Noninvasive diffusing capacity and cardiac output in exercising dogs

1988 ◽  
Vol 65 (2) ◽  
pp. 669-674 ◽  
Author(s):  
J. I. Carlin ◽  
S. S. Cassidy ◽  
U. Rajagopal ◽  
P. S. Clifford ◽  
R. L. Johnson
Keyword(s):  
Blood Flow ◽  
Body Weight ◽  
Cardiac Output ◽  
Steady State ◽  
Pulmonary Blood Flow ◽  
Maximal Exercise ◽  
O2 Consumption ◽  
Diffusing Capacity ◽  
Metabolic Capacity ◽  
End Tidal

We have developed a rebreathing procedure to determine diffusing capacity (DLCO) and pulmonary blood flow (Qc) in the awake, exercising dog. A low dead space, leak-free respiratory mask with an incorporated mouthpiece was utilized to achieve mixing between the rebreathing bag and the dog's lung. The rebreathing bag was initially filled with approximately 1.0 liter of gas containing 0.6% C2H2, 0.3% C18O, 9% He, and 35-40% O2. End-tidal gas concentrations were measured with a respiratory mass spectrometer. The disappearance of C2H2 and C18O was measured with respect to He to calculate Qc and DLCO. Values for DLCO in dogs, expressed per kilogram of body weight, were much larger than those reported in humans. However, at a given level of absolute O2 consumption, measurements of absolute DLCO in dogs were comparable to those reported in humans by both rebreathing and steady-state methods at rest and near-maximal exercise. These results suggest that DLCO is more closely matched to the metabolic capacity (i.e., maximal O2 consumption) than to body size between these two species.

O2 consumption during exercise in dogs--roles of splenic contraction and alpha-adrenergic vasoconstriction

1986 ◽  
Vol 251 (3) ◽  
pp. H502-H509 ◽  
Author(s):  
J. C. Longhurst ◽  
T. I. Musch ◽  
G. A. Ordway
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Adrenergic Receptor ◽  
Maximal Exercise ◽  
Adrenergic Blockade ◽  
Receptor Blockade ◽  
O2 Consumption ◽  
Alpha Adrenergic Receptor ◽  
O2 Extraction ◽  
Adrenergic Receptor Blockade

To examine the influence of alpha-adrenergic vasoconstriction on the aerobic capacity of dogs, we calculated O2 consumption (VO2) by the Fick method during submaximal and maximal exertion before and during alpha-adrenergic blockade with phentolamine. Regional blood flow was measured with radioactive microspheres. alpha-Adrenergic receptor blockade reduced VO2 by 12.9% during submaximal and 17.9% during maximal exercise. Arterial and venous lactic acid approximately doubled during both levels of stress in the presence of alpha-adrenergic receptor blockade. Calculated VO2 decreased because arteriovenous O2 (A-V)O2 extraction was reduced by 11.6% during submaximal exercise. During maximal exercise a 16.7% decrease in (A-V)O2 extraction and a 5.7% decrease in cardiac output contributed to the decrease in maximal VO2. During both levels of stress, (A-V)O2 extraction was reduced because arterial O2 content was decreased. Since circulating hematocrits during exercise were reduced by alpha-adrenergic receptor blockade (43-38%), we postulate that splenic contraction likely was inhibited. Additionally, distribution of blood flow to skeletal muscle and visceral organs was unaltered by alpha-blockade. To examine the importance of splenic contraction during maximal exercise, we examined hemodynamic and metabolic responses before and after splenectomy. Compared with the spleen-intact condition, splenectomized dogs demonstrated a 12.6% reduction in VO2 as a result of 7.7 and 5.5% reductions in (A-V)O2 extraction and cardiac output, respectively. (A-V)O2 extraction was reduced because arterial O2 content and circulating hematocrit during exercise were decreased. Therefore, in the exercising dog, alpha-adrenergic receptor blockade reduces O2 consumption and causes a shift to anaerobic metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Kinetics of CO uptake and diffusing capacity in transition from rest to steady-state exercise

1992 ◽  
Vol 72 (5) ◽  
pp. 1764-1772 ◽  
Author(s):  
J. R. Kinker ◽  
A. S. Haffor ◽  
M. Stephan ◽  
T. L. Clanton
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Pulmonary Blood Flow ◽  
Time Course ◽  
Significant Rise ◽  
Diffusing Capacity ◽  
Incremental Test ◽  
Content Difference ◽  
Kinetics Of ◽  
Alveolar Capillary

