Effects of feeding on arterial blood gases in the American alligator Alligator mississippiensis

2000 ◽  
Vol 203 (20) ◽  
pp. 3117-3124 ◽  
Author(s):  
M. Busk ◽  
J. Overgaard ◽  
J.W. Hicks ◽  
A.F. Bennett ◽  
T. Wang
Keyword(s):  
Metabolic Rate ◽  
Oxygen Affinity ◽  
Alligator Mississippiensis ◽  
Ph Effects ◽  
Blood Oxygen ◽  
Blood Gas ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Oxygen Affinity ◽  
Alkaline Tide

Reptiles habitually ingest large meals at infrequent intervals, leading to changes in acid-base status as the net secretion of acid to the stomach causes a metabolic alkalosis (the alkaline tide). In chronically cannulated and undisturbed amphibians and reptiles, the pH changes in arterial blood are, nevertheless, reduced by a concomitant respiratory acidosis (increased P(CO2) caused by a relative hypoventilation). Alligators (Alligator mississippiensis) have been reported to exhibit exceptionally large increases in plasma [HCO3(−)] following feeding, but these studies were based on blood samples obtained by cardiac puncture, so stress and disturbance may have affected the blood gas levels. Furthermore, crocodilian haemoglobin is characterised by a unique binding of HCO3(−) that act to reduce blood oxygen-affinity, and it has been proposed that this feature safeguards oxygen offloading by counteracting pH effects on blood oxygen-affinity. Therefore, to study acid-base regulation and the interaction between the alkaline tide and oxygen transport in more detail, we describe the arterial blood gas composition of chronically cannulated and undisturbed alligators before and after voluntary feeding (meal size 7.5+/−1% of body mass). Digestion was associated with an approximately fourfold increase in metabolic rate (from 0.63+/−0.04 to 2.32+/−0.24 ml O(2) min(−1)kg(−1)) and was accompanied by a small increase in the respiratory gas exchange ratio. The arterial P(O2) of fasting alligators was 60.3+/−6.8 mmHg (1 mmHg = 0.133 kPa) and reached a maximum of 81.3+/−2.7 mmHg at 96 h following feeding; there was only a small increase in lactate levels, so the increased metabolic rate seems to be entirely aerobic. Plasma [HCO3(−)] increased from 24.4+/−1.1 to 36.9+/−1.7 mmol l(−1) (at 24 h), but since arterial P(CO2) increased from 29.0+/−1.1 to 36.8+/−1.3 mmHg, arterial pH remained virtually unaffected (changing from 7.51+/−0.01 to 7.58+/−0.01 at 24 h). The changes in plasma [HCO3(−)] were mirrored by equimolar reductions in plasma [Cl(−)]. The in vitro blood oxygen-affinity was reduced during the post-prandial period, whereas the estimated in vivo blood oxygen-affinity remained virtually constant. This supports the view that the specific HCO3(−) effect prevents an increased blood oxygen-affinity during digestion in alligators.

Increased blood oxygen affinity during digestion in the snakePython molurus

2002 ◽  
Vol 205 (21) ◽  
pp. 3327-3334 ◽  
Author(s):  
Johannes Overgaard ◽  
Tobias Wang
Keyword(s):  
Partial Pressure ◽  
Oxygen Transport ◽  
Oxygen Affinity ◽  
Arterial Oxygen ◽  
Blood Oxygen ◽  
Arterial Blood ◽  
Oxygen Dissociation ◽  
Blood Oxygen Affinity ◽  
Dissociation Curves

SUMMARYMany snakes exhibit large increases in metabolic rate during digestion that place extensive demands on efficient oxygen transport. In the present study,we describe blood oxygen affinity following three weeks of fasting and 48 h after feeding in the Burmese python (Python molurus). We also report simultaneous measurements of arterial blood gases and haematological parameters. Arterial blood was obtained from chronically implanted catheters,and blood oxygen-dissociation curves were constructed from oxygencontent measurements at known oxygen partial pressure(PO2) values at 2% and 5% CO2. Arterial pH remained constant at approximately 7.6 after feeding, but digestion was associated with an approximately 6 mmol l-1 increase in [HCO3-], while CO2 partial pressure(PCO2) increased from 2.21±0.13 kPa in fasted animals to 2.89±0.17 kPa at 48 h after feeding. Blood oxygen affinity in vivo was predicted on the basis of pH in vivoand the blood oxygen-dissociation curves obtained in vitro. The blood oxygen affinity in vivo increased during digestion, with P50 values decreasing from 4.58±0.11 kPa to 3.53±0.24 kPa. This increase was associated with a significant decrease in the red blood cell [NTP]/[Hb4] ratio (relationship between the concentrations of organic phosphates and total haemoglobin) and a significant decrease in mean cellular haemoglobin content, which is indicative of swelling of the red blood cells. Our data for blood oxygen affinity and arterial oxygen levels, together with previously published values of oxygen uptake and blood flows, allow for a quantitative evaluation of oxygen transport during digestion. This analysis shows that a large part of the increased metabolism during digestion is supported by an increased venous extraction, while arterial PO2(PaO2) and haemoglobin saturation do not vary with digestive status. Thus, we predict that venous PO2 (PvO2) is reduced from a fasting value of 5.2 kPa to 1.6 kPa during digestion.

Blood oxygen affinity in high- and low-altitude populations of the deer mouse

1982 ◽  
Vol 48 (1) ◽  
pp. 89-105 ◽  
Author(s):  
Lee R.G. Snyder ◽  
Stephen Born ◽  
Andrew J. Lechner
Keyword(s):  
Deer Mouse ◽  
Oxygen Affinity ◽  
Blood Oxygen ◽  
Blood Oxygen Affinity ◽  
Low Altitude

scholarly journals Temporal changes of plasma erythropoietin level in hypobaric hypoxic mice and the influence of an altered blood oxygen affinity.

