Temperature-induced changes in blood acid-base status in the alligator, Alligator mississipiensis

1978 ◽  
Vol 45 (6) ◽  
pp. 922-926 ◽  
Author(s):  
D. G. Davies
Keyword(s):  
Carbon Dioxide ◽  
Body Temperature ◽  
Minute Ventilation ◽  
Carbon Dioxide Production ◽  
Carbon Dioxide Partial Pressure ◽  
Acid Base ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Body Temperature Increase ◽  
Alligator Mississipiensis

Gas exchange and arterial blood acid-base status were measured in 13 conscious alligators, Alligator mississipiensis, at 15, 25, and 35 degrees C. Arterial pH decreased by 0.250 units (from 7.635 to 7.385) and arterial carbon dioxide partial pressure increased by 11.4 Torr (from 11.8 to 23.2) as body temperature increased from 15 to 35 degrees C. No statistically significant changes occurred in arterial bicarbonate concentration. When OH-/H+ and alpha-imidazole were compared at each temperature, more variability was observed in OH-/H+, which increased from 8.7 to 12.0 as temperature increased from 15 to 35 degrees C. alpha-Imidazole remained essentially constant (0.76 at 15 degrees C and 0.80 at 35 degrees C). Body temperature increase caused marked increases in minute ventilation (VE), oxygen consumption (VO2), and carbon dioxide production (VCO2). The relative changes in these parameters resulted in a decrease in both VE/VO2 and VE/VCO2. The data of the present study are consistent with the concept that poikilotherms regulate their alveolar ventilation with changes in body temperature in order to keep OH-/H+ or alpha-imidazole constant.

Relative effects of carbonic anhydrase infusion or inhibition on carbon dioxide transport and acid-base status in the sea lamprey Petromyzon marinus following exercise

1996 ◽  
Vol 199 (4) ◽  
pp. 933-940
Author(s):  
B Tufts ◽  
S Currie ◽  
J Kieffer
Keyword(s):  
Carbon Dioxide ◽  
Carbonic Anhydrase ◽  
Venous Blood ◽  
Extracellular Fluid ◽  
Respiratory Acidosis ◽  
Acid Base ◽  
Carbon Dioxide Transport ◽  
Co2 Transport ◽  
Arterial Blood ◽  
Acid Base Status

In vivo experiments were carried out to determine the relative effects of carbonic anhydrase (CA) infusion or inhibition on carbon dioxide (CO2) transport and acid-base status in the arterial and venous blood of sea lampreys recovering from exhaustive exercise. Infusion of CA into the extracellular fluid did not significantly affect CO2 transport or acid-base status in exercised lampreys. In contrast, infusion of the CA inhibitor acetazolamide resulted in a respiratory acidosis in the blood of recovering lampreys. In acetazolamide-treated lampreys, the post-exercise extracellular pH (pHe) of arterial blood was significantly lower than that in the saline-infused (control) lampreys. The calculated arterial and venous partial pressure of carbon dioxide (PCO2) and the total CO2 concentration in whole blood (CCO2wb) and red blood cells (CCO2rbc) during recovery in the acetazolamide-infused lampreys were also significantly greater than those values in the saline-infused control lampreys. These results suggest that the CO2 reactions in the extracellular compartment of lampreys may already be in equilibrium and that the access of plasma bicarbonate to CA is probably not the sole factor limiting CO2 transport in these animals. Furthermore, endogenous red blood cell CA clearly has an important role in CO2 transport in exercising lampreys.

Effect of body temperature on ventilatory control in the alligator

1982 ◽  
Vol 52 (1) ◽  
pp. 114-118 ◽  
Author(s):  
D. G. Davies ◽  
J. L. Thomas ◽  
E. N. Smith
Keyword(s):  
Body Temperature ◽  
Pulmonary Ventilation ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Base Balance ◽  
Alligator Mississipiensis ◽  
Induced Changes

Pulmonary ventilation and arterial blood acid-base balance were measured in six unanesthetized alligators, Alligator mississipiensis, at 15, 25, and 35 degree C. The animals exhibited pronounced ventilatory responses to hypercapnia at all temperatures studied. Arterial PCO2 increased and pH decreased with increases in body temperature during both normocapnia and hypercapnia. The fractional dissociation of imidazole (alpha Pr) remained constant with changes in body temperature during normocapnia, but increased with temperature during hypercapnia. Ventilatory sensitivity, defined as delta (VE/VO2/delta (alpha Pr), was independent of body temperature. We conclude that the control of breathing in the alligator is a physiological defense of alpha Pr and that ventilatory responses occur following nontemperature-induced changes in blood acid-base balance, which tend to return alpha Pr to a normal value.

