Influence of vagal blockade on respiratory and circulatory functions in hypothermic dogs

1962 ◽  
Vol 17 (5) ◽  
pp. 833-836 ◽  
Author(s):  
John Salzano ◽  
F. G. Hall
Keyword(s):  
Cardiac Output ◽  
Body Temperature ◽  
Dead Space ◽  
Alveolar Ventilation ◽  
Normal Body Temperature ◽  
Vagal Blockade ◽  
Physiologic Dead Space ◽  
Anesthetized Dogs ◽  
Output Ratio ◽  
Carbon Dioxide Pressure

Anatomical and physiological dead spaces were enlarged as a result of reduction in body temperature to 28 C in spontaneously respiring anesthetized dogs. Respiratory dead space at 32 C was not significantly different from that at normal body temperature. Vagal blockade resulted in an increase in tidal volume and decrease in respiratory frequency and increased anatomic and physiologic dead space at normal and reduced temperatures. Alveolar ventilation and cardiac output declined equally (percentagewise) with reduction in body temperature to 32 C; at 28 C alveolar ventilation fell more precipitously so that alveolar ventilation-cardiac output ratio (ventilation-perfusion) at 28 C was approximately one-half that at 37 and 32 C. Arterial-alveolar carbon dioxide pressure differences were independent of temperature and vagal blockade. The results indicate no impairment of gas transport or gas exchange at 32 or 28 C in spontaneously respiring anesthetized dogs. Submitted on January 11, 1962

Dead space ventilation promotes alveolar hypocapnia reducing surfactant secretion by altering mitochondrial function

Thorax ◽  
2019 ◽  
Vol 74 (3) ◽  
pp. 219-228 ◽  
Author(s):  
Martina Kiefmann ◽  
Sascha Tank ◽  
Marc-Oliver Tritt ◽  
Paula Keller ◽  
Kai Heckel ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Dead Space ◽  
Lung Compliance ◽  
Alveolar Ventilation ◽  
Alveolar Epithelial Cells ◽  
Perfusion Failure ◽  
Physiologic Dead Space ◽  
Surfactant Secretion ◽  
Dead Space Ventilation

BackgroundIn acute respiratory distress syndrome (ARDS), pulmonary perfusion failure increases physiologic dead space ventilation (VD/VT), leading to a decline of the alveolar CO2 concentration [CO2]iA. Although it has been shown that alveolar hypocapnia contributes to formation of atelectasis and surfactant depletion, a typical complication in ARDS, the underlying mechanism has not been elucidated so far.MethodsIn isolated perfused rat lungs, cytosolic or mitochondrial Ca2+ concentrations ([Ca2+]cyt or [Ca2+]mito, respectively) of alveolar epithelial cells (AECs), surfactant secretion and the projected area of alveoli were quantified by real-time fluorescence or bright-field imaging (n=3–7 per group). In ventilated White New Zealand rabbits, the left pulmonary artery was ligated and the size of subpleural alveoli was measured by intravital microscopy (n=4 per group). Surfactant secretion was determined in the bronchoalveolar lavage (BAL) by western blot.ResultsLow [CO2]iA decreased [Ca2+]cyt and increased [Ca2+]mito in AECs, leading to reduction of Ca2+-dependent surfactant secretion, and alveolar ventilation in situ. Mitochondrial inhibition by ruthenium red or rotenone blocked these responses indicating that mitochondria are key players in CO2 sensing. Furthermore, ligature of the pulmonary artery of rabbits decreased alveolar ventilation, surfactant secretion and lung compliance in vivo. Addition of 5% CO2 to the inspiratory gas inhibited these responses.ConclusionsAccordingly, we provide evidence that alveolar hypocapnia leads to a Ca2+ shift from the cytosol into mitochondria. The subsequent decline of [Ca2+]cyt reduces surfactant secretion and thus regional ventilation in lung regions with high VD/VT. Additionally, the regional hypoventilation provoked by perfusion failure can be inhibited by inspiratory CO2 application.