1989 ◽  
Vol 39 (6) ◽  
pp. 833-846 ◽  
Author(s):  
Satoshi SHIMIZU ◽  
Susumu SAKATA ◽  
Yasunori ENOKI ◽  
Yoshimi OHGA ◽  
Izumi OKI ◽  
...  
Keyword(s):  
Oxygen Affinity ◽  
Temporal Changes ◽  
Blood Oxygen ◽  
Blood Oxygen Affinity ◽  
Altered Blood ◽  
Erythropoietin Level

scholarly journals Autosomal dominant polycythemia

Blood ◽  
1985 ◽  
Vol 66 (5) ◽  
pp. 1208-1214 ◽  
Author(s):  
JT Prchal ◽  
WM Crist ◽  
E Goldwasser ◽  
G Perrine ◽  
JF Prchal
Keyword(s):  
Autosomal Dominant ◽  
Oxygen Affinity ◽  
Colony Growth ◽  
Blood Oxygen ◽  
Autosomal Dominant Trait ◽  
Volume Measurements ◽  
Blood Oxygen Affinity ◽  
Low Levels ◽  
Stimulation Of

Two families with polycythemia inherited as an autosomal dominant trait are described. Serial hemoglobin determinations in multiple family members and RBC volume measurements in selected affected subjects documented their polycythemia. Measurements of arterial p02s, p50s, and blood oxygen affinity were normal in all affected individuals from each family who were tested. Erythropoietin (EPO) levels were low in affected individuals from family 1 and normal in affected members of family 2. Stimulation of in vitro CFU-E colony growth by low levels of EPO was significantly increased in subjects from family 1, but normal in those affected from family 2. We conclude that although the inheritance pattern for the polycythemia in both of these families appeared to be the same, the biologic defect leading to the disorder in each of these unique families was different. The precise mechanism of the increased EPO sensitivity noted in affected subjects from family 1 awaits elucidation.

scholarly journals The Circulatory Response to Acute Hypoxia in Octopus

1983 ◽  
Vol 104 (1) ◽  
pp. 59-71 ◽  
Author(s):  
M.J. WELLS ◽  
J. WELLS
Keyword(s):  
Oxygen Uptake ◽  
Acute Hypoxia ◽  
Oxygen Affinity ◽  
Octopus Vulgaris ◽  
Blood Oxygen ◽  
Total Oxygen ◽  
Circulatory Response ◽  
The Central Nervous System ◽  
Blood Oxygen Affinity ◽  
Cutaneous Respiration

Octopus vulgaris can regulate its oxygen uptake in a closed respirometer down to a Poo2 of less than 70 mmHg. As the tankwater Poo2 falls the hearts slow down. Pulse amplitudes and mean pressures fall in the afferent branchial vessels and in the dorsal aorta. Despite behavioural changes - expansion of the interbrachial web and extension of the arms - that might imply this, the proportion of the total oxygen uptake attributable to cutaneous respiration (less than 13%) does not alter as the external Poo2 falls. The response of the hearts to a low Poo2 is not affected by severing the nerve supply from the central nervous system, or by removal of the heart ganglia. It is evidently determined by oxygen lack and not by the accumulation of CO2 or other metabolites, since the same effects are achieved by placing the animals in water where the Poo2 has been reduced by boiling. The conclusion that regulation does not depend upon circulatory responses to hypoxia is considered in the light of recent work on the changes in blood oxygen affinity associated with acute hypoxia in cephalopods.

Physiological effects of lowered blood oxygen affinity in dogs

1978 ◽  
Vol 33 (3) ◽  
pp. 263-270 ◽  
Author(s):  
Michael A. Krall ◽  
James D. Bristow ◽  
J. Eugene Welch ◽  
James Metcalfe
Keyword(s):  
Oxygen Affinity ◽  
Physiological Effects ◽  
Blood Oxygen ◽  
Blood Oxygen Affinity

Postnatal regulation of canine oxygen delivery: erythrocyte components affecting Hb function

1980 ◽  
Vol 238 (1) ◽  
pp. H73-H79 ◽  
Author(s):  
P. A. Mueggler ◽  
G. Jones ◽  
J. S. Peterson ◽  
J. M. Bissonnette ◽  
R. D. Koler ◽  
...  
Keyword(s):  
Oxygen Affinity ◽  
Fetal Hemoglobin ◽  
Blood Oxygen ◽  
Oxygen Dissociation ◽  
Affinity Change ◽  
Blood Oxygen Affinity ◽  
Postnatal Change ◽  
2,3 Dpg

A rightward shift in the blood oxygen dissociation curve occurs during the 1st mo of canine life. A detailed peptide analysis indicated that dogs do not have a separate fetal hemoglobin. Other erythrocyte components such as ATP, K+, Na+, and H+ were excluded as significant mediators of the postnatal oxygen affinity change. Erythrocyte 2,3-DPG levels essentially zero in fetal dogs, increased rapidly during the 1st mo of canine life. There was a significant correlation between this postnatal 2,3-DPG increase and the postnatal decrease in blood oxygen affinity. Dialyzed hemolysates of fetal or adult canine blood have the same intrinsic oxygen affinity and the same response to normal adult levels of 2,3-DPG. Furthermore, the magnitude and direction of this 2,3-DPG-induced decrease in oxygen affinity in vitro are comparable to the in vivo postnatal change in oxygen affinity.

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