Mixed-effects Modeling of the Intrinsic Ventilatory Depressant Potency of Propofol in the Non-steady State

2004 ◽  
Vol 100 (2) ◽  
pp. 240-250 ◽  
Author(s):  
Thomas Bouillon ◽  
Joergen Bruhn ◽  
Lucian Radu-Radulescu ◽  
Corina Andresen ◽  
Carol Cohane ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Time Course ◽  
Minute Ventilation ◽  
Carbon Dioxide Production ◽  
Response Model ◽  
Indirect Response Model ◽  
Indirect Response ◽  
Arterial Blood ◽  
Ventilatory Depression

Background Despite the ubiquitous use of propofol for anesthesia and conscious sedation and numerous publications about its effect, a pharmacodynamic model for propofol-induced ventilatory depression in the non-steady state has not been described. To investigate propofol-induced ventilatory depression in the clinically important range (at and below the metabolic hyperbola while carbon dioxide is accumulating because of drug-induced ventilatory depression), the authors applied indirect effect modeling to Paco2 data at a fraction of inspired carbon dioxide of 0 during and after administration of propofol. Methods Ten volunteers underwent determination of their carbon dioxide responsiveness by a rebreathing design. The parameters of a power function were fitted to the end-expiratory carbon dioxide and minute ventilation data. The volunteers then received propofol in a stepwise ascending pattern with use of a target-controlled infusion pump until significant ventilatory depression occurred (end-tidal pressure of carbon dioxide > 65 mmHg and/or imminent apnea). Thereafter, the concentration was reduced to 1 microg/ml. Propofol pharmacokinetics and the Paco2 were determined from frequent arterial blood samples. An indirect response model with Bayesian estimates of the pharmacokinetics and carbon dioxide responsiveness in the absence of drug was used to describe the Paco2 time course. Because propofol reduces oxygen requirements and carbon dioxide production, a correction factor for propofol-induced decreasing of carbon dioxide production was included. Results The following pharmacodynamic parameters were found to describe the time course of hypercapnia after administration of propofol (population mean and interindividual variability expressed as coefficients of variation): F (gain of the carbon dioxide response), 4.37 +/- 36.7%; ke0, CO2, 0.95 min-1 +/- 59.8%; baseline Paco2, 40.9 mmHg +/- 12.8%; baseline minute ventilation, 6.45 l/min +/- 36.3%; kel, CO2, 0.11 min-1 +/- 34.2%; C50,propofol, 1.33 microg/ml +/- 49.6%; gamma, 1.68 +/- 21.3%. Conclusion Propofol at common clinical concentrations is a potent ventilatory depressant. An indirect response model accurately described the magnitude and time course of propofol-induced ventilatory depression. The indirect response model can be used to optimize propofol administration to reduce the risk of significant ventilatory depression.

scholarly journals Contrast‐enhanced ultrasound imaging can be used to evaluate fetal cerebral perfusion: potential implications for fetal surgery

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Kendall M. Lawrence ◽  
Barbara E. Coons ◽  
Anush Sridharan ◽  
Avery C. Rossidis ◽  
Marcus G. Davey ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Cerebral Perfusion ◽  
Fetal Surgery ◽  
Time Dependent ◽  
Contrast Enhanced Ultrasound ◽  
Acid Base ◽  
Fetal Sheep ◽  
Contrast Enhanced ◽  
Support Device ◽  
Acid Base Status

