 l/min) to the final phase (14.1 l/min) of sustained hypoxia (P less than 0.05). Compared with the control (50.9 Torr), jugular venous PCO2 significantly decreased to 47.4 Torr at the initial phase of hypoxia but did not differ among the phases of hypoxia (47.2 Torr for the intermediate phase and 47.7 Torr for the final phase). We classified the subjects into two groups by hypoxic ventilatory response during progressive hypoxia at the mean value. The decrease in VE during sustained hypoxia was significant in the low responders (n = 9) [13.2 (initial phase) to 9.3 l/min (final phase of hypoxia), P less than 0.01], but not in the high responders (n = 6) (20.9–21.3 l/min, NS). This finding could not be explained by the change of arterial or jugular venous gases, which did not significantly change during sustained hypoxia in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral blood flow and interstitial fluid adenosine during hemorrhagic hypotension

1988 ◽  
Vol 255 (5) ◽  
pp. H1211-H1218 ◽  
Author(s):  
D. G. Van Wylen ◽  
T. S. Park ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Adenosine Receptor ◽  
Cerebral Autoregulation ◽  
Interstitial Fluid ◽  
Adenosine Receptor Antagonist ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
Adenosine Concentration ◽  
Group 2

This study was designed to assess the role of adenosine in autoregulation of cerebral blood flow (CBF) with the use of the brain dialysis technique to sample cerebral interstitial fluid (ISF) and hydrogen clearance to measure local CBF in ketamine-anesthetized rats. In group 1 (n = 11), animals were hemorrhaged to reduce mean arterial blood pressure (MABP) from control levels (MABP = 101.1 +/- 2.6) to 80, 70, 60, 50, 40, and 30 mmHg. Cerebral autoregulation was evidenced by no significant decrease in CBF until MABP decreased to 60 mmHg. However, dialysate adenosine concentration did not increase until MABP decreased to 50 mmHg. In group 2 (bilateral dialysis; n = 11), in which the left carotid artery was ligated before reductions in MABP, left-side dialysate adenosine concentration increased at a MABP of 70 mmHg. In group 3 (bilateral dialysis; n = 6), one dialysis probe was perfused with artificial cerebrospinal fluid containing 10(-3) M 8(p-sulfophenyl)theophylline (8-SPT), an adenosine receptor antagonist, during reduction of MABP to 50 mmHg. Although there were similar reductions in CBF with or without adenosine receptor blockade, dialysate adenosine concentration was greater on the side of locally infused 8-SPT at a MABP of 50 mmHg. These data suggest that adenosine is not responsible for cerebral autoregulation at blood pressures greater than 50 mmHg but may contribute to the decrease in cerebral vascular resistance observed at arterial pressures below the autoregulatory range.

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