Ventilatory responses to partial cardiopulmonary bypass at rest and exercise in dogs

1986 ◽  
Vol 61 (2) ◽  
pp. 575-583 ◽  
Author(s):  
A. Huszczuk ◽  
B. J. Whipp ◽  
A. Oren ◽  
E. C. Shors ◽  
M. Pokorski ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Peripheral Vascular ◽  
Descending Aorta ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Co2 Flow ◽  
Induced Changes ◽  
Different Levels ◽  
Rest And Exercise

We determined the role of blood flow-induced changes in CO2 load to the lungs on ventilatory control, at rest and in the steady-state of electrically induced exercise, in the anesthetized dog. A portion of the vena caval blood was diverted to the descending aorta following “arterialization” through an extracorporeal gas exchanger. Ventilation typically decreased, both at rest and during exercise (i.e., at 2 different levels of mixed venous CO2), in proportion to the CO2 loss; arterial PCO2 was consequently regulated. There were concomitant increases of the pulmonary and peripheral vascular resistance. Bilateral cervical vagosympathectomy markedly attenuated the ventilatory response at rest, thus disrupting arterial PCO2 homeostasis, but not so during exercise. The results therefore provide evidence for and support the suggestion of CO2 flow-related hyperpnea both at rest and during muscular exercise.

Role of VCO2 in control of breathing of awake exercising dogs

1984 ◽  
Vol 56 (5) ◽  
pp. 1335-1339 ◽  
Author(s):  
F. M. Bennett ◽  
R. D. Tallman ◽  
F. S. Grodins
Keyword(s):  
Directional Statistics ◽  
Direct Signal ◽  
Arterial Pco2 ◽  
Average Decrease ◽  
Ventilatory Responses ◽  
Co2 Output ◽  
Exercise Hyperpnea ◽  
Co2 Flow ◽  
End Tidal

Steady-state ventilatory responses to CO2 inhalation, intravenous CO2 loading (loading), and intravenous CO2 unloading (unloading) were measured in chronic awake dogs while they exercised on an air-conditioned treadmill at 3 mph and 0% grade. End-tidal PO2 was maintained at control levels by manipulation of inspired gas. Responses obtained in three dogs demonstrated that the response to CO2 loading [average increase in CO2 output (Vco2) of 216 ml/min or 35%] was a hypercapnic hyperpnea in every instance. Also, the response to CO2 unloading [average decrease in Vco2 of 90 ml/min or 15% decrease] was a hypocapnic hypopnea in every case. Also, the analysis of the data by directional statistics indicates that there was no difference in the slopes of the responses (change in expiratory ventilation divided by change in arterial Pco2) for loading, unloading, and inhalation. These results indicate that the increased CO2 flow to the lung that occurs in exercise does not provide a direct signal to the respiratory controller that accounts for the exercise hyperpnea. Therefore, other mechanisms must be important in the regulation of ventilation during exercise.

Carotid chemoreceptors in ventilatory responses to changes in venous CO2 load

1981 ◽  
Vol 51 (6) ◽  
pp. 1398-1403 ◽  
Author(s):  
E. A. Phillipson ◽  
G. Bowes ◽  
E. R. Townsend ◽  
J. Duffin ◽  
J. D. Cooper
Keyword(s):  
Ventilatory Response ◽  
Venous Blood ◽  
Major Influence ◽  
Arterial Pco2 ◽  
Peripheral Venous Blood ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Co2 Excretion

We examined the role of the carotid chemoreceptors in the ventilatory response to changes in venous CO2 load in 12 awake sheep using a venovenous extracorporeal perfusion circuit and two carbon dioxide membrane lungs (CDML). Three of the sheep had undergone surgical denervation of the carotid bodies (CBD). In the nine intact sheep, as CO2 was removed from or added to the peripheral venous blood through the CDML under normoxic conditions, there was a linear relationship between the rate of pulmonary CO2 excretion (VCO2) and the resulting rate of ventilation over a VCO2 range of 0--800% of control, so that arterial PCO2 remained close to isocapnic. In contrast, in the three CBD sheep, the ventilatory response to changes in VCO2 was significantly decreased under normoxic conditions, resulting in marked hypercapnia. The results indicate that the carotid chemoreceptors exert a major influence on the ventilatory response to changes in venous CO2 load.

