Changes in caridac output and hemolymph flow during hypoxic exposure in the gravid grass shrimp, Palaemonetes pugio

Abstract

The cardiovascular response of decapod crustaceans to hypoxic exposure is well documented; however, information is limited concerning the influence of reproductive state on cardiovascular demands during hypoxic exposure. Given the additional metabolic demand of reproduction, we investigated the cardiovascular adjustments employed by gravid grass shrimp Palaemonetes pugio to maintain oxygen delivery during hypoxic stress. Cardiac output values were elevated in gravid compared to nongravid grass shrimp. Gravid grass shrimp were exposed to hypoxia and the stroke volume, heart rate, cardiac output and hemolymph flow were determined using video-microscopy and dimensional analysis. Oxygen consumption rates were determined using respirometry. There where no changes in the cardiac output values of gravid females until reaching 6.8 kPa O2, with a significant redistribution of hemolymph flow at 13.7 kPa O2. Flow was significantly decreased to the anterior lateral arteries that supply the ovaries and hepatopancreas, the anterior aorta and the posterior aorta. The redistribution of hemolymph flow away from these vessels results in an enhanced hemolymph flow to the sternal artery that supplies the ventral segmental system, the gills, the buccal apparatus and the ventral nerve cord. The data suggest that during hypoxic stress, gravid females place a priority on survival.

Changes in cardiac performance during hypoxic exposure in the grass shrimpPalaemonetes pugio

“…In these animals, we did not observe an increase in V S as expected, despite the maintenance of V b at 6.8kPaO 2 (Wheatly and Taylor, 1981;McMahon and Wilkens, 1975;Reiber and McMahon, 1998). In previous studies, when grass shrimp were exposed to 2h of hypoxia at a level of 6.8kPaO 2 (Guadagnoli and Reiber, 2005), and in this study, V b was maintained near normoxic values with increases (although not statistically significant) in stroke volume. At 2.2kPaO 2 , a value well below the P crit value of the animal (Harper and Reiber, 1999;Cochran and Burnett, 1996), grass shrimp were unable to maintain cardiac output, with the fall in ƒ H not supported by sufficient increases in V S .…”

“…The contraction and relaxation of the abdominal musculature and/or the extension or retraction of the tail region (Taylor, 1990;Reiber et al, 1997) can modulate peripheral vascular resistance. An extension of the tail region and increased pleopod fanning have been observed in grass shrimp exposed to severe hypoxia (Guadagnoli and Reiber, 2005). The ejection curve of grass shrimp P-A loops generated during exposure to hypoxia becomes progressively curvilinear, which is consistent with a reduction in vascular resistance (Keller et al, 1991).…”

“…The animal was held in place and positioned within the experimental chamber with a micromanipulator (World Precision Instruments, Sarasota, FL, USA). The video camera was placed over the chamber so that digital images of the heart could be captured through the transparent exoskeleton (Harper and Reiber, 1999;Harper and Reiber, 2001;Guadagnoli and Reiber, 2005;Guadagnoli et al, 2005a;Guadagnoli et al, 2005b).…”

“…Numerous studies have demonstrated that decapod crustaceans can redistribute hemolymph flow among their arterial systems (Guadagnoli and Reiber, 2005;McGaw et al, 1994;Reiber and McMahon, 1998). Redistribution of arterial flow is accomplished by muscular cardioarterial valves located at the entrance to each arterial system (Maynard, 1960) and has been demonstrated in several species [in Bathynomus: by Kihara and Kuwasawa (Kihara and Kuwasawa, 1984); in Cancer magister: by McGaw and colleagues (McGaw et al, 1994); in Panulirus japonicas: by Kuramoto and Ebara (Kuramoto and Ebara, 1984); and in Procambarus clarkii: by Reiber (Reiber, 1994)].…”

Elasticity, unexpected contractility and the identification of actin and myosin in lobster arteries

“…Since the arteries do not appear to be innervated (M.J.C., K. S. Chan and J.L.W., unpublished), cardioactive drugs must be acting directly on the vessel walls to cause contraction while an unknown relaxing factor, possibly nitric oxide (Mahadevan et al, 2004), circulating in the haemolymph or released by surrounding tissues, could cause vessel dilation. Such local control of arterial radius, plus the participation of cardioarterial valves and DAA-lateral artery valves, will be important in regional haemolymph distribution patterns among the seven arteries leaving the heart (Airriess and McMahon, 1992;Davidson et al, 1998;McGaw and Reiber, 2002;Guadagnoli and Reiber, 2005). …”