Brain extracellular fluid pH and blood flow during isocapnic and hypocapnic hypoxia

1982 ◽  
Vol 53 (1) ◽  
pp. 247-252 ◽  
Author(s):  
W. P. Nolan ◽  
D. G. Davies
Keyword(s):  
Blood Flow ◽  
Partial Pressure ◽  
Extracellular Fluid ◽  
Co2 Partial Pressure ◽  
Brain Extracellular Fluid ◽  
O2 Partial Pressure ◽  
Total Brain ◽  
New Zealand White Rabbits ◽  
Cerebral Vasodilation ◽  
Ph Microelectrodes

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.

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
Keyword(s):  
Blood Flow ◽  
Extracellular Fluid ◽  
Brain Blood Flow ◽  
Vascular Response ◽  
Radioactive Microspheres ◽  
Vascular Responses ◽  
Control Value ◽  
Total Brain ◽  
The Brain ◽  
Ph Microelectrodes

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.

Pulmonary and circulatory changes in conscious sheep exposed to 100% O2 at 1 ATA

1982 ◽  
Vol 53 (1) ◽  
pp. 110-116 ◽  
Author(s):  
S. Matalon ◽  
M. S. Nesarajah ◽  
L. E. Farhi
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Partial Pressure ◽  
Regional Blood Flow ◽  
Respiratory Acidosis ◽  
Right Atrial ◽  
Base Line ◽  
Co2 Partial Pressure ◽  
O2 Partial Pressure ◽  
Mixed Venous

We have measured the effects of normobaric hyperoxia on arterial and mixed venous gas tensions, cardiac output, heart rate, right atrial, pulmonary, and aortic pressures in 12 conscious chronically instrumented sheep. Regional blood flow to brain, heart, kidney, intestines, and respiratory muscles was assessed in five sheep by injecting 15-micrometers microspheres labeled with gamma-emitting isotopes. Survival time ranged from 60 to 120 h (mean = 80 h). All variables except arterial O2 partial pressure (PaO2) and mixed venous O2 partial pressure remained at base-line level during the first 40 h of exposure, after which PaO2 decreased gradually but remained above 200 Torr at death. After this there was a progressive uncompensated respiratory acidosis with terminal arterial CO2 partial pressure values exceeding 90 Torr. There was a considerable rise in the brain blood flow, whereas flow to the other organs either remained unchanged or increased in proportion to cardiac output. Our experiments also showed that systemic hyperoxic vasoconstriction did not occur, and any local changes were not of sufficient magnitude to affect perfusion.

Ventrolateral medullary surface blood flow determined by hydrogen clearance

1984 ◽  
Vol 56 (1) ◽  
pp. 150-154 ◽  
Author(s):  
P. J. Feustel ◽  
M. J. Stafford ◽  
J. S. Allen ◽  
J. W. Severinghaus
Keyword(s):  
Blood Flow ◽  
White Matter ◽  
Partial Pressure ◽  
Surface Flow ◽  
Co2 Partial Pressure ◽  
Pyramidal Tracts ◽  
O2 Partial Pressure ◽  
Chemosensitive Areas ◽  
Hydrogen Clearance ◽  
Matter Flow

The H2 clearance technique was used to determine the blood flow of the postulated respiratory chemosensitive areas near the ventrolateral surface of the medulla. In 12 pentobarbital sodium-anesthetized cats, flow (mean +/- SD) was measured from 25-micron Teflon-coated platinum wire electrodes implanted to a depth of 0.3–0.7 mm. Flow (in ml X min-1 X 100 g-1, n = 35) was 52.8 +/- 28.5 in hypocapnia [arterial CO2 partial pressure (PaCO2) = 21.8 +/- 1.6 Torr], 57.8 +/- 27.5 in normocapnia (PaCO2 = 31.9 +/- 2.2 Torr), and 75.0 +/- 31.7 in hypercapnia (PaCO2 = 44.5 +/- 3.0 Torr). Flow determined from 15 electrodes in adjacent pyramidal tracts (white matter) was less at all levels of CO2; 22.9 +/- 12.3 in hypocapnia, 29.1 +/- 15.9 in normocapnia, and 33.9 +/- 13.9 in hypercapnia. In hypoxia [arterial O2 partial pressure (PaO2) = 39.9 +/- 6.3 Torr] ventrolateral surface flow rose to 87.9 +/- 47.6, and adjacent white matter flow was 35.8 +/- 15.6. These results indicate that flow in the postulated central chemoreceptor areas exceeds that of white matter and is sensitive to variations in PaCO2 and PaO2.