In the transition from rest to steady-state exercise, O2 uptake from the lungs (VO2) depends on the product of pulmonary blood flow and pulmonary arteriovenous O2 content difference. The kinetics of pulmonary blood flow are believed to be somewhat faster than changes in pulmonary arteriovenous O2 content difference. We hypothesized that during CO breathing, the kinetics of CO uptake (VCO) and diffusing capacity for CO (DLCO) should be faster than VO2 because changes in pulmonary arteriovenous CO content difference should be relatively small. Six subjects went abruptly from rest to constant exercise (inspired CO fraction = 0.0005) at 40, 60, and 80% of their peak VO2, measured with an incremental test (VO2peak). At all exercise levels, DLCO and VCO rose faster than VO2 (P less than 0.001), and DLCO rose faster than VCO (P less than 0.001). For example, at 40% VO2peak, the time constant (tau) for DLCO in phase 2 was 19 +/- 5 (SD), 24 +/- 5 s for VCO, and 33 +/- 5 s for VO2. Both VCO and DLCO increased with exercise intensity but to a lesser degree than VO2 at all exercise intensities (P less than 0.001). In addition, no significant rise in DLCO was observed between 60 and 80% VO2peak. We conclude that the kinetics of VCO and DLCO are faster than VO2, suggesting that VCO and DLCO kinetics reflect, to a greater extent, changes in pulmonary blood flow and thus recruitment of alveolar-capillary surface area. However, other factors, such as the time course of ventilation, may also be involved.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of a systemic A-V fistula and of pulmonary embolization on diffusing capacity

1963 ◽  
Vol 18 (3) ◽  
pp. 553-556 ◽  
Author(s):  
M. Henry Williams ◽  
Bruce J. Sobol
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Pulmonary Blood Flow ◽  
Glass Beads ◽  
Diffusing Capacity ◽  
Anesthetized Dogs ◽  
Pulmonary Embolization

Opening an aortic-caval fistula in anesthetized dogs was associated with slight but significant increase of the steady-state diffusing capacity of the lungs. Extensive pulmonary embolization with glass beads resulted in a slight and insignificant fall of the diffusing capacity. Increased pulmonary blood flow and obstruction to pulmonary arterioles do not appear to be associated with marked increase and decrease of the diffusing capacity. Submitted on October 5, 1962

Gastrointestinal blood flow and oxygen consumption in awake newborn piglets: effect of feeding

1983 ◽  
Vol 245 (5) ◽  
pp. G697-G702 ◽  
Author(s):  
P. T. Nowicki ◽  
B. S. Stonestreet ◽  
N. B. Hansen ◽  
A. C. Yao ◽  
W. Oh
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
O2 Consumption ◽  
Gi Tract ◽  
Local Blood Flow ◽  
O2 Uptake ◽  
O2 Extraction ◽  
Gastrointestinal Blood Flow ◽  
O2 Delivery ◽  
Effect Of Feeding

Regional and total gastrointestinal (GI) blood flow, O2 delivery, and whole-gut O2 extraction and O2 consumption were measured before and 30, 60, and 120 min after feeding in nonanesthetized, awake 2-day-old piglets. Cardiac output and blood flow to kidneys, heart, brain, and liver were also determined. Blood flow was measured using the radiolabeled microsphere technique. In the preprandial condition, total GI blood flow was 106 +/- 9 ml X min-1 X 100 g-1, while O2 extraction was 17.2 +/- 0.9% and O2 consumption was 1.99 +/- 0.19 ml O2 X min-1 X 100 g-1. Thirty minutes after slow gavage feeding with 30 ml/kg artificial pig milk, O2 delivery to the GI tract and O2 extraction rose significantly (P less than 0.05) by 35 +/- 2 and 33 +/- 2%, respectively. The increase in O2 delivery was effected by a significant increase in GI blood flow, which was localized to the mucosal-submucosal layer of the small intestine. O2 uptake by the GI tract increased 72 +/- 4% 30 min after feeding. Cardiac output and blood flow to non-GI organs did not change significantly with feeding, whereas arterial hepatic blood flow decreased significantly 60 and 120 min after feeding. The piglet GI tract thus meets the oxidative demands of digestion and absorption by increasing local blood flow and tissue O2 extraction.

