Influence of doxapram and intermittent 10% carbon dioxide inspiration on cardiovascular and laryngeal functions in anesthetized dogs

2021 ◽  
Author(s):  
Daniel M. Sakai ◽  
Shenise L. Howard ◽  
Rachel A. Reed ◽  
Jane E. Quandt ◽  
Michele Barletta ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Anesthetized Dogs

Role of myocardial oxygen and carbon dioxide in coronary autoregulation

1992 ◽  
Vol 262 (4) ◽  
pp. H1231-H1237 ◽  
Author(s):  
T. P. Broten ◽  
E. O. Feigl
Keyword(s):  
Carbon Dioxide ◽  
Left Main Coronary Artery ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Vascular Conductance ◽  
Anesthetized Dogs ◽  
Coronary Conductance ◽  
A Prospective Study

Myocardial oxygen (PO2) and carbon dioxide tensions (PCO2) are likely mediators of the local control of coronary blood flow. A previous study demonstrated that myocardial PO2 and PCO2, estimated by coronary venous values, interact synergistically to determine coronary flow. This synergistic relation was used in a prospective study to test the hypothesis that myocardial PO2 and PCO2 mediate changes in coronary vascular conductance during autoregulation. The left main coronary artery was pump perfused at controlled pressures in closed-chest anesthetized dogs. Autoregulation curves were obtained by increasing coronary perfusion pressure from 80 to 160 mmHg in 20-mm increments. Steady-state measurements of coronary venous PO2 and PCO2 and coronary conductance were obtained at each perfusion pressure. The coronary venous PO2 and PCO2 were used in the previously determined synergistic relation to predict the coronary vascular conductance during autoregulation. The predicted changes in coronary vascular conductance were compared with the actual changes in coronary vascular conductance for the pressure range of 80-160 mmHg. The data indicate that the synergistic interaction of oxygen and carbon dioxide accounts for approximately 23% of the change in coronary vascular conductance during autoregulation. These results suggest that other factors are also involved in autoregulation.

Physiological effects of carbon dioxide gas introduced into coronary arteries

1959 ◽  
Vol 196 (6) ◽  
pp. 1308-1311 ◽  
Author(s):  
Morton J. Oppenheimer ◽  
Herbert M. Stauffer ◽  
Louis A. Soloff ◽  
Thomas M. Durant
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Short Duration ◽  
Coronary Arteries ◽  
Control Period ◽  
Physiological Effects ◽  
Carbon Dioxide Gas ◽  
Normal Configuration ◽  
Anesthetized Dogs

Carbon dioxide gas is well tolerated when introduced directly into coronary arteries of anesthetized dogs. There were no fatalities in either normal or freshly infarcted hearts. Intracoronary carbon dioxide gas produced no persisting changes in the electrocardiogram or in blood pressure when injected slowly. Rapid injections under pressure produced extrasystoles at the time of injection and caused some subsequent changes of short duration in the electrocardiogram. These short duration changes were alterations of S-T segment deviations (which purposely had been produced previously in the control period) toward a more normal configuration. During this same period of time coupled extrasystoles produced in the control period were suppressed.

Ventilatory response to fixed acid evaluated by ‘iso-Pco2’ technique

1959 ◽  
Vol 14 (4) ◽  
pp. 557-561 ◽  
Author(s):  
Dario B. Domizi ◽  
John F. Perkins ◽  
Joan S. Byrne
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Carbon Dioxide Tension ◽  
Ion Concentration ◽  
Hydrogen Ion Concentration ◽  
Control Value ◽  
Anesthetized Dogs ◽  
Increased Sensitivity ◽  
Small Increments ◽  
Fixed Acid

In order to avoid changes in a second stimulus to ventilation, i.e. carbon dioxide, while measuring the response to fixed acid, a technique was utilized whereby alveolar carbon dioxide tension (PaCOCO2) could be held constant. This technique includes continuous recording of PaCOCO2 with an infrared type analyzer and addition of sufficient CO2 to the inspired air to keep PaCOCO2 at its control value (near 40 mm Hg). The response of anesthetized dogs to infusion of 0.5 m HCl was measured when the PaCOCO2 was held at the control value and also at various other levels. Other experiments measured the effect of CO2 when it was not allowed to change arterial hydrogen ion concentration [H+]. It was found that both these substances are potent respiratory stimuli and that their effects may be considered essentially separate and additive, as suggested by Gray. The experiments also demonstrated a slightly increased sensitivity to CO2 at increased arterial [H+], but this effect was not found necessary to explain the response to acid. Responses to successive small increments in PaCOCO2 failed to reveal any ‘threshold,’ even with CO2 tensions as low as 15 mm during acidosis. Submitted on December 29, 1958

scholarly journals Transcutaneous oxygen and carbon dioxide monitoring in anesthetized dogs.