Role of NO in goat basal cerebral circulation and after vasodilatation to hypercapnia or brief ischemias

1993 ◽  
Vol 265 (6) ◽  
pp. R1410-R1415 ◽  
Author(s):  
G. Dieguez ◽  
J. L. Garcia ◽  
N. Fernandez ◽  
A. L. Garcia-Villalon ◽  
L. Monge ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Methyl Ester ◽  
Cerebral Circulation ◽  
Systemic Arterial Pressure ◽  
Nitric Oxide Production ◽  
Hemodynamic Effects ◽  
Arterial Pco2 ◽  
Different Levels

The role of nitric oxide (NO) in the cerebral circulation under basal conditions and after vasodilatation to hypercapnia or reactive hyperemias was studied in 17 anesthetized goats. The intravenous administration of NG-nitro-L-arginine methyl ester (L-NAME, 3-4 or 8-10 mg/kg), an inhibitor of nitric oxide production, reduced middle cerebral artery (MCA) flow (electromagnetically measured) by 19 and 30% and increased systemic arterial pressure by 21 and 26%, respectively, whereas heart rate did not significantly change; MCA resistance increased by 48 and 86%, respectively. These hemodynamic effects were reversed by L-arginine (200-300 mg/kg iv; 5 goats). Different levels of hypercapnia (PCO2 of 30-35, 40-45, and 55-65 mmHg) (12 goats) produced arterial PCO2-dependent increases in MCA flow that were similar under control and L-NAME treatment. Graded cerebral hyperemia occurred after 5, 10, and 20 s of MCA occlusion in 5 goats, but its magnitude was decreased during L-NAME treatment. It suggests that, in the cerebral circulation, nitric oxide 1) produces a basal vasodilator tone and 2) is probably not involved in the vasodilatation to hypercapnia but may mediate hyperemic responses after short brain ischemias.

scholarly journals Ventilatory responses to ozone are reduced in immature rats

2000 ◽  
Vol 88 (6) ◽  
pp. 2023-2030 ◽  
Author(s):  
S. A. Shore ◽  
J. H. Abraham ◽  
I. N. Schwartzman ◽  
G. G. Krishna Murthy ◽  
J. D. Laporte
Keyword(s):  
Bronchoalveolar Lavage ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Ventilatory Responses ◽  
Sprague Dawley Rats ◽  
Immature Rats ◽  
Old Rats ◽  
Induced Changes

During ozone (O3) exposure, adult rats decrease their minute ventilation (V˙e). To determine whether such changes are also observed in immature animals, Sprague-Dawley rats, aged 2, 4, 6, 8, or 12 wk, were exposed to O3(2 ppm) in nose-only-exposure plethysmographs. BaselineV˙e normalized for body weight decreased with age from 2.1 ± 0.1 ml ⋅ min−1⋅ g−1in 2-wk-old rats to 0.72 ± 0.03 ml ⋅ min−1⋅ g−1in 12-wk-old rats, consistent with the higher metabolic rates of younger animals. In adult (8- and 12-wk-old) rats, O3caused 40–50% decreases in V˙e that occurred primarily as the result of a decrease in tidal volume. In 6-wk-old rats, O3-induced changes inV˙e were significantly less, and in 2- and 4-wk-old rats, no significant changes inV˙e were observed during O3exposure. The increased baseline V˙e and the smaller decrements in V˙e induced by O3in the immature rats imply that their delivered dose of O3is much higher than in adult rats. To determine whether these differences in O3dose influence the extent of injury, we measured bronchoalveolar lavage protein concentrations. The magnitude of the changes in bronchoalveolar lavage induced by O3was significantly greater in 2- than in 8-wk-old rats (267 ± 47 vs. 165 ± 22%, respectively, P < 0.05). O3exposure also caused a significant increase in PGE2in 2-wk-old but not in adult rats. The results indicate that the ventilatory response to O3is absent in 2-wk-old rats and that lack of this response, in conjunction with a greater specific ventilation, leads to greater lung injury.

scholarly journals The role of pulmonary CO2 flow in the control of the phase I ventilatory response to exercise in humans

