Relationship between cardiac glycogen and tolerance to anoxia in the Western painted turtle, Chrysemys picta bellii

Expression of the constitutive Hsp73, inducible Hsp72 and Hsp90 was investigated in brain, heart, liver and skeletal muscle of the anoxia-tolerant western painted turtle Chrysemys picta bellii in response to 2, 6, 12, 18, 24 and 30·h forced dives and following 1·h recovery from 12, 24 and 30·h forced dives at 17°C. During a dive, expression of all three Hsps examined remained at control levels for at least 12·h in all tissues examined except the liver, where Hsp72 showed a decrease at 12·h, reaching a significant threefold decrease by 24·h. Brain and liver Hsp73, 72 and 90 expression increased two-to threefold at 18, 24 and 30·h. Heart and muscle Hsp73 and heart Hsp90 expression remained at normoxic levels throughout the entire dive, while heart and muscle Hsp72 and muscle Hsp90 increased two-to fourfold at 24 and 30·h. Following reoxygenation, Hsp expression increased in all tissues examined. These data indicate that increased Hsp expression is not critical in the early adaptation to anoxic survival and that short-term anoxia is probably not a stress for species adapted to survive long periods without oxygen. However, the late upregulation of heat shock proteins during anoxia suggests that stress proteins play a role in promoting long-term anoxia tolerance.

Section: Discussionsupporting

confidence: 81%

Section: Discussionsupporting

confidence: 60%

Time-dependent expression of heat shock proteins 70 and 90 in tissues of the anoxic western painted turtle

Ramaglia

Buck

2004

“…Turtles are also anoxia tolerant, but their cardiac strategy during anoxia involves a switch to a radical hypometabolic state rather than maintenance or near maintenance of cardiac performance. During anoxia, cold-acclimated freshwater turtles reduced cardiac power output and metabolic rate in parallel to about 5% of routine (Arthur et al, 1997;Farrell and Stecyk, 2007;Herbert and Jackson, 1985;Hicks and Farrell, 2000a;Hicks and Farrell, 2000b;Jackson and Ultsch, 1982), even though the initial response (1-2h) was to increase the glycolytic rate (Daw et al, 1967;Lutz et al, 2005;Wasser et al, 1991). Even warm-acclimated turtles (22°C) reduced cardiac PO by 5-fold during anoxia (Hicks and Farrell, 2000a).…”

Section: Cardiovascular Responses To Severe Hypoxia and Anoxiamentioning

confidence: 99%

Cardiac responses to anoxia in the Pacific hagfish,Eptatretus stoutii

Cox

Sandblom

Farrell

2010

SUMMARYIn the absence of any previous study of the cardiac status of hagfishes during prolonged anoxia and because of their propensity for oxygen-depleted environments, the present study tested the hypothesis that the Pacific hagfish Eptatretus stoutii maintains cardiac performance during prolonged anoxia. Heart rate was halved from the routine value of 10.4±1.3beatsmin -1 by the sixth hour of an anoxic period and then remained stable for a further 30h. Cardiac stroke volume increased from routine (1.3±0.1mlkg . During recovery from prolonged anoxia, cardiac output and heart rate increased to peak values within 1.5h. Thus, the Pacific hagfish should be acknowledged as hypoxic tolerant in terms of its ability to maintain around 70% of their normoxic cardiac performance during prolonged anoxia. This is only the second fish species to be so classified.

“…During anoxia, turtles must meet their energy demands through anaerobic metabolism, with glucose as the primary substrate. Glucose is derived from catecholamine-mediated breakdown of hepatic and skeletal muscle glycogen stores (Daw et al, 1967;Penny, 1974;Keiver and Hochachka, 1991;Wasser and Jackson, 1991;Keiver et al, 1992), thus, maintained blood flow to the liver and muscle during anoxia may facilitate glucose export to other organs. Indeed, 6·h of anoxia at 21°C resulted in an increased %Q .…”

Section: -Adrenergic Blood Flow Regulation In Anoxic Turtlesmentioning

confidence: 99%

α-Adrenergic regulation of systemic peripheral resistance and blood flow distribution in the turtleTrachemys scriptaduring anoxic submergence at 5°C and 21°C

Stecyk

Overgaard

Farrell

et al. 2004

SUMMARYAnoxic exposure in the anoxia-tolerant freshwater turtle is attended by substantial decreases in heart rate and blood flows, but systemic blood pressure (Psys) only decreases marginally due to an increase in systemic peripheral resistance (Rsys). Here,we investigate the role of the α-adrenergic system in modulating Rsys during anoxia at 5°C and 21°C in the turtle Trachemys scripta, and also describe how anoxia affects relative systemic blood flow distribution(%Q̇sys) and absolute tissue blood flows. Turtles were instrumented with an arterial cannula for measurement of Psys and ultrasonic flow probes on major systemic blood vessels for determination of systemic cardiac output(Q̇sys). α-Adrenergic tone was assessed from vascular injections of α-adrenergic agonists and antagonists (phenylephrine and phentolamine, respectively) during normoxia and following either 6 h (21°C) or 12 days (5°C) of anoxic submergence. Coloured microspheres, injected through a left atrial cannula during normoxia and anoxia, as well as after α-adrenergic stimulation and blockade during anoxia at both temperatures, were used to determine relative and absolute tissue blood flows.Anoxia was associated with an increased Rsys and functional α-adrenergic vasoactivity at both acclimation temperatures. However, while anoxia at 21°C was associated with a high systemicα-adrenergic tone, the progressive increase of Rsysat 5°C was not mediated by α-adrenergic control. A redistribution of blood flow away from ancillary vascular beds towards more vital circulations occurred with anoxia at both acclimation temperatures.%Q̇sys and absolute blood flow were reduced to the digestive and urogenital tissues (approximately 2- to 15-fold), while %Q̇sys and absolute blood flows to the heart and brain were maintained at normoxic levels. The importance of liver and muscle glycogen stores in fueling anaerobic metabolism were indicated by increases in%Q̇sys to the muscle at 21°C (1.3-fold) and liver at 5°C (1.7-fold). As well, the crucial importance of the turtle shell as a buffer reserve during anoxic submergence was indicated by 40-50% of Q̇sys being directed towards the shell during anoxia at both 5°C and 21°C. α-Adrenergic stimulation and blockade during anoxia caused few changes in%Q̇sys and absolute tissue blood flow. However, there was evidence of α-adrenergic vasoactivity contributing to blood flow regulation to the liver and shell during anoxic submergence at 5°C.