Chronotropic response to intravenous infusion in the anesthetized dog

1963 ◽  
Vol 204 (3) ◽  
pp. 423-426 ◽  
Author(s):  
Gulzar Ahmad ◽  
Paul A. Nicoll
Keyword(s):  
Heart Rate ◽  
Body Temperature ◽  
Jugular Vein ◽  
Normal Body Temperature ◽  
Chronotropic Response ◽  
Negative Results ◽  
Intravenous Saline ◽  
Anesthetized Dogs ◽  
Flow Through ◽  
Normothermic Group

Ninety-four anesthetized dogs at normal body temperature received 293 intravenous saline infusions by gravity flow through either a femoral or jugular vein. Also nine dogs with body temperature lowered to 27 C received 30 similar infusions. Heart rate and blood pressure were monitored by transducer and oscillographic recording. The chronotropic response of the normothermic group varied with the preinfusion heart rate, with those below 140/min generally showing increases and those above showing no response or a decrease. Negative results with hypothermic animals also having slow preinfusion rates indicate the Bainbridge effect requires the slow preinfusion heart rate to be under vagal inhibition.

Unanesthetized dogs with increased respiratory dead space

1960 ◽  
Vol 15 (5) ◽  
pp. 838-842 ◽  
Author(s):  
Thomas B. Barnett ◽  
Richard M. Peters
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Dead Space ◽  
Minute Volume ◽  
Alveolar Ventilation ◽  
Physiologic Dead Space ◽  
Consistent Change ◽  
The Dead ◽  
Animal Preparation ◽  
Respiratory Dead Space

A method is described for maintaining a permanent tracheostomy in dogs. This animal preparation has been used to study the effects of artificially increased respiratory dead space. Trained dogs with tracheostomies have made possible measurements of ventilation without anesthesia. It has been found that additions to the respiratory dead space in the form of tubing of frac34 in. i.d. result in an increase in physiologic dead space of the same magnitude as the volume of tubing added. Increasing the dead space in this manner resulted in an increased minute volume which was accomplished principally by an increase in tidal volume without a significant or consistent change in respiratory rate. Alveolar ventilation remained unchanged even with large additions to the dead space (20–30 cc/kg of animal wt.). Arterial pCO2 was significantly higher in these animals than in the controls. The CO2 tension was similarly elevated when extra dead space of lesser volume (5–20 cc/kg) was allowed to remain on the dogs for more than 48 hours. Submitted on April 13, 1960

scholarly journals Human thermoregulatory responses during serial cold-water immersions

1998 ◽  
Vol 85 (1) ◽  
pp. 204-209 ◽  
Author(s):  
John W. Castellani ◽  
Andrew J. Young ◽  
Michael N. Sawka ◽  
Kent B. Pandolf
Keyword(s):  
Body Temperature ◽  
Rectal Temperature ◽  
Heat Production ◽  
Alternative Explanation ◽  
Cold Water ◽  
Metabolic Heat Production ◽  
Normal Body Temperature ◽  
Repeat Trial ◽  
Metabolic Heat ◽  
Made In

This study examined whether serial cold-water immersions over a 10-h period would lead to fatigue of shivering and vasoconstriction. Eight men were immersed (2 h) in 20°C water three times (0700, 1100, and 1500) in 1 day (Repeat). This trial was compared with single immersions (Control) conducted at the same times of day. Before Repeat exposures at 1100 and 1500, rewarming was employed to standardize initial rectal temperature. The following observations were made in the Repeat relative to the Control trial: 1) rectal temperature was lower and heat debt was higher ( P < 0.05) at 1100; 2) metabolic heat production was lower ( P < 0.05) at 1100 and 1500; 3) subjects perceived the Repeat trial as warmer at 1100. These data suggest that repeated cold exposures may impair the ability to maintain normal body temperature because of a blunting of metabolic heat production, perhaps reflecting a fatigue mechanism. An alternative explanation is that shivering habituation develops rapidly during serially repeated cold exposures.

A New Equal Area Method to Calculate and Represent Physiologic, Anatomical, and Alveolar Dead Spaces

2006 ◽  
Vol 104 (4) ◽  
pp. 696-700 ◽  
Author(s):  
Yongquan Tang ◽  
Martin J. Turner ◽  
A Barry Baker
Keyword(s):  
Carbon Dioxide ◽  
Dead Space ◽  
Graphical Method ◽  
Mean Difference ◽  
Equal Area ◽  
Area Method ◽  
Physiologic Dead Space ◽  
Anatomical Dead Space ◽  
The Mean ◽  
The Difference

