Short-term emersion affects cardiac function and regional haemolymph distribution in the crab Cancer magister

1996 ◽  
Vol 199 (3) ◽  
pp. 569-578
Author(s):  
C Airriess ◽  
B Mcmahon

Changes in cardiac function and arterial haemolymph flow associated with 6 h of emersion were investigated in the crab Cancer magister using an ultrasonic flowmeter. This species is usually found sublittorally but, owing to the large-scale horizontal water movements associated with extreme tides, C. magister may occasionally become stranded on the beach. Laboratory experiments were designed such that the emersion period was typical of those that might be experienced by this crab in its natural environment. The frequency of the heart beat began to decline sharply almost immediately after the start of the experimental emersion period. Cardiac stroke volume fell more gradually. The combined reduction in these two variables led to a maximum decrease in cardiac output of more than 70 % from the control rate. Haemolymph flow through all the arteries originating at the heart, with the exception of the anterior aorta, also declined markedly during emersion. As the water level in the experimental chamber fell below the inhalant branchial openings, a stereotypical, dramatic increase in haemolymph flow through the anterior aorta began and this continued for the duration of the emersion period. The rapid time course of the decline in heart-beat frequency and the increase in haemolymph flow through the anterior aorta suggest a neural mechanism responding to the absence of ventilatory water in the branchial chambers. These responses may be adaptations, respectively, to conserve energy by reducing the minute volume of haemolymph pumped by the heart and to protect the supply of haemolymph to cephalic elements of the central nervous system. The decline in cardiac stroke volume, which occurs more slowly over the emersion period, may be a passive result of the failure to supply sufficient O2 to meet the aerobic demands of the cardiac ganglion.

1994 ◽  
Vol 190 (1) ◽  
pp. 23-41 ◽  
Author(s):  
C Airriess ◽  
B Mcmahon

Unrestrained crabs instrumented with probes for ultrasonic measurement of arterial haemolymph flow were subjected to 6 h of hypoxic exposure. During this interval, the inhalant O2 partial pressure was reduced in steps from 18 to 3 kPa. Measurement of haemolymph flow through all arteries leaving the heart allowed direct calculation of cardiac output, stroke volume and the distribution of cardiac output for both non-stressed and hypoxic animals. Resting levels of cardiac output were low compared with previously reported values for this and other species of decapod crustaceans. During exposure to the most severe level of hypoxia tested, haemolymph flow through the anterior arteries decreased while flow through the posterior aorta and sternal artery increased by 55 % and 27 % respectively. Cardiac output increased from a control value of 9.8±1.6 to 11.9±1.2 ml kg-1 min-1 despite a decrease in heart-beat frequency. Scaphognathite beat frequency increased from 82.1±4.3 min-1 to more than 120 min-1 after 90 min of hypoxic exposure and remained at this level for the duration of the exposure period. The decrease in haemolymph flow, via the anterior arteries, to the antero-dorsal region of the animal concurrent with an increase in flow to the posterior and antero-ventral regions, via the posterior aorta and sternal artery, implicates an active mechanism for redistribution of haemolymph flow during hypoxic exposure. The high rate of scaphognathite pumping, presumably to maximise O2 uptake during experimental hypoxia, was probably made possible by an increased blood supply to these organs, which are perfused by downstream branches of the sternal artery.


1995 ◽  
Vol 198 (12) ◽  
pp. 2547-2550 ◽  
Author(s):  
I J McGaw ◽  
J L Wilkens ◽  
B R McMahon ◽  
C N Airriess

Peptide neurohormones exist as functionally similar analogues in a wide variety of invertebrate and vertebrate phyla, and many have been implicated as cardiovascular regulators. In decapod crustaceans, these include the pentapeptide proctolin, crustacean cardioactive peptide (CCAP) and the FMRF amide-related peptides F1 and F2, all of which are found in the pericardial organs located immediately upstream of the heart. Cardioexcitatory activity has been demonstrated by these four peptides in both isolated and semi-isolated arthropod hearts; CCAP, however, has minimal effects on the heart of Cancer magister. In the present study, we determined the effects of proctolin, F1 and F2 on the heart of the crab C. magister in both in vitro (semi-isolated heart) and in vivo (whole animal) preparations. In semi-isolated hearts, infusion of each peptide caused cardioexcitation, increasing the rate and stroke volume of the heart. In whole crabs, the peptides were cardioinhibitory; the strongest effects were observed with F1 and F2, which dramatically decreased heart rate, cardiac stroke volume and cardiac output. These results cast doubt on current perceptions of the functional role of cardioactive peptides in the regulation of invertebrate cardiovascular performance in vivo.


