Homeoviscous Properties Implicated by the Interactive Effects of Pressure and Temperature on the Hydrothermal Vent Crab Bythograea thermydron

7 Pages·1994·3.1 MB·English

by  C N Airriess

Reference: Biol. Bull 187: 208-214. (October. 1994)
Homeoviscous Properties Implicated by the Interactive
Effects of Pressure and Temperature on the
Hydrothermal Vent Crab Bythograea thermydron
CHRIS N. AIRRIESS1 * AND JAMES J. CHILDRESS2
^Department ofBiologicalSciences, UniversityofCalgary, 2?<)l) L'niversity Dr. N.W., Calgary.
Alberta, T2N 1N4. Canada, and2Department ofBiological Sciences andMarine Science Institute.
University ofCalifornia at Santa Barbara. Santa Barbara, California 93106
Abstract. Specimens of the hydrothermal vent crab biological systems, with the primary loci foreffectsbeing
Bythograea thermydron, collected from 13 N on the enzymeand membrane systems(Macdonald and Miller,
East Pacific Rise, wereexposed to pressuresgreaterthan 1976; Wann and Macdonald, 1980; Siebenaller and So-
those in their natural habitat over a range oftempera- mero, 1989; Somero, 1992). At the enzymatic level,
turesto assess how increased hydrostatic pressure affects pressureexertsan inhibitoryeffectwhen thereisa volume
a species that requires high pressure to survive. We increase associated with substrate binding or catalytic
measured heart beat frequency and contraction wave- activity (Siebenaller and Somero, 1989; Somero, 1992).
form at pressures ranging from 28 MPa (normal envi- In membranes, the structure ofthe membrane is altered
ronmental pressure for this species) to 62 MPa at 5, by the greater compressibility of lipid as compared to
10. and 20C. At 5C, increased hydrostatic pressure waterand other membranecomponents(Macdonald and
induced bradycardia or acardia in conjunction with Miller, 1976).
marked disruption ofthe ventricularcontraction wave- Both enzyme and membrane adaptations have been
form. The animals did not survive following de- found in deep-sea organisms. The enzymatic adapta-
compression. Theeffectsofincreased pressurewere less tions involve a reduction in the volume change that
pronounced at 10C and almost negligible at 20C. Our occurs in the enzymes of deep-sea organisms during
results support previous findings at subambient pres- catalysis. As a result, enzyme-substrate affinity and
sures which suggest that the lipid bilayers of cell and other catalytic properties ofthe enzymes ofdeeper-liv-
organelle membranes are the primary sites affected by ing species are more independent ofpressure (Sieben-
short-term pressure variation indeep-seaorganisms. We aller and Somero, 1989; Somero, 1992). At the mem-
also found evidence ofan adaptive mechanism ofpres- brane level, the adaptations involve ashift in membrane
sure-temperature interaction in these animals from the lipid composition with increasing depth. This shift
eurythermic h.; '"the hydrothermal vents. maintains optimal fluidity (homeoviscous adaptation)
in the face ofincreasing pressure, which would tend to
Introduction
order the membrane lipids (Cossins and Macdonald,
Hydrostatic pressure increases by one atmosphere 1984. 1986, 1989; Cossins and Sinensky, 1986). The
m
(101.3 kPa) for each 10 ofdepth in the ocean; thus, effects of homeoviscous adaptation are expected to be
organisms living at greater depths experience greater especially prominent in excitable tissues and. unlike
pressures (Saunders and Fofonoff, 1976). Elevated pres- those of enzymatic adaptation, to show profound in-
sures have been shown to have a variety of effects on teraction with temperature: lower temperatures ame-
liorate the effects of lower pressures and higher tem-
of*RZeoPcorleeoisgveyen,dtU7andiDdvreeecrsessi:mtbyLearobfo1Cr9aa9tm3ob;rryaicdcogefep,MtoeDldoewc18unliJanurlgySSit1gr9ne9ae4lt.l,inCga,mbDreipdagretmCeBn2t tpehrraotuugrhestheaimreloipoproastietetehfefecetfsfecotns tohfe hfliugihdeirtyporfesmseurme-s
3EJ, UK. brane lipids (Cossins and Macdonald, 1989). In addi-
208
PRESSURE EFFECTS IN B THERMYDRON 209
lion, one would not expect homeoviscous adaptation deep-sea animal that requires high pressure for survival:
to reduce the sensitivity to pressure, as is the case for second, to examine the interactive effects ofthese ele-
enzymatic adaptations, but rather to shift the tolerated vated pressures with temperature.