Background Physiologic dead space is usually estimated by the Bohr-Enghoff equation or the Fletcher method. Alveolar dead space is calculated as the difference between anatomical dead space estimated by the Fowler equal area method and physiologic dead space. This study introduces a graphical method that uses similar principles for measuring and displaying anatomical, physiologic, and alveolar dead spaces. Methods A new graphical equal area method for estimating physiologic dead space is derived. Physiologic dead spaces of 1,200 carbon dioxide expirograms obtained from 10 ventilated patients were calculated by the Bohr-Enghoff equation, the Fletcher area method, and the new graphical equal area method and were compared by Bland-Altman analysis. Dead space was varied by varying tidal volume, end-expiratory pressure, inspiratory-to-expiratory ratio, and inspiratory hold in each patient. Results The new graphical equal area method for calculating physiologic dead space is shown analytically to be identical to the Bohr-Enghoff calculation. The mean difference (limits of agreement) between the physiologic dead spaces calculated by the new equal area method and Bohr-Enghoff equation was -0.07 ml (-1.27 to 1.13 ml). The mean difference between new equal area method and the Fletcher area method was -0.09 ml (-1.52 to 1.34 ml). Conclusions The authors' equal area method for calculating, displaying, and visualizing physiologic dead space is easy to understand and yields the same results as the classic Bohr-Enghoff equation and Fletcher area method. All three dead spaces--physiologic, anatomical, and alveolar--together with their relations to expired volume, can be displayed conveniently on the x-axis of a carbon dioxide expirogram.

Comparison of cardiac output measurements using electrical velocimetry and lithium dilution with thermodilution in anesthetized dogs

2021 ◽  
Vol 48 (6) ◽  
pp. S997
Author(s):  
V. Paranjape ◽  
N. Henao-Guerrero ◽  
G. Menciotti ◽  
F. Garcia-Pereira ◽  
C. Ricco-Pereira
Keyword(s):  
Cardiac Output ◽  
Electrical Velocimetry ◽  
Anesthetized Dogs ◽  
Cardiac Output Measurements

Postural variations in dead space and CO2 gradients breathing air and O2

1962 ◽  
Vol 17 (3) ◽  
pp. 417-420 ◽  
Author(s):  
C. P. Larson ◽  
J. W. Severinghaus
Keyword(s):  
Dead Space ◽  
Normal Limit ◽  
Healthy Adult ◽  
Sitting Position ◽  
Alveolar Dead Space ◽  
Vascular Bed ◽  
Postural Changes ◽  
Physiologic Dead Space ◽  
Pulmonary Vascular Bed

Effects of postural changes on anatomic and physiologic dead space and arterial-alveolar CO2gradients were studied in 11 healthy, adult subjects breathing air and O2. Results indicate that, on moving from the supine to the sitting position, Vads and Vpds increased by corresponding amounts (42 and 37 ml) with no increase in alveolar dead space or volume of lung which is nonperfused. Arterial-alveolar CO2 gradients were unaffected by posture, but more than doubled with O2 breathing, suggesting that O2 may relax the pulmonary vascular bed and diminish perfusion of highest lung segments. Isoproterenol aerosol (0.5%) produced significant bronchodilatation (27 ml increase in Vads), but only small and inconsistent increases in alveolar dead space and CO2 gradients. The PDS/Vt ratio in these subjects while sitting, breathing air, averaged 31 ± 6%, which is higher than the normally accepted value of 30%. As a result, the upper normal limit for PDS/Vt has been increased to 40% in our laboratories. Submitted on January 22, 1962

Appearance of excess lactate in anesthetized dogs during anemic and hypoxic hypoxia

1965 ◽  
Vol 209 (3) ◽  
pp. 604-610 ◽  
Author(s):  
Stephen M. Cain
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Oxygen Transport ◽  
Liver Dysfunction ◽  
Hypoxic Hypoxia ◽  
Blood Gas ◽  
Total Oxygen ◽  
Anesthetized Dogs ◽  
Lactate And Pyruvate ◽  
Mixed Venous

Ten anesthetized, splenectomized dogs were made progressively anemic by replacement of blood with warmed dextran to approximate hematocrits of 30, 20, 15, and 10%. A second group of 10 dogs was made progressively hypoxic by having them inspire 11.4, 9.5, 8.0, and 5.9% O2 in N2. Blood gas contents, pH, and gas tensions were measured in arterial and mixed venous bloods. Cardiac output was calculated from the arteriovenous O2 difference and the O2 uptake. Excess lactate was calculated from measured levels of lactate and pyruvate in blood water. Excess lactate appeared at higher mixed venous Po2 in anemic animals than in hypoxic, 40 mm Hg versus 20 mm Hg. When related to total oxygen transport, however, excess lactate appeared at about the same point (12 ml/kg per min) in both groups. Because liver has been shown to reduce its oxygen uptake with any lowering of perfusate oxygen content, it was suggested that the excess lactate measured during both anemic and hypoxic hypoxia in anesthetized dogs is largely the result of liver dysfunction with respect to lactate.

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