Costal vs. crural diaphragmatic blood flow during submaximal and near-maximal exercise in ponies

1988 ◽  
Vol 65 (4) ◽  
pp. 1514-1519 ◽  
Author(s):  
M. Manohar
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Left Atrium ◽  
Maximal Exercise ◽  
Muscle Blood Flow ◽  
Intercostal Muscle ◽  
Quiet Breathing ◽  
Blood Flows ◽  
Graded Exercise ◽  
Crural Diaphragm

The present study was carried out 1) to compare blood flow in the costal and crural regions of the equine diaphragm during quiet breathing at rest and during graded exercise and 2) to determine the fraction of cardiac output needed to perfuse the diaphragm during near-maximal exercise. By the use of radionuclide-labeled 15-micron-diam microspheres injected into the left atrium, diaphragmatic and intercostal muscle blood flow was studied in 10 healthy ponies at rest and during three levels of exercise (moderate: 12 mph, heavy: 15 mph, and near-maximal: 19-20 mph) performed on a treadmill. At rest, in eucapnic ponies, costal (13 +/- 3 ml.min-1.100 g-1) and crural (13 +/- 2 ml.min-1.100 g-1) phrenic blood flows were similar, but the costal diaphragm received a much larger percentage of cardiac output (0.51 +/- 0.12% vs. 0.15 +/- 0.03% for crural diaphragm). Intercostal muscle perfusion at rest was significantly less than in either phrenic region. Graded exercise resulted in significant progressive increments in perfusion to these tissues. Although during exercise, crural diaphragmatic blood flow was not different from intercostal muscle blood flow, these values remained significantly less (P less than 0.01) than in the costal diaphragm. At moderate, heavy, and near-maximal exercise, costal diaphragmatic blood flow (123 +/- 12, 190 +/- 12, and 245 +/- 18 ml.min-1.100 g-1) was 143%, 162%, and 162%, respectively, of that for the crural diaphragm (86 +/- 10, 117 +/- 8, and 151 +/- 14 ml.min-1.100 g-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of ouabain on cardiac output and pulmonary blood flow in dogs

1972 ◽  
Vol 84 (3) ◽  
pp. 371-376 ◽  
Author(s):  
Elmer Treat ◽  
Harvey Ulano ◽  
Marc Pfeffer ◽  
Walter Massion ◽  
Linda L. Shanbour ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Pulmonary Blood Flow

Single-Breath Breath Holding Measurement of Pulmonary Blood Flow: Comparison to Direct Fick Cardiac Output

1986 ◽  
Vol 71 (s15) ◽  
pp. 36P-36P ◽  
Author(s):  
A.H. Kendrick ◽  
A. Rozkovec ◽  
M. Papouchado ◽  
J. West ◽  
J.E. Bees ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Pulmonary Blood Flow ◽  
Breath Holding ◽  
Single Breath

Abstract WP432: Non-invasive Respiratory Impedance Enhances Cerebral Perfusion

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Christopher G Favilla ◽  
Ashwin B Parthasarathy ◽  
John A Detre ◽  
Michael T Mullen ◽  
Scott E Kasner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Flow Velocity ◽  
Cerebral Perfusion ◽  
Respiratory Impedance ◽  
Mean Flow ◽  
Non Invasive ◽  
End Tidal ◽  
High Level ◽  
Mean Flow Velocity

Background: Optimization of cerebral blood flow is the cornerstone of clinical management in a number of neurologic diseases, most notably ischemic stroke. Intra-thoracic pressure influences cardiac output and has the potential to impact cerebral blood flow (CBF). Here we aim to quantify cerebral hemodynamic changes in response to increased respiratory impedance using a non-invasive respiratory device. Methods: Cerebral perfusion was measured under varying levels of respiratory impedance (6cm H 2 0, 9cm H 2 0, and 12 cm H 2 0) in 20 healthy volunteers. Simultaneous measurements of microvascular CBF and middle cerebral artery mean flow velocity (MFV), respectively, were performed with optical diffuse correlation spectroscopy (DCS) and transcranial Doppler ultrasound (TCD). Results: At the high level of respiratory impedance, mean flow velocity increased by 6.4% compared to baseline (p=0.004), but changes in cortical CBF were smaller and non-significant (Figure). Heart rate, cardiac output, respiratory rate, and end tidal CO 2 remained stable during all levels of respiratory impedance. There was small increase in mean arterial blood pressure, 1.7% (p=0.006), at the high level of respiratory impedance. In a multivariable linear regression model accounting for end tidal CO 2 and individual variability, respiratory impedance was associated with increases in both mean flow velocity (coefficient: 0.49, p<0.001) and cortical CBF (coefficient: 0.13, p<0.001). Conclusions: Manipulating intrathoracic pressure via non-invasive respiratory impedance was well tolerated and produced a small but measurable increase in cerebral perfusion in healthy individuals. Future studies in acute ischemic stroke patients with impaired cerebral autoregulation is warranted in order to assess whether respiratory impedance is feasible as a novel non-invasive therapy for stroke.

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