range ofpressure in the same way that it does in tem-
perature adaptation (Sinensky, 1974). There is some Materials and Methods
indication that the membranes of fishes living at Collection and maintenance
depths greater than 2500 m have reduced compressi-
bility (Behan ct at.. 1992). Along with reducing the ef- Baited traps deployed and retrieved by the Deep Sub-
fects ofpressure variation on membrane function, this mergence Vehicle Alvin were used to collect specimens
adaptation would preserve the activity of membrane- ofB. thermydron, ofeither sex, from the hydrothermal
associated enzymes which are critically dependent vent field at 13 N on the East Pacific Rise. Crabs were
on the physical state of the membrane (Gibbs and brought to the surface in insulated containers that kept
Somero. 1989). temperature, but not pressure, relatively constant. Once
Although it is clear from the work cited above that atthesurface, crabswereexaminedtoobtaindemographic
both enzyme and membrane adaptations are found in data, then placed in steel vessels that were maintained at
deep-sea organisms, the evaluation oftheir relative im- apressureof21 MPa(204atm)andsuppliedwith flowing
portance must come from studies ofthe functioning of seawater at approximately 8C. Under such conditions,
deep-sea animals. Much work on hydrostatic pressure survival for more than 18 months has been reported
effects has been concerned with the effects ofelevated (Mickel and Childress. 1982a).
pressures on organisms that normally live at 1 atm. Animalpreparation
Other pressure studies havebeen concerned with species
of fishes and crustaceans that live at depths of about In preparation for experimental use. crabs were slowly
1000 m and have typically demonstrated mild responses depressurized, removed from the maintenance vessel, and
to reduced pressure in conjunction with somewhat transferredtoa shallowglasscontainerfilledwith ice-cold
greater tolerance of elevated pressures (Belman and seawater. Instrumentation ofthe animals for impedance
Gordon. 1979: Quetin and Childress, 1980). Recent pneumography was accomplished as quickly as possible
studies that used pressure traps to recover specimens to minimize disturbance and hypobaric trauma.
demonstrated that species living below 2000 m are de- To measure heart beat frequency, holeswere drilled in
pendent on elevated pressures (Macdonald and Gil- the dorsal carapace on either side of the heart and two
christ. 1980. 1982: Yayanos, 1981). Animals living at fine silverwires were inserted so that their endsjust pen-
depths ofabout 2500 m around hydrothermal vents on etrated the pericardia! sinus. To prevent bleedingand hold
the Galapagos Rift also require high pressure for long- the wires in position, dental dam was placed over the
term survival, although many can survive decompres- wires and holes and fixed to the carapace with cyano-
sion to 1 atm ifthis is soon followed by recompression acrylate cement. Changes in impedance associated with
(Arp and Childress. 1981; Mickel and Childress. ventricular contraction were detected by an impedance
1982a,b; Arp ct a!.. 1984). These animals are also converter (UFI, model 2991) and recorded on a Gould
uniquely suited to studies of pressure-temperature in- two-channel pen recorder.
teractions because, unlike other deep-sea animals, they Although not reported as a part ofthis study, the fre-
experiencewide natural temperature ranges. Mickel and quency ofscaphognathite beating was recorded as an in-
Childress( 1982a) havedemonstrated thatwhen the vent dicator of the physiological state of the animals. Two
crab Bythogrui'ti thcrmydron is exposed to pressures impedance pneumography electrodes were affixed inside
substantially lower than those of its natural habitat, the exhalant channel ofthe right branchial chamber and
heart rate is reduced and the EKG wave form becomes impedance changescaused by movement ofthe scaphog-
irregular. Furthermore, the onset ofthese effects was at nathite were recorded as above.
higher pressures at higher temperatures and at lower Following preparation, crabs were placed without ad-
pressures at lower temperatures, a result which the au- ditional restraint in a 6-1 stainless steel vessel (Autoclave
thors interpreted as evidence that membrane lipid Engineers) filled with aerated, filtered seawater. Experi-
properties are important in determining the pressure mental temperatureswere maintained insidethepressure
sensitivity ofthis species. This study did not, however, vessel by awater-jacket surrounding the chamber. A hand
test for the effects of superambient pressures on this pump (Enerpac) connected via Hastelloy C tubing and
species, and no othersuch studies have been conducted Autoclave Engineers fittings was used to pressurize the
on any deep-sea animal. The purpose of the present vessel to 28 MPa(272 atm); pressurewas monitored using
study was twofold: first, to determine at what pressures a gauge on the pump. The entire system was rated to 69
an elevation in pressure affects the functioning of a MPa (680 atm) working pressure with a 4:1 safety factor.