1989 ◽  
Vol 20 (1/2) ◽  
pp. 9-11
Author(s):  
Hideki TABARU ◽  
Hitoshi WATANABE ◽  
Jun-ichi NAGAMATSU ◽  
Mikio TANAKA ◽  
Sanenori NAKAMA
Keyword(s):  
Carbon Dioxide ◽  
Transcutaneous Oxygen ◽  
Anesthetized Dogs ◽  
Carbon Dioxide Monitoring

Renal handling of exogenous and metabolic carbon dioxide

1964 ◽  
Vol 206 (2) ◽  
pp. 362-368 ◽  
Author(s):  
Francis P. Chinard ◽  
Mary F. Nolan ◽  
Theodore Enns
Keyword(s):  
Carbon Dioxide ◽  
Carbonic Anhydrase ◽  
Renal Handling ◽  
Dissolved Carbon ◽  
Multiple Indicator Dilution ◽  
Excretion Pattern ◽  
Dissolved Carbon Dioxide ◽  
Early Peak ◽  
Anesthetized Dogs ◽  
Multiple Indicator

The multiple-indicator-dilution technique has been applied to a study of the permeability of proximal and distal portions of the nephrons to dissolved carbon dioxide and bicarbonate ion in anesthetized dogs. Under control conditions with mannitol loading, the excreted carbon dioxide appears considerably earlier than the simultaneously injected creatinine whether dissolved CO2 or bicarbonate ion is injected. After inhibition of carbonic anhydrase by acetazolamide, there is relatively little effect on the excretion pattern of dissolved CO2. However, the excretion pattern of bicarbonate ion becomes nearly parallel to that of creatinine: the early peak disappears. On the basis of these results, it is concluded that the distal portions of the nephrons are permeable to dissolved CO2 but impermeable to bicarbonate ion and that, under control conditions, carbonic anhydrase serves to establish a catalytically mediated diffusion exchange for the transfer of CO2 derived from bicarbonate ion. Similar conclusions may apply to the proximal portions of the nephrons. On taking into account other data, it appears that the collecting ducts are impermeable to dissolved carbon dioxide. Carbon dioxide produced by decarboxylation of pyruvate has excretion patterns similar to those obtained for dissolved carbon dioxide. It is concluded that the decarboxylation product is dissolved CO2 and not bicarbonate ion.

Effect of hypoglycemia on cerebral metabolism and carbon dioxide responsivity

1989 ◽  
Vol 256 (3) ◽  
pp. H697-H706 ◽  
Author(s):  
F. E. Sieber ◽  
S. A. Derrer ◽  
C. D. Saudek ◽  
R. J. Traystman
Keyword(s):  
Carbon Dioxide ◽  
Cerebral Metabolism ◽  
Carbon Dioxide Tension ◽  
Cerebrovascular Reactivity ◽  
Cerebral Oxygen ◽  
Cerebral Vasoconstriction ◽  
Sagittal Sinus ◽  
Cerebral Metabolites ◽  
Anesthetized Dogs ◽  
Beta Hydroxybutyrate

This study examined the effects of hypoglycemia (HG) on cerebral metabolism and cerebrovascular reactivity to carbon dioxide. Cerebral blood flow (CBF) was determined using radiolabeled microspheres in pentobarbital-anesthetized dogs. Cerebral oxygen, glucose, lactate, pyruvate, acetoacetate, and beta-hydroxybutyrate uptakes were calculated using the respective concentrations measured in arterial and sagittal sinus blood samples. EEG was recorded throughout each experiment. HG was induced with insulin to obtain a blood glucose less than 30 mg/100 ml. Hypercapnia was studied in 10 animals (3 control, 7 HG) by increasing arterial carbon dioxide tension (PaCO2) from control (35 +/- 4; mean +/- SE) to 54 +/- 2 Torr during normoglycemia (NG) and HG. Hypocapnia was studied in 11 animals (3 control, 8 HG) by decreasing PaCO2 from control (39 +/- 1) to 14 +/- 1 Torr in NG and HG. Measurements were taken after reaching steady-state PaCO2 in both groups at each control and altered PaCO2 state. In the hypercapnic group, glucose decreased from 71 +/- 3 to 28 +/- 3 mg/100 ml. CBF increased with hypercapnia to 175% of control in both NG and HG. Cerebral metabolic rate of oxygen and electroencephalogram (EEG) did not change in the hypercapnic group. In the hypocapnic group glucose decreased from 71 +/- 3 to 19 +/- 2 mg/100 ml. CBF decreased with hypocapnia to 62 +/- 5% of control in NG but remained at control in HG. This was not accompanied by changes in cerebral oxygen consumption; however, a flat EEG occurred in all HG hypocapnic animals. No change occurred in uptake of the other cerebral metabolites measured in any group. This study shows that the CBF hypercapnic response remains intact during HG; however, hypocapnia causes severe EEG disturbances and impairs the cerebral vasoconstriction response.

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