1996 ◽  
Vol 72 (3) ◽  
pp. 285-285
Author(s):  
Paolo Cerretelli ◽  
Bruno Grassi ◽  
Lei Xi ◽  
Federico Schena ◽  
Claudio Marconi ◽  
...  
Keyword(s):  
Phase I ◽  
Ventilatory Response ◽  
Co2 Flow ◽  
Response To Exercise ◽  
Exercise In Humans

P6467Pressure-mediated changes in the ventricular septum shape during exercise in patients with pulmonary hypertension: a 3-d echocardiography study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G D'Alesio ◽  
F Migliavacca ◽  
J F Rodriguez Matas ◽  
F Bandera ◽  
M Losito ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Interventricular Septum ◽  
Systolic Pulmonary Artery Pressure ◽  
3D Data ◽  
Pressure Changes ◽  
Induced Changes ◽  
Volume Acquisition ◽  
Full Volume ◽  
Rest And Exercise

Abstract Background The role of interventricular (IV) septum in mediating the mechanical interaction between the two ventricles is well recognized. This interaction is promoted by several structural and hemodynamic determinants. We aimed at assessing the geometrical RV changes in patients with pulmonary hypertension (PH) compared to normal, evaluating RV curvature at rest and during stress testing addressing the specific role of pressure-induced changes in IV septum curvature. Methods Thirty-four subjects (15 controls; 19 PH patients) underwent RV real-time 3D full volume acquisition at rest and during exercise-echo. The 3D data were analysed off-line using the 4D RV TomTec software. The 3D mesh of the RV model was post-processed using a custom developed software. The value of mean regional curvature was assessed for the interventricular septum (IVS) at end-diastole (ED) and at end systole (ES). Results In controls the IVS curvature, assessed at end-diastole (ED) and end-systole (ES), was significantly (p<0.001) more concave (at rest −0.31±0.06 at ED, and −0.29±0.06 at ES; during exercise −0.28±0.09 at ED, and −0.28±0.08 at ES) than in PH patients (at rest −0.09±0.14 at ED, and −0.09±0.11 at ES ; during exercise −0.05±0.18 at ED, and −0.02±0.18 at ES). There was no significant variation in any of RV IVS curvatures between rest and exercise or between ES and ED. In PH subjects, IVS curvature at ES weakly increased from −0.09±0.11 (SD) at rest to −0.02±0.18 during exercise (p=0.179).Nonetheless, the degree of IVS curvature was strongly related to systolic pulmonary artery pressure (PASP), both at rest (r=0.743 at ES, p<0.01; r=0.794, p<0.001 at ED) and during exercise (r=0.823 at ES, p<0.0001; r=0.812 at ED, p<0.0001). Conclusions These data provide new perspectives on how the interventricular septum morphology adapts during exercise in PH patients vs controls. Changes in IVS curvature are linearly related to pulmonary pressure changes and occur with different slope (rest-exercise) in PH vs controls.

Metabolic role of the exercise-induced increment in epinephrine in the dog

1988 ◽  
Vol 255 (4) ◽  
pp. E428-E436 ◽  
Author(s):  
J. M. Moates ◽  
D. B. Lacy ◽  
R. E. Goldstein ◽  
A. D. Cherrington ◽  
D. H. Wasserman
Keyword(s):  
Glucose Production ◽  
Plasma Glucagon ◽  
Metabolic Role ◽  
Exercise Period ◽  
Exercise Induced ◽  
Glucagon And Insulin ◽  
Induced Changes ◽  
Response To Exercise ◽  
Rest And Exercise

The role of the exercise-induced increment in epinephrine was studied in five adrenalectomized (ADX) and in six normal dogs (C). Experiments consisted of an 80-min equilibration period, a 40-min basal period, and a 150-min exercise period. ADX were studied with epinephrine replaced to basal levels during rest and to increased levels during exercise to simulate its normal rise (HE) and on a separate day with epinephrine maintained at basal levels throughout the study (BE). Cortisol was replaced during rest and exercise in ADX so as to simulate the levels seen in C. Glucose was infused as needed in ADX to maintain the glycemia evident during exercise in C. Glucose production (Ra) and utilization (Rd) were assessed isotopically. In C, epinephrine had risen by 95 +/- 25 pg/ml by the end of exercise. In HE, the increment in epinephrine (117 +/- 29 pg/ml) was similar to that seen in C, whereas in BE epinephrine fell by 18 +/- 9 pg/ml. Basal norepinephrine levels were 139 +/- 9, 260 +/- 25, and 313 +/- 33 pg/ml in C, HE, and BE, respectively. In response to exercise, norepinephrine increased by nearly twofold in all protocols. Basal and exercise-induced changes in plasma glucagon and insulin were similar in C and ADX. Ra increased similarly in C (5.3 +/- 0.6 mg.kg-1.min-1) and HE (4.9 +/- 0.6 mg.kg-1.min-1). In BE, Ra rose normally for the initial 90 min but then declined resulting in a rise of only 2.9 +/- 0.5 mg.kg-1.min-1 after 150 min of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The role of pulmonary CO2 flow in the control of the phase i ventilatory response to exercise in humans

