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.

Cardiac output distribution and regional blood flow during hypocarbia in monkeys

1985 ◽  
Vol 58 (4) ◽  
pp. 1225-1230 ◽  
Author(s):  
S. Gelman ◽  
K. C. Fowler ◽  
S. P. Bishop ◽  
L. R. Smith
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Arterial Blood Flow ◽  
Tissue Blood Flow ◽  
Base Line ◽  
Output Distribution ◽  
Arterial Blood ◽  
Cardiac Output Distribution ◽  
The Brain

Cardiac output distribution and regional blood flow were studied during hypocarbia independent of changes in ventilatory parameters. Fifteen cynomolgus monkeys were anesthetized with methohexital sodium (8 mg/kg im) and hyperventilated through an endotracheal tube. Hypocarbia at two levels, 28 +/- 1.8 and 17 +/- 0.6 Torr, was achieved by a stepwise decreasing CO2 flow into the semiclosed system. Regional blood flow was determined with labeled microspheres. At each stage of experiments two sets of microspheres (9 and 15 microns diam) were used simultaneously. The use of two microsphere sizes allowed evaluation of the relationship between total (nutritive and nonnutritive) tissue blood flow, determined with 15-microns spheres, and nutritive blood flow, determined with 9-microns spheres. There was no change in cardiac output or arterial pressure during both degrees of studied hypocarbia. Hypocarbia was accompanied by a decrease in myocardial blood flow determined with 15-microns spheres and preservation of the flow determined with 9-microns spheres. Splenic blood flow was decreased, whereas hepatic arterial blood flow was increased during both levels of hypocarbia. Blood flow through the brain, renal cortex, and gut showed a biphasic response to hypocarbia: during hypocarbia at 28 +/- 1.8 Torr, blood flow determined with 15-microns spheres was unchanged (in the gut) or decreased (in the brain and kidneys), whereas blood flow determined with 9-microns spheres was decreased. During hypocarbia at 17 +/- 0.6 Torr, blood flow determined with 9-microns spheres had a tendency to restore to base-line values.

Vasopressin responses to asphyxia and hemorrhage in newborn pigs

1987 ◽  
Vol 252 (1) ◽  
pp. R122-R126
Author(s):  
C. W. Leffler ◽  
D. W. Busija ◽  
D. P. Brooks ◽  
J. T. Crofton ◽  
L. Share ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Partial Pressure ◽  
Cyclooxygenase Inhibition ◽  
Co2 Partial Pressure ◽  
Plasma Vasopressin ◽  
Lysine Vasopressin ◽  
O2 Partial Pressure ◽  
Newborn Pigs

Vasopressin may be important in maintenance of arterial pressure and redistribution of cardiac output in hypotensive and asphyxiated newborns. We used chronically instrumented, unanesthetized, 4-day-old pigs to investigate the effects of hypotensive hemorrhage and asphyxia on plasma vasopressin concentration and to determine the effects of cyclooxygenase inhibition on these responses. Asphyxia [arterial O2 partial pressure (PaO2) = 40-50 Torr, arterial CO2 partial pressure (PaCO2) = 60-80 Torr) increases plasma lysine vasopressin (LVP) from 2.2 +/- 0.8 to 52.4 +/- 15.0 microU/ml. Neither the baseline nor stimulated plasma LVP was affected by indomethacin (5 mg/kg) or meclofenamate (5 mg/kg). Hemorrhage (30 ml/kg) increased plasma LVP from 2.8 +/- 0.8 to 163.4 +/- 28.1 (20 min) and 135.1 +/- 18.5 microU/ml (60 min). The effects of vehicle and indomethacin (5 mg/kg) 20 min after hemorrhage on plasma LVP 60 min after hemorrhage were not different. Changes in plasma vasopressin caused by asphyxia and hemorrhage in the unanesthetized newborn pig are similar to the responses observed in adults of other species. This study does not suggest that prostanoids are involved in these responses in newborn pigs.

Effect of enkephalins on cardiac output and regional blood flow in conscious dogs

1989 ◽  
Vol 256 (6) ◽  
pp. H1651-H1658
Author(s):  
C. L. Rosen ◽  
A. Cote ◽  
G. G. Haddad
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Base Line ◽  
Brain Blood Flow ◽  
O2 Consumption ◽  
Blood Gas ◽  
Blood Flow Redistribution

To investigate the effects of enkephalins on cardiac output and regional blood flow, we administered D-Ala-D-Leu-enkephalin (DADLE) intracisternally (ic) to 14 chronically instrumented unanesthetized dogs. Measurements were made at base line, 20, 45, and 75 min after DADLE (25 or 125 micrograms/kg) and 15 min after naloxone (5 micrograms/kg ic). After 125 micrograms/kg DADLE, all animals developed hypoventilation, bradycardia, and decreased O2 consumption without hypotension. Cardiac output decreased (-34%), but brain blood flow increased (+110%). Blood flow decreased to the diaphragm (-38%), heart (-21%), skeletal muscle (-40%), skin (-67%), pancreas (-79%), and gastrointestinal tract (-26%). After 25 micrograms/kg DADLE, there were no consistent changes in cardiac output or regional blood flow. Four additional animals (without DADLE) were exposed to altered inspired gases to reproduce the blood gas changes after DADLE. These animals developed hyperventilation without bradycardia and increased brain (+114%) and diaphragm (+649%) blood flow. We conclude that centrally administered enkephalins produce 1) a parallel decrease in ventilation, heart rate, O2 consumption, and cardiac output and 2) a major blood flow redistribution, primarily dictated by the effects of opioids on ventilation, heart rate, and metabolism.