Ventilatory changes associated with changes in pulmonary blood flow in dogs

1983 ◽  
Vol 54 (4) ◽  
pp. 997-1002 ◽  
Author(s):  
J. F. Green ◽  
M. I. Sheldon
Keyword(s):  
Blood Flow ◽  
Partial Pressure ◽  
Pulmonary Blood Flow ◽  
Median Sternotomy ◽  
Blood Gases ◽  
Arterial Pco2 ◽  
Co2 Partial Pressure ◽  
Arterial Blood ◽  
O2 Partial Pressure ◽  
The Right

To examine the influence of pulmonary blood flow (Qp) on spontaneous ventilation (VE), we isolated the systemic and pulmonary circulations and controlled the arterial blood gases and blood flow (Q) in each circuit as we measured VE. Each dog was anesthetized with ketamine and maintained with halothane. Systemic Q was drained from the right atrium and pumped through an oxygenator and heat exchanger and returned to the aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and pumping it to the pulmonary artery. The heart was fibrillated, all cannulas were brought through the chest wall, and the median sternotomy was closed. The dog was then allowed to breathe spontaneously. The arterial O2 partial pressure (PO2) of both circuits was maintained greater than 300 Torr. Systemic Q was maintained at 0.080 l X min-1 X kg-1. Initially the arterial CO2 partial pressure (PCO2) of both circuits was set at 40 Torr as Qp was varied randomly between approximately 0.025 and 0.175 l X min-1 X kg-1. The average VE-Qp relationship was linear with a slope of 1.45 (P less than 0.0005). Increasing the arterial PCO2 of both circuits to 60 Torr elevated VE an average of 0.37 l X min-1 X kg-1 at each level of Qp (P less than 0.0005). Vagotomy abolished the effect of Qp on VE. Increasing Qp affected the systemic arterial PCO2-VE response curve by shifting it upward without altering its slope. These results demonstrate that increases in Qp are associated with increases in VE. This phenomenon may contribute to exercise hyperpnea.

Separation of carotid body chemoreceptor responses to O2 and CO2 by oligomycin and by antimycin A

1982 ◽  
Vol 242 (3) ◽  
pp. C200-C206 ◽  
Author(s):  
E. Mulligan ◽  
S. Lahiri
Keyword(s):  
Steady State ◽  
Carbonic Anhydrase ◽  
Partial Pressure ◽  
Carotid Body ◽  
Body Tissue ◽  
Antimycin A ◽  
Tissue Ph ◽  
Co2 Partial Pressure ◽  
O2 Partial Pressure ◽  
Metabolic Hypothesis

The cat carotid chemoreceptor O2 and CO2 responses can be separated by oligomycin and by antimycin A. Both of these agents greatly diminish or abolish the chemoreceptor O2 response but not the nicotine or CO2 responses. After either oligomycin or antimycin, the responses to increases and decreases in arterial CO2 partial pressure (PaCO2) consisted of increases and decreases in activity characterized respectively by exaggerated overshoots and undershoots. These were eliminated by the carbonic anhydrase inhibitor, acetazolamide, suggesting that they resulted from changes in carotid body tissue pH. The steady-state PaCO2 response remaining after oligomycin was no longer dependent on arterial O2 partial pressure (PaO2). All effects of antimycin were readily reversible in about 20 min. The separation of the responses to O2 and CO2 indicates that there may be at least partially separate pathways of chemoreception for these two stimuli. The similarity of the oligomycin and antimycin results supports the metabolic hypothesis of chemoreception.

Interaction of hypoxia and hypercapnia on cerebral hemodynamics and brain electrical activity in dogs

1987 ◽  
Vol 253 (4) ◽  
pp. H890-H897 ◽  
Author(s):  
R. W. McPherson ◽  
D. Eimerl ◽  
R. J. Traystman
Keyword(s):  
Partial Pressure ◽  
Elevated Level ◽  
Severe Hypoxia ◽  
O2 Uptake ◽  
Animal Group ◽  
Moderate Hypoxia ◽  
Co2 Partial Pressure ◽  
Arterial Blood ◽  
O2 Partial Pressure ◽  
O2 Delivery