1995 ◽  
Vol 71 (4) ◽  
pp. 287-294 ◽  
Author(s):  
Paolo Cerretelli ◽  
Bruno Grassi ◽  
Lei Xi ◽  
Federico Schena ◽  
Claudio Marconi ◽  
...  
Keyword(s):  
Phase I ◽  
Ventilatory Response ◽  
Co2 Flow ◽  
Response To Exercise ◽  
Exercise In Humans

Effect of different levels of bacterial probiotic on broilers performance

2003 ◽  
Vol 2003 ◽  
pp. 185-185
Author(s):  
M. R. Abdollahi ◽  
A. Kamyab ◽  
A. Bazzazzadekan ◽  
A. Nik-Khah ◽  
A. Z. Shahneh
Keyword(s):  
Alimentary Tract ◽  
Management Practices ◽  
Animal Health ◽  
Critical Role ◽  
Microbial Populations ◽  
Feed Management ◽  
Induced Changes ◽  
Symbiotic Organisms ◽  
Different Levels

The microbial populations in the gastrointestinal tracts of poultry play a key role in normal digestive processes and in maintaining animal health. Disease- and stress-induced changes in the physicochemical environment in the gastrointestinal tract, or simple changes in feed management practices can significantly influence the microbial populations and their effects on animal performance and health. In the last five decades, increased knowledge of the factors that influence the activities of microorganisms in the alimentary tract has helped to define the critical role of these symbiotic organisms. Probiotics, competitive exclusion and direct-fed microbial feed supplements can be used as a strategic tool for managing these microbial populations. The aim of this trial was study of effect of different levels of bacterial probiotic on broilers performance and some of blood factors.

Interaction between CO2 production and ventilation in the hypoxic kitten

1993 ◽  
Vol 74 (2) ◽  
pp. 905-910 ◽  
Author(s):  
J. P. Mortola ◽  
T. Matsuoka
Keyword(s):  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Co2 Production ◽  
Depressant Effect ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Parallel Increase ◽  
Shallow Breathing

We hypothesized that in the hypoxic newborn the drop in metabolic rate, and particularly in CO2 production (VCO2), contributes to the magnitude of the ventilatory response. Experiments were performed on unanesthetized newborn kittens in a warm [28–30 degrees C ambient temperature (Ta)] or cold (20 degrees C) environment. Breathing pattern and gaseous metabolism were measured by the barometric technique and the inflow-outflow O2 and CO2 difference, respectively. At 30 degrees C, hypoxia (10% O2) decreased VCO2 and induced rapid and shallow breathing, with little effect on minute ventilation (VE). Normoxic exposure to 20 degrees C determined a parallel increase in VE and metabolism; at this Ta, hypoxia decreased VCO2 more than at the higher Ta, and the drop in tidal volume (VT) was also proportionally larger; hence, at 20 degrees C, hypoxic VE was markedly below the normoxic values. Despite these changes in breathing pattern, at neither Ta during hypoxia did arterial PCO2 increase above the normoxic value; in fact, arterial PCO2 at 20 degrees C was slightly decreased because of the important drop in VCO2. Exposure to hypoxia with a CO2 load (inspired CO2 = 1, 3, or 5%) did not abolish the hypometabolic response; the hypoxic depressant effect on VT was either unchanged (by 1% CO2), completely offset (by 3% CO2), or reversed (by 5% CO2), with parallel effects on VE. The results are consistent with the hypothesis that in the newborn the level of CO2, by controlling VT, could represent a link between the metabolic and ventilatory responses to acute hypoxia.

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