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

1965 ◽  
Vol 209 (3) ◽  
pp. 604-610 ◽  
Author(s):  
Stephen M. Cain

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.

1979 ◽  
Vol 80 (1) ◽  
pp. 271-285 ◽  
Author(s):  
B. R. McMAHON ◽  
D. G. McDONALD ◽  
C. M. WOOD

Scaphognathite and heart-pumping frequencies, ventilation volume, cardiac output, oxygen uptake and oxygen transport by haemolymph have been studied in unrestrained Dungeness crabs (Cancer magister) before, immediately after, and during recovery from 20 min of enforced exhausting activity. Exercise increased oxygen uptake 4-fold. This increase was achieved by more than 2-fold elevation of both ventilation volume and cardiac output and by greater participation of haemocyanin in oxygen delivery. The elevated ventilation volume resulted entirely from an increase in scaphognathite pumping frequency, while the rise in cardiac output resulted largely from increase in stroke volume. Prior to exercise haemocyanin accounts for less than 50% of the oxygen delivered to the tissues. Following exercise this increases to over 80%, the additional oxygen release being mediated by a depression of prebranchial oxygen tension and a substantial Bohr effect resulting from build up of lactate ion in the haemolymph and subsequent fall in pH. These changes allowed % oxygen extraction from branchial water to be maintained at 28% despite a 2-fold increase in ventilation volume, and allowed an increase in %. oxygen extraction by the tissues. Despite these changes oxygen supply fell below demand during exercise, and considerable anaerobic metabolism resulted, as evidenced by a 9-fold increase in haemolymph lactate concentration. The resulting oxygen debt required 8–24 h for repayment. Aerobic metabolic scope, and mechanisms of increasing oxygen uptake and transport in this crab are compared with those of a range of fish species.


Author(s):  
William J.M. Kinnear ◽  
James H. Hull

This chapter outlines how dividing the volume of oxygen uptake (VO2) by the pulse rate gives an estimate of the stroke volume of the heart. The amount of oxygen taken up with each heartbeat is called the oxygen pulse (O2 pulse). It should increase steadily on exercise to a value above 10 ml/beat and may continue to rise during the recovery phase. A low O2 pulse can be an indicator of low cardiac output. If the maximum VO2 (VO2max) is normal, caution should be used in the interpretation of a low O2 pulse. Sometimes the O2 pulse is abnormal because of a fall in peripheral arterial oxygen saturation (SpO2) or mixed venous oxygen levels.


1981 ◽  
Vol 51 (5) ◽  
pp. 1103-1107 ◽  
Author(s):  
P. W. Jones ◽  
W. French ◽  
M. L. Weissman ◽  
K. Wasserman

Cardiac output changes were induced by step changes of heart rate (HR) in six patients with cardiac pacemakers during monitoring of ventilation and gas exchange, breath-by-breath. Mean low HR was 48 beats/min; mean high HR was 82 beats/min. The change of oxygen uptake immediately after the HR change was used as an index of altered cardiac output. After HR increase, oxygen uptake (V02) rose by 34 +/- 20% (SD), and after HR decrease, Vo2 fell by 24 +/- 11%. There was no change in arterial blood pressure. After HR increase, ventilation increased, after a mean delay of 19 +/- 4 s; after HR reduction, ventilation fell, after a mean delay of 29 +/- 7 s. In the period between HR increase and the resulting increase in ventilation, end-tidal PCO2 (PETCO2) rose by 2.6 +/- 2.0 Torr, and in the period between HR decreases and the fall in ventilation, PETCO2 dropped by 2.9 +/- 2.2 Torr. The response time and end-tidal gas tension changes implicate the chemoreceptors in the reflex correction of blood gas disturbances that may result from imbalances between cardiac output and ventilation.


1977 ◽  
Vol 42 (3) ◽  
pp. 403-407 ◽  
Author(s):  
J. A. Wagner ◽  
S. M. Horvath ◽  
T. E. Dahms

Cardiovascular and metabolic parameters were studied in dogs anesthetized with pentobarbital sodium, and while awake resting or exercising for 30 min at either 6.4 km/h, 10% grade (32% VO2 max) or 8.0 km/h, 16% grade (50% VO2 max). The anesthetized dogs had lower cardiac outputs, stroke volumes, arterial-mixed venous oxygen differences, oxygen uptakes, rectal temperatures, and higher diastolic and mean arterial pressures than awake resting dogs. Heart rates and arterial systolic pressures were similar in the two conditions. The increased oxygen uptakes during exercise were associated with approximately equal percentage increments in cardiac outputs and oxygen extractions. Cardiac output increases during exercise were largely due to increases in heart rates. Arterial CO2 tension and CO2 contents as well as venous O2 and CO2 gas tensions and contents declined, and pH and rectal temperatures increased during exercise. The dogs became alkalotic during exercise. Elevated central body temperatures appeared to be the major factor controlling respiration.


1981 ◽  
Vol 240 (1) ◽  
pp. R99-R105 ◽  
Author(s):  
P. S. Rutledge

Heart and ventilation frequencies, oxygen uptake rate, hemocyanin concentration, and pre- and postbranchial PO2 and pH were measured in unrestrained crayfish (Pacifastacus leniuculus) immediately following routine and forced (maximum) activity. Experiments were performed at 20 degrees C, the temperature of maximum scope for activity in this species, and at 10 and 25 degrees C. A procedure for using N-ethylmaleimide as an anticoagulant in hemolymph sampling is described. Hemocyanin oxygen saturation, oxygen content of pre- and postbranchial hemolymph, cardiac output, and stroke volume were estimated from the measured parameters. PO2 of postbranchial hemolymph sampled immediately after routine activity was low (9-12 Torr), accompanied by hemocyanin oxygen saturations of 55-75%. Maximum forced activity for 10 min caused further reduction in these values. Thus hemocyanin is apparently not usually saturated with oxygen in these crayfish. Cardiac output, as estimated by the Fick principle, was high (at 20 degrees C, 236 ml x kg-1 x min-1 for routine activity and 969 ml x kg-1 x min-1 for forced activity). Evidence is presented that ventilation, rather than circulation, limits active oxygen uptake and scope for activity both above and below 20 degrees C.


1961 ◽  
Vol 16 (2) ◽  
pp. 279-282 ◽  
Author(s):  
John T. Reeves ◽  
Robert F. Grover ◽  
Giles F. Filley ◽  
S. Gilbert Blount

Cardiac output and femoral A-V oxygen difference were measured in each of seven normal men at rest and during several stints of supine exercise to investigate the mechanisms of oxygen transport for stepwise increments of oxygen uptake. The femoral A-V oxygen difference increased sharply for mild exercise and showed smaller further increase for heavier exercise stints. The pulmonary A-V oxygen difference followed a similar behavior where the changes were of smaller magnitude. For mild exercise, increasing oxygen transport apparently depends to a greater extent on increasing femoral tissue oxygen extraction and to a lesser extent on increased femoral and total blood flow. For heavier exertion, increasing oxygen transport depends to a greater extent on increasing flow and to a smaller extent on a widening tissue oxygen extraction. Mechanisms which are utilized to meet the increased metabolic demands of exercise depend in part upon the severity of the exertion. Cardiac output appears not to be a simple linear function of oxygen uptake for various metabolic demands ranging from rest to heavy exercise. Submitted on August 8, 1960


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