The interaction of hypoxic hypoxia, hypercapnia, and mean arterial blood pressure (MABP) was studied in 15 pentobarbital-anesthetized ventilated dogs. In one group of animals (n = 5) hypercapnia [arterial CO2 partial pressure (PaCO2) approximately 50 Torr] was added to both moderate hypoxia and severe hypoxia. Moderate hypoxia [arterial O2 partial pressure (PaO2) = 36 mmHg] increased MABP and cerebral blood flow (CBF) without changes in cerebral O2 uptake (CMRO2). Superimposed hypercapnia increased CBF and MABP further with no change in CMRO2. In another group of animals (n = 5), a MABP increase of approximately 40 mmHg during moderate hypoxia without hypercapnia did not further increase CBF, suggesting intact autoregulation. Thus, during moderate hypoxia, hypercapnia is capable of increasing CBF. Severe hypoxia (PaO2 = 22 mmHg) increased CBF, but MABP and CMRO2 declined. Superimposed hypercapnia further decreased MABP and decreased CBF from its elevated level and further decreased CMRO2. Raising MABP under these circumstances in another animal group (n = 5) increased CBF above the level present during severe hypoxia alone and increased CMRO2. The change in CBF and CMRO2 during severe hypoxia plus hypercapnia with MABP elevation were not different from that severe hypoxia alone. We conclude that, during hypoxia sufficiently severe to impair CMRO2, superimposed hypercapnia has a detrimental influence due to decreased MABP, which causes a decrease in CBF and cerebral O2 delivery.

scholarly journals Maximal exercise at extreme altitudes on Mount Everest

1983 ◽  
Vol 55 (3) ◽  
pp. 688-698 ◽  
Author(s):  
J. B. West ◽  
S. J. Boyer ◽  
D. J. Graber ◽  
P. H. Hackett ◽  
K. H. Maret ◽  
...  
Keyword(s):  
Partial Pressure ◽  
Maximal Exercise ◽  
Ambient Air ◽  
O2 Uptake ◽  
Mount Everest ◽  
Air Breathing ◽  
Co2 Partial Pressure ◽  
O2 Partial Pressure ◽  
Low Levels ◽  
Arterial Po2

Maximal exercise at extreme altitudes was studied during the course of the American Medical Research Expedition to Everest. Measurements were carried out at sea level [inspired O2 partial pressure (PO2) 147 Torr], 6,300 m during air breathing (inspired PO2 64 Torr), 6,300 m during 16% O2 breathing (inspired PO2 49 Torr), and 6,300 m during 14% O2 breathing (inspired PO2 43 Torr). The last PO2 is equivalent to that on the summit of Mt. Everest. All the 6,300 m studies were carried out in a warm well-equipped laboratory on well-acclimatized subjects. Maximal O2 uptake fell dramatically as the inspired PO2 was reduced to very low levels. However, two subjects were able to reach an O2 uptake of 1 l/min at the lowest inspired PO2. Arterial O2 saturations fell markedly and alveolar-arterial PO2 differences increased as the work rate was raised at high altitude, indicating diffusion limitation of O2 transfer. Maximal exercise ventilations exceeded 200 l/min at 6,300 m during air breathing but fell considerably at the lowest values of inspired PO2. Alveolar CO2 partial pressure was reduced to 7-8 Torr in one subject at the lowest inspired PO2, and the same value was obtained from alveolar gas samples taken by him at rest on the summit. The results help to explain how man can reach the highest point on earth while breathing ambient air.

Inhibition of CO2 Assimilation by Supraoptimal CO2: Effect of Light and Temperature

1983 ◽  
Vol 10 (1) ◽  
pp. 75 ◽  
Author(s):  
KC Woo ◽  
SC Wong
Keyword(s):  
Partial Pressure ◽  
Co2 Concentration ◽  
Co2 Assimilation ◽  
Quantum Yields ◽  
Co2 Partial Pressure ◽  
Low Co2 ◽  
O2 Partial Pressure ◽  
Partial Pressures ◽  
High Partial Pressure ◽  
Partial Pressure Of Co2

In cotton the rate of CO2 assimilation, at O2 partial pressures up to 200 mbar, increased to a maximum and then declined as the intercellular partial pressure of CO2 was increased. The specific intercellular partial pressure of CO2 at which rate of assimilation began to decline depended on the environmental conditions. At 19 mbar partial pressure of O2 the decline occurred at CO2 partial pressure >390 �bar. At 200 mbar partial pressure of O2 it occurred at CO2 partial pressure > 534 �bar. O2 increased the CO2 partial pressure required for inhibition but it did not appear to affect the steepness of the decline of rate of assimilation with further increase in partial pressure of CO2 once the decline became apparent. The decline was more readily observed at low temperature and low O2 partial pressure, and in plants grown at low light and NO3- levels. It was also observed in cowpea and sunflower. Changes in quantum efficiency in cotton at high and low CO2 concentrations were observed. At ambient CO2 concentration (300 �bar), the quantum yields measured at 19 and 200 mbar partial pressure of O2 were 0.072 � 0.0003 and 0.053 � 0.0060 mol CO2 per mol absorbed quanta, respectively. In contrast, at 900 �bar CO2 partial pressure the respective values were 0.050 � 0.0023 and 0.070 � 0.0006 mol CO2 per mol absorbed quanta. The nature of the inhibition of CO2 assimilation by high partial pressure of CO2 is discussed.

