scholarly journals Improving estimates of diving lung volume in air-breathing marine vertebrates

2020 ◽  
Vol 223 (12) ◽  
pp. jeb216846
Author(s):  
Andreas Fahlman ◽  
Katsufumi Sato ◽  
Patrick Miller
1982 ◽  
Vol 96 (1) ◽  
pp. 295-306
Author(s):  
NEAL J. SMATRESK ◽  
JAMES N. CAMERON

Transfer from fresh water to 50% sea water (SW) at 26 °C increased the blood osmolarity of spotted gar (Lepisosteus oculatus) from 275 to 310 mosmol during the first 24 h. It then returned slowly to freshwater levels by 5 days after the transfer. The arterial pH dropped sharply, from 7.69 in fresh water to 7.46 in 50% SW, as a result of a small elevation in the blood CO2 partial pressure, and a marked metabolic acidosis. The respiratory (CO2) portion of the acidosis appeared to be a result of the reduction in branchial ventilation, and possibly permeability as well. The metabolic portion of the acidosis was not due to the accumulation of lactic acid, but probably involved a disruption of the extracellular strong ion difference in the saltier medium. The metabolic acidosis did not diminish during 5 days. The rate of air breathing rose from 7 to 20 bph during 50 % SW exposure. The control of pulmonary ventilation was directly responsive to the availability of O2, in general increasing when O2 was limiting (e.g. 50% SW transfer, hypoxia) and decreasing in hyperoxia. CO2 had no affect on the rate of air breathing. Withdrawal from 5–20% of total lung volume elicited an immediate air breath during hypoxia, but the response was inconsistent in normally aerated water. Lung inflation with O2 prolonged the interval between air breaths, but inflation with N2 did not change the rate of air breathing. Thus, pulmonary ventilation was secondarily controlled by lung volume. Gill ventilation frequency fell in 50 % SW, despite a respiratory and metabolic acidosis, while gill ventilation increased in response to treatment with acetazolamide. Hyperoxia caused a marked depression of gill ventilation, despite a respiratory acidosis. The gill ventilation rate appears to be most closely linked to oxygen, but may be affected indirectly by CO2 through the Root or Bohr effects.


2018 ◽  
Vol 285 (1877) ◽  
pp. 20180482 ◽  
Author(s):  
Daniel Garcia Párraga ◽  
Michael Moore ◽  
Andreas Fahlman

Hydrostatic lung compression in diving marine mammals, with collapsing alveoli blocking gas exchange at depth, has been the main theoretical basis for limiting N 2 uptake and avoiding gas emboli (GE) as they ascend. However, studies of beached and bycaught cetaceans and sea turtles imply that air-breathing marine vertebrates may, under unusual circumstances, develop GE that result in decompression sickness (DCS) symptoms. Theoretical modelling of tissue and blood gas dynamics of breath-hold divers suggests that changes in perfusion and blood flow distribution may also play a significant role. The results from the modelling work suggest that our current understanding of diving physiology in many species is poor, as the models predict blood and tissue N 2 levels that would result in severe DCS symptoms (chokes, paralysis and death) in a large fraction of natural dive profiles. In this review, we combine published results from marine mammals and turtles to propose alternative mechanisms for how marine vertebrates control gas exchange in the lung, through management of the pulmonary distribution of alveolar ventilation ( ) and cardiac output/lung perfusion ( ), varying the level of in different regions of the lung. Man-made disturbances, causing stress, could alter the mismatch level in the lung, resulting in an abnormally elevated uptake of N 2 , increasing the risk for GE. Our hypothesis provides avenues for new areas of research, offers an explanation for how sonar exposure may alter physiology causing GE and provides a new mechanism for how air-breathing marine vertebrates usually avoid the diving-related problems observed in human divers.


Pneumologie ◽  
2014 ◽  
Vol 68 (S 01) ◽  
Author(s):  
C Pizarro ◽  
R Schueler ◽  
C Hammerstingl ◽  
J Kreuz ◽  
U Juergens ◽  
...  

Pneumologie ◽  
2015 ◽  
Vol 69 (S 01) ◽  
Author(s):  
C Pizarro ◽  
H Ahmadzadehfar ◽  
M Essler ◽  
G Nickenig ◽  
D Skowasch

2016 ◽  
Vol 562 ◽  
pp. 93-100 ◽  
Author(s):  
RA Cumming ◽  
R Nikula ◽  
HG Spencer ◽  
JM Waters

2003 ◽  
Vol 29 (1) ◽  
pp. 117-123 ◽  
Author(s):  
G. R. Hillman ◽  
B. Würsig ◽  
G. A. Gailey ◽  
N. Kehtarnavaz ◽  
A. Drobyshevsky ◽  
...  

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