Abstract Background Fetal surgery is increasingly performed to correct congenital defects. Currently, fetal brain perfusion cannot be assessed intra-operatively. The purpose of this study was to determine if contrast-enhanced ultrasound (CEUS) could be used to monitor fetal cerebral perfusion during fetal surgery and if parameters correlate with fetal hemodynamics or acid/base status. Methods Cannulated fetal sheep were insufflated with carbon dioxide gas in an extra-uterine support device and in utero to mimic fetal surgery. Fetal heart rate, mean arterial pressure, and arterial blood gases were serially measured. CEUS examinations of the brain were performed and time-dependent metrics were quantified to evaluate perfusion. The relationships between measured parameters were determined with mixed linear effects models or two-way repeated measures analysis of variance. Results 6 fetal sheep (113 ± 5 days) insufflated at multiple time-points (n = 20 experiments) in an extra-uterine support device demonstrated significant correlations between time-dependent perfusion parameters and fetal pH and carbon dioxide levels. In utero, 4 insufflated fetuses (105 ± 1 days) developed hypercarbic acidosis and had reductions in cerebral perfusion parameters compared to age-matched controls (n = 3). There was no significant relationship between cerebral perfusion parameters and fetal hemodynamics. Conclusions CEUS-derived cerebral perfusion parameters can be measured during simulated fetal surgery and strongly correlate with fetal acid/base status.

Cardiovascular and metabolic responses to temperature in Coluber constrictor

1987 ◽  
Vol 253 (2) ◽  
pp. R222-R227 ◽  
Author(s):  
J. N. Stinner
Keyword(s):  
Blood Pressure ◽  
Body Temperature ◽  
Stroke Volume ◽  
Minute Ventilation ◽  
Marked Change ◽  
Effect Of Temperature ◽  
Metabolic Demand ◽  
Thermal Dependence ◽  
Arterial Blood ◽  
Coluber Constrictor

The cardiovascular adjustments associated with elevated metabolic demand caused by rising body temperature were investigated in Coluber constrictor. From 16 to 35 degrees C, O2 consumption increased roughly ninefold. Systemic blood flow, determined by the Fick method, increased approximately 4.5-fold and arteriovenous O2 difference increased approximately 2-fold. Heart rate steadily increased over the temperature range examined. At the cooler temperatures stroke volume also increased but, above approximately 25 degrees C, stroke volume declined with rising temperature. The changes in stroke volume may result from the direct effect of temperature on myocardial contractility. The thermal dependence of blood convection requirement in C. constrictor is similar to changes in air convection requirement determined in a previous study. Consequently the minute ventilation-to-perfusion ratio appears to be independent of temperature, at least from 20 to 35 degrees C. Systemic arterial blood pressure increases with rising body temperature due to the rise in cardiac output, whereas vascular resistance declines. Blood pressure in snakes disturbed by the investigator is roughly two times higher than in resting animals at all temperatures studied. This marked change in blood pressure suggests an "alarm reaction" mediated by the sympathetic nervous system.

scholarly journals Hyperlactacemia in critically ill children: comparison of traditional and Fencl-Stewart methods

2007 ◽  
Vol 47 (1) ◽  
pp. 35
Author(s):  
Hari Kushartono ◽  
Antonius H. Pudjiadi ◽  
Susetyo Harry Purwanto ◽  
Imral Chair ◽  
Darlan Darwis ◽  
...  
Keyword(s):  
Base Excess ◽  
Pediatric Intensive Care ◽  
Blood Gases ◽  
Critically Ill Children ◽  
Strongly Correlated ◽  
Acid Base ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Lactate Levels ◽  
Elevated Lactate

Background Base excess is a single variable used to quantifymetabolic component of acid base status. Several researches havecombined the traditional base excess method with the Stewartmethod for acid base physiology called as Fencl-Stewart method.Objective The purpose of the study was to compare two differentmethods in identifying hyperlactacemia in pediatric patients withcritical illness.Methods The study was performed on 43 patients admitted tothe pediatric intensive care unit of Cipto MangunkusumoHospital, Jakarta. Sodium, potassium, chloride, albumin, lactateand arterial blood gases were measured. All samples were takenfrom artery of all patients. Lactate level of >2 mEq/L was definedas abnormal. Standard base excess (SBE) was calculated fromthe standard bicarbonate derived from Henderson-Hasselbalchequation and reported on the blood gas analyzer. Base excessunmeasured anions (BE UA ) was calculated using the Fencl-Stewartmethod simplified by Story (2003). Correlation between lactatelevels in traditional and Fencl-Stewart methods were measuredby Pearson’s correlation coefficient .Results Elevated lactate levels were found in 24 (55.8%) patients.Lactate levels was more strongly correlated with BE UA (r = - 0.742,P<0.01) than with SBE (r = - 0.516, P<0.01).Conclusion Fencl-Stewart method is better than traditionalmethod in identifying patients with elevated lactate levels, so theFencl-Stewart method is suggested to use in clinical practice.