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.

Systemic hemodynamics affecting cardiac output during hypocapnic and hypercapnic hypoxia

1986 ◽  
Vol 60 (4) ◽  
pp. 1230-1236 ◽  
Author(s):  
D. Davidson ◽  
S. A. Stalcup ◽  
R. B. Mellins
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Partial Pressure ◽  
Transit Time ◽  
Systemic Circulation ◽  
Systemic Arterial Pressure ◽  
Base Line ◽  
Systemic Hemodynamic ◽  
Arterial Partial Pressure ◽  
Hypercapnic Hypoxia

Systemic hemodynamic adjustments involved in the control of cardiac output (CO) were examined in chronically instrumented unanesthetized sheep inhaling gas mixtures resulting in hypocapnic hypoxia (H) [arterial pH (pHa) = 7.53, arterial partial pressure of O2 (Pao2) = 30 Torr, arterial partial pressure of CO2 (Paco2) = 29 Torr] or hypercapnic hypoxia (HCH) (pHa = 7.14, Pao2 = 34 Torr, Paco2 = 72 Torr) for 1 h. H (n = 7) and HCH (n = 6) resulted in 26% and 61% increases in CO, respectively, and mean systemic arterial pressure rose to a greater extent during HCH. Both H and HCH resulted in increased blood flow (microsphere method) to the peripheral systemic circulation including the brain, heart, diaphragm, and nonrespiratory skeletal muscle (the latter blood flow increased 120% during H and 380% during HCH). Gastrointestinal and renal blood flow remained unchanged during H and HCH. Transit time of green dye from the pulmonary artery to regional veins in the hindlimb and intestine was 5.0 and 8.2 s, respectively, during base-line conditions and remained unchanged with HCH. During HCH, regional O2 consumption increased 274% for the hindlimb and decreased 39% for the intestine. Total catecholamines rose 250% during H and 3,700% during HCH. During hypocapnic and hypercapnic hypoxia, CO is augmented in part by systemic hemodynamic adjustments that include a redistribution of blood flow and a translocation of blood volume to the fast transit time peripheral systemic circuit. The sympathetic nervous system may play an important role in mediating these systemic hemodynamic adjustments.

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.

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.

Cardiorespiratory responses to hypoxia in intact and bilaterally vagotomized pigeons

1986 ◽  
Vol 61 (4) ◽  
pp. 1340-1345 ◽  
Author(s):  
G. M. Barnas ◽  
M. Gleeson ◽  
W. Rautenberg
Keyword(s):  
Partial Pressure ◽  
Respiratory Exchange Ratio ◽  
Cardiovascular Responses ◽  
Co2 Production ◽  
Co2 Partial Pressure ◽  
Carotid Bodies ◽  
O2 Partial Pressure ◽  
O2 Concentration ◽  
Cervical Vagotomy ◽  
Mixed Venous

Bilateral, cervical vagotomy in birds denervates, among other receptors, the carotid bodies. To test whether such neural section removes sensitivity to hypoxia, we measured respiratory, cardiovascular, and blood gas responses to hypoxia at 84-, 70-, and 49-Torr inspiratory O2 partial pressure (PIO2) in five pigeons with intact vagi and in five bilaterally, cervically vagotomized pigeons. Normoxic respiratory frequency (fresp) and expiratory flow rate (VE) were decreased after vagotomy. Intact pigeons showed large increases in VE in response to hypoxia, effected mostly by increases in fresp. VE also increased greatly in response to hypoxia in vagotomized pigeons, but increases were largely the result of tidal volume. O2 consumption, CO2 production, and respiratory exchange ratio increased slightly in all pigeons during hypoxia. Normoxic heart rate was greater after vagotomy; cardiac output increased in all pigeons in response to hypoxia, but stroke volume increased only in intact pigeons. During normoxia, arterial and mixed venous O2 partial pressure, O2 concentration, and pH were lower and arterial and mixed venous CO2 partial pressure was higher, after vagotomy. In all pigeons during hypoxia, arterial and mixed venous O2 and CO2 partial pressure and O2 concentration decreased and arterial and mixed venous pH increased; changes were roughly parallel in intact and vagotomized pigeons. The arteriovenous O2 concentration differences during normoxia and hypoxia were similar in all pigeons. We conclude that bilateral, cervical vagotomy in the pigeon causes hypoventilation and tachycardia during normoxia, but strong respiratory and cardiovascular responses to hypoxia are still present.

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.

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