scholarly journals Myocardial force generation and anoxia tolerance in the common cockle, Cerastoderma edule

Author(s):  
William Joyce ◽  
Karlina Ozolina ◽  
Holly A Shiels

The myocardium of molluscs exhibits profound anoxia tolerance, however the cellular mechanisms underlying heart performance during normoxia and anoxia are not well understood. In the present study we investigated the role of the sarcoplasmic reticulum (SR) during normoxia and chemical anoxia (2 mM sodium cyanide) in electrically paced ventricle preparations from the common cockle (Cerastoderma edule) at ~19°C. Acute anoxia caused a substantial increase in resting tension but did not significantly affect the force of contraction, rate of contraction or rate of relaxation in myocardial preparations. SR inhibition (ryanodine, 10 µM; thapsigargin, 2 µM) attenuated the increase in resting tension, and also caused a significant decrease in the force of contraction during anoxia. During normoxia, SR inhibition reduced the force and rate of contraction by 20-30 % at contraction frequencies of 0.2 Hz and 0.5 Hz. SR inhibition also elicited an increase in resting tension at 0.5 Hz. Our results suggest that the SR plays a role in maintaining cardiac performance during anoxia in cockle myocardium. Furthermore, the SR is operative during normoxia and is relatively more important in the cockle heart than in many ectothermic vertebrates. As efforts to understand the evolution of the SR are advanced, anoxia tolerant invertebrates may serve as valuable model organisms.

2014 ◽  
Author(s):  
William Joyce ◽  
Karlina Ozolina ◽  
Holly A Shiels

The myocardium of molluscs exhibits profound anoxia tolerance, however the cellular mechanisms underlying heart performance during normoxia and anoxia are not well understood. In the present study we investigated the role of the sarcoplasmic reticulum (SR) during normoxia and chemical anoxia (2 mM sodium cyanide) in electrically paced ventricle preparations from the common cockle (Cerastoderma edule) at ~19°C. Acute anoxia caused a substantial increase in resting tension but did not significantly affect the force of contraction, rate of contraction or rate of relaxation in myocardial preparations. SR inhibition (ryanodine, 10 µM; thapsigargin, 2 µM) attenuated the increase in resting tension, and also caused a significant decrease in the force of contraction during anoxia. During normoxia, SR inhibition reduced the force and rate of contraction by 20-30 % at contraction frequencies of 0.2 Hz and 0.5 Hz. SR inhibition also elicited an increase in resting tension at 0.5 Hz. Our results suggest that the SR plays a role in maintaining cardiac performance during anoxia in cockle myocardium. Furthermore, the SR is operative during normoxia and is relatively more important in the cockle heart than in many ectothermic vertebrates. As efforts to understand the evolution of the SR are advanced, anoxia tolerant invertebrates may serve as valuable model organisms.


2019 ◽  
Vol 286 (1905) ◽  
pp. 20191072 ◽  
Author(s):  
Ilan M. Ruhr ◽  
Heather McCourty ◽  
Afaf Bajjig ◽  
Dane A. Crossley ◽  
Holly A. Shiels ◽  
...  

For some species of ectothermic vertebrates, early exposure to hypoxia during embryonic development improves hypoxia-tolerance later in life. However, the cellular mechanisms underlying this phenomenon are largely unknown. Given that hypoxic survival is critically dependent on the maintenance of cardiac function, we tested the hypothesis that developmental hypoxia alters cardiomyocyte physiology in a manner that protects the heart from hypoxic stress. To test this hypothesis, we studied the common snapping turtle, which routinely experiences chronic developmental hypoxia and exploits hypoxic environments in adulthood. We isolated cardiomyocytes from juvenile turtles that embryonically developed in either normoxia (21% O 2 ) or hypoxia (10% O 2 ), and subjected them to simulated anoxia and reoxygenation, while simultaneously measuring intracellular Ca 2+ , pH and reactive oxygen species (ROS) production. Our results suggest developmental hypoxia improves cardiomyocyte anoxia-tolerance of juvenile turtles, which is supported by enhanced myofilament Ca 2+ -sensitivity and a superior ability to suppress ROS production. Maintenance of low ROS levels during anoxia might limit oxidative damage and a greater sensitivity to Ca 2+ could provide a mechanism to maintain contractile force. Our study suggests developmental hypoxia has long-lasting effects on turtle cardiomyocyte function, which might prime their physiology for exploiting hypoxic environments.


2012 ◽  
Vol 14 (2) ◽  
pp. 451-466 ◽  
Author(s):  
Ilaria Coscia ◽  
Peter E. Robins ◽  
Joanne S. Porter ◽  
Shelagh K. Malham ◽  
Joseph E. Ironside

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