scholarly journals Tanshinone IIA ameliorates acute lung injury by inhibition of the NLRP3 inflammasome

2019 ◽  
Vol 71 (2) ◽  
pp. 315-320 ◽  
Author(s):  
Tianyu Chen ◽  
Shaoyun Qin ◽  
Ying Dai
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Partial Pressure ◽  
Nlrp3 Inflammasome ◽  
Weight Ratio ◽  
Dry Weight ◽  
Tanshinone Iia ◽  
Inflammasome Activation ◽  
Co2 Partial Pressure ◽  
O2 Partial Pressure

Tanshinone IIA is the phenanthrenequinone derivative extracted from the perennial plant Salvia miltiorrhiza Bunge (red sage). We investigated whether inhibition of the nucleotide-binding oligomerization domain (NOD)-like receptor family protein 3 (NLRP3) inflammasome mediates the protective effect of tanshinone IIA in acute lung injury (ALI) induced in rats by oleic acid (OA) injection. Compared with the control treatment, OA injection induced pulmonary histological impairment, increased the lung wet/dry weight ratio (7.0?1.1 vs 4.?0.6 ) and CO2 partial pressure (PaCO2) (52?6.4 vs 40?3.6 mmHg), decreased arterial O2 partial pressure (PaO2) (63?8.4 vs 100?3.0 mmHg), and increased tumor necrosis factor ? (TNF?) (8.8?2.3 vs 5.2 ?1.5 pg/mL), monocyte chemoattractant protein-1 (MCP-1) (36.1?4.9 vs 25.2?6.6 pg/mL) and interleukin-1? (IL-1?) (15.9?3.2 vs 4.6?1.3 pg/mL) in the bronchoalveolar lavage (BAL) fluid. Tanshinone IIA provided protection against ALI, observed as a reduction in the lung wet/dry weight ratio and CO2 partial pressure, and increased O2 partial pressure. The cytokine increase was also prevented. Tanshinone IIA attenuated increased protein levels of NLRP3, caspase-1 and IL-1? in pulmonary tissues, suggesting that it ameliorates ALI by preventing NLRP3 inflammasome activation.

Pressure increases oxygen affinity of whole blood and erythrocyte suspensions

1986 ◽  
Vol 61 (2) ◽  
pp. 486-494 ◽  
Author(s):  
R. B. Reeves ◽  
R. A. Morin
Keyword(s):  
Partial Pressure ◽  
Whole Blood ◽  
Oxygen Affinity ◽  
Partial Molal Volume ◽  
Erythrocyte Suspension ◽  
Molal Volume ◽  
Co2 Partial Pressure ◽  
Physiological Conditions ◽  
O2 Partial Pressure ◽  
Effect Of Hydrostatic Pressure

Effect of hydrostatic pressure (HP) on whole blood (WB) or erythrocyte suspension hemoglobin (Hb) O2 affinity has been studied using newly developed techniques. O2 partial pressure at which hemoglobin is half-saturated with O2 (P50) measurements were made at 5 HP (1, 26, 51, 76, and 126 ATA) on thin films of human WB or erythrocytes at 37 degrees C. CO2 partial pressure of WB was either 28 or 57 Torr (film pH 7.51 or 7.31). HP increased affinity of erythrocytes and WB. For erythrocytes in tris(hydroxymethyl)aminomethane buffer, the ratio (r) of P50 (1 ATA)/P50 (51 ATA) was 1.089 (P less than 0.01) at pH 7.0. WB P50 decreased with HP at a rate of -3.3 X 10(-2) Torr X atm-1; change in P50 at higher HP vs. 1 ATA was highly significant (P less than 0.01). No effect of HP was seen on the CO2 Bohr coefficient. Inert gas choice, N2 vs. helium (He), had no effect. Measurement of decrease of P50 with HP at 76 ATA in hemolyzed WB gave an r of 1.15, as great or greater than that found in WB, indicates that Donnan equilibrium alteration is not involved. No effect of HP was found in WB on the ratio of P50 of erythrocytes with normal (5 mmol/l erythrocytes) 2,3-diphosphoglycerate (DPG) to P50 of erythrocytes with less than 5% of normal DPG; i.e., no effect of pressure was seen on the independent influence of DPG on P50. WB measurements of Hb O2 uptake under simulated physiological conditions are characterized by a net decrease in partial molal volume on oxygenation of 30–35 ml/mol Hb4.

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