Studies on the Pathophysiology of Encephalopathy in Reye's Syndrome: Hyperammonemia in Reye's Syndrome

PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 999-1004
Author(s):  
Daniel C. Shannon ◽  
Robert De Long ◽  
Barry Bercu ◽  
Thomas Glick ◽  
John T. Herrin ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Venous Drainage ◽  
Respiratory Alkalosis ◽  
Ammonia Concentration ◽  
Reye's Syndrome ◽  
Acid Base ◽  
Arterial Blood ◽  
Cerebral Venous Drainage ◽  
Acid Base Status ◽  
The Brain

The initial acid-base status of eight survivors of Reye's syndrome was characterized by acute respiratory alkalosis (Pco2=32 mm Hg; Hco3-= 22.0 mEq/liter) while that of eight children who died was associated with metabolic acidosis as well (HCO3-=10.0 mEq/liter). Arterialinternal jugular venous ammonia concentration differences on day 1 (299 mg/100 ml) and day 2 (90 mg/ 100 ml) reflected cerebral uptake of ammonia while those on days 3 and 4 (-43 and -55 mg/100 ml) demonstrated cerebral release. Arterial blood hyperammonemia can be detoxified safely in the brain as long as the levels do not exceed approximately 300µg/100 ml. Beyond that level lactic acidosis is observed, particularly in cerebral venous drainage. Arterial blood hyperammonemia was also related to the extent of alveolar hyperventilation. These findings are very similar to those seen in experimental hyperammonemia and support the concept that neurotoxicity in children with Reye's syndrome is at least partly due to impaired oxidative metabolism secondary to hyperammonemia.

Ventilatory and blood acid-base adjustments to a decrease in body temperature from 30 to 10YC in black racer snakes Coluber constrictor

1996 ◽  
Vol 199 (4) ◽  
pp. 815-823
Author(s):  
J Stinner ◽  
M Grguric ◽  
S Beaty
Keyword(s):  
Steady State ◽  
Body Temperature ◽  
Minute Ventilation ◽  
Co2 Production ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Slow Increase ◽  
Coluber Constrictor ◽  
Steady State Levels ◽  
Time Required

There is increasing evidence that many amphibian and reptilian species use relatively slow ion-exchange mechanisms in addition to ventilation to adjust pH as body temperature changes. Large changes in blood bicarbonate concentration with changes in temperature have previously been reported for the snake Coluber constrictor. The purpose of the present study was to determine the ventilatory and pH adjustments associated with the increase in CO2 stores when the snakes are cooled. Body temperature was lowered from 30 to 10 &deg;C within 4 h, at which time measurements of inspired minute ventilation (V.air), O2 consumption (VO2) and CO2 production (V.CO2) were started and continued for 56 h. The decrease in temperature produced a transient fall in the respiratory exchange ratio (V.CO2/VO2) to 0.2-0.3 and a steady-state value of 0.65&plusmn;0.14 (mean &plusmn; s.d., N=7) was not achieved until about 35 h. There were concomitant transient reductions in V.air and V.air/V.O2. However, V.air/V.CO2 initially increased, with a corresponding reduction in arterial PCO2 (PaCO2) and increase in arterial pH. By 35 h, V.air/V.CO2 had decreased and PaCO2 had increased to steady-state levels, but pH decreased very little because of a gradual increase in bicarbonate concentration. We conclude that the drop in temperature imposed a metabolic acidosis for approximately 35 h because of the time required to increase bicarbonate concentration, and that the acidosis was compensated for by an elevated V.air/V.CO2. Steady-state breathing and acid-base status were not achieved until the relatively slow increase in CO2 stores had been completed.

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