1996 ◽  
Vol 199 (3) ◽  
pp. 627-633 ◽  
Author(s):  
B Wachter ◽  
B Mcmahon

Adult male Cancer magister (Dana) were equipped with pulsed-Doppler flowmeters and pressure transducers for simultaneous measurement of heart and ventilation frequencies, haemolymph flow through each of the major arterial systems and cardiac output and for calculation of stroke volume. Each variable was measured at rest and during two consecutive periods of moderate treadmill walking activity and recovery. During activity, haemolymph flow through the sternal and anterolateral arteries increased, while flow through the hepatic arterial system decreased. This resulted in a redistribution of haemolymph flow in which a proportion of cardiac output was shifted from the anterior, posterior and hepatic arterial systems to the sternal arterial system. The relative proportion of the cardiac output flowing through the anterolateral artery remained constant. This indicated that oxygen supply was shifted away from the digestive system to the muscles of the walking legs and the respiratory system. Cardiac output, heart rate and stroke volume all increased in response to activity. The increase in cardiac output is the result of a large increase in stroke volume and a small increase in heart rate. A doubling of ventilation rate also occurred during activity. Both the circulatory and ventilatory systems were restored to pre-activity values by 60 min of recovery.


2006 ◽  
Vol 27 (5) ◽  
pp. S139-S146 ◽  
Author(s):  
S Zlochiver ◽  
D Freimark ◽  
M Arad ◽  
A Adunsky ◽  
S Abboud

1997 ◽  
Vol 200 (11) ◽  
pp. 1695-1702 ◽  
Author(s):  
J M Jones ◽  
A K Gamperl ◽  
A P Farrell ◽  
D P Toews

Flow from the posterior lymph hearts of Bufo marinus was measured using Doppler flow probes. These probes were placed on the posterior vertebral vein and recorded flow as lymph was ejected from the heart. In resting, hydrated toads, mean lymph flow from one of the paired posterior lymph hearts was 25.9 +/- 4.9 ml kg-1 h-1, stroke volume was 8.9 +/- 1.4 microL kg-1 and lymph heart rate was 47.5 +/- 3.7 beats min-1. We estimate that, together, the paired posterior lymph hearts are capable of generating flows that are approximately one-sixtieth of the resting cardiac output. Mean peak systolic pressure developed by the posterior lymph hearts was 1.62 +/- 0.08 kPa. Simultaneous measurements of lymph heart pressure development and flow revealed that the outflow pore of the heart opened at a pressure of 0.71 +/- 0.04 kPa, approximately 113 +/- 5 ms into systole. When toads were moderately disturbed, stroke volume increased by as much as fourfold with little change in lymph heart rate (< 5 beats min-1). When toads were dehydrated, lymph flow decreased by 70% at 12h and by 80% and 24h. Since there was only a modest non-significant decrease in lymph heart rate (30%), this reduction in flow was attributed to decreases in stroke volume (approximately 80%). Lymph heart flow and stroke volume returned to control values 30 min after adding water back into the experimental chamber. Stroke volume was clearly more important in regulating lymph flow than lymph heart rate under these conditions in Bufo marinus.


2007 ◽  
Vol 98 (4) ◽  
pp. 2382-2398 ◽  
Author(s):  
Robert J. Calin-Jageman ◽  
Mark J. Tunstall ◽  
Brett D. Mensh ◽  
Paul S. Katz ◽  
William N. Frost

This research examines the mechanisms that initiate rhythmic activity in the episodic central pattern generator (CPG) underlying escape swimming in the gastropod mollusk Tritonia diomedea. Activation of the network is triggered by extrinsic excitatory input but also accompanied by intrinsic neuromodulation and the recruitment of additional excitation into the circuit. To examine how these factors influence circuit activation, a detailed simulation of the unmodulated CPG network was constructed from an extensive set of physiological measurements. In this model, extrinsic input alone is insufficient to initiate rhythmic activity, confirming that additional processes are involved in circuit activation. However, incorporating known neuromodulatory and polysynaptic effects into the model still failed to enable rhythmic activity, suggesting that additional circuit features are also required. To delineate the additional activation requirements, a large-scale parameter-space analysis was conducted (∼2 × 106 configurations). The results suggest that initiation of the swim motor pattern requires substantial reconfiguration at multiple sites within the network, especially to recruit ventral swim interneuron-B (VSI) activity and increase coupling between the dorsal swim interneurons (DSIs) and cerebral neuron 2 (C2) coupling. Within the parameter space examined, we observed a tendency for rhythmic activity to be spontaneous and self-sustaining. This suggests that initiation of episodic rhythmic activity may involve temporarily restructuring a nonrhythmic network into a persistent oscillator. In particular, the time course of neuromodulatory effects may control both activation and termination of rhythmic bursting.


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