C. N. AIRRIESS AND J. J. CHILDRESS
Animals were allowed to recover at normal environ- 120
mental pressure until the '-..-art beat frequency stabilized
and the scaphognathin .;egan to alternate between pe- 100
riodsofcontinuou .nigand inactivity in the fashion
typical ofnonstrc:>..:J decapod crustaceans (McMahon 80 20 'C
and Wilkens, 1972). Animalsthatdid not regain typical,
stable readings of heart and scaphognathite activity o" 60
within 2 h of instrumentation were not used in subse-
0- 40
quent experiments.
i.
u.
20
Experimentalprotocol
Once the crabs appeared to have recovered, the chart
speedwasincreased toallowresolution ofindividual con- 40 50 60 70
tractions of the ventricle. Heart beat frequency was ob-
Pressure (MPa)
tained bycountingthewaveform peaksovera 30-speriod.
Natural
Ventricular contraction pattern was quantified by cal- environmental
culatingthe standard deviation of 10 successive interbeat pressure
intervals. Immediately after this control recording, the Figure 1. The effect ofaltered pressure on heart beat frequency in
pressure inside the experimental chamber was increased Bythograeaihermydronatthreetemperatures. Forcomparison,thedata
from 28 to 31 MPa. The animals were allowed 10 min to ofMickelandChildress(1982a;opensymbols)arepresentedalongwith
those from the present study (solid symbols). The middle curve from
adjust, then the chart speed was increased for determi- theformerstudywasobtainedfromexperimentsconductedat 12 rather
nation of ventricular contraction frequency and pattern than 10C.At5C()theratefellalmostlinearlytoitsminimum value
before the pressure was raised to 34 MPa. This protocol aspressurewasincreased;however,contractionfrequencywasmaintained
cthoentmianuxeidm,uwmithprpersessusreurteesitnecdr(e6a2siMngPain)3w-asMPraeasctheepds.,Aufntteilr Tpunrhteeislshuterhaeerstpbrreealstosewuroe5f2crreMaaPbcash.etdebsuattbedotuhatten522d0eMcClPia(nVe)dinallecssrsoabsrseevtmeeraseitlneydedtahtcaon1nsi0ntCan1t(0A)aC.t
30 min, the vessel pressure was gradually lowered to 28 crabs. Generally, the decline in heart rate brought about by hypobaric
MPa. Data were obtained 30 min after return to the orig- exposurewasamelioratedbylowertemperatures, whereashightemper-
inal pressure, and the chamber was subsequently depres- atures buffered the effects ofhyperbaric exposure. Although the crabs
surized for removal ofthe crabs. used in these two studies were obtained from sites thousands ofmiles
The effects ofpressure and temperature on heart beat caeplalretntanagdretheemeenxtpeorfitmheentnaolrmtoebchanriiqcuedsatvaarsiuepdposrtosmetwhehavtaliidnitdyetoafilc,oemx--
frequency and contraction pattern were estimated using biningthedatasets.Spearman rankcorrelationcoefficients(r,)forheart
analysisofvariance with repeated measures(ANOVAR). rate and pressure (data from the present study) were calculated as: r,
ANOVARs significant at the 0.05 level were further an- -0.940, n = 60, P < 0.01 at 5C; rs = -0.923, n = 30, P< 0.01 at
alyzed using Tukey's HSD multiple-comparison test. In 10C; rs = -0.706, n = 60. P < 0.01 at 20C. Normal environmental
addition, Spearman rank correlation was used to deter- pressureisabout28MPaforthisspecies. Datashownasmean I SEM.
mine the relationship between pressure and heart beat
frequency ateach temperature. All values are reported as
the mean 1 SEM. n = 60, P< 0.01). Heart beat frequency was significantly
different from the control value at all pressures greater
Results than 41 MPa at this temperature (F = 72.05, P < 0.01).
Following 30 min ofrecovery at 28 MPa, heart rate was
Contractionfreq\ still markedly different from the pre-exposure value (P
recTohveercfornotmrotlheheianist,rum .flraetiqounepnrcoycoefducrreabwsasalplosoiwteidveltyo < 0T.h0e1;hTeaabrtlebeI)a.t frequency ofcrabs tested at 10C fell
correlated with experiniL , \\ temperature (rs = 0.937, from 60.7 4.8to3.0 1.5 min"1 overthesame pressure
= 15, P < 0.01). The relationship between temperature range asabove (Fig. 1). The correlation between pressure
andcontraction frequencydid not, however, remain con- and heart rate (rs = -0.923, n = 30, P < 0.01) was also
stant as pressure within the experimental chamber in- significant, but the difference between control and ex-
creased (Fig. 1). perimental contraction frequencies was significant only
At 5C, heart rate dropped 92% from its control value at pressures greater than 52 MPa (F = 32.76, P < 0.05).
at 28 MPa to 3.3 1.3 min"1 after 10 min at 62 MPa The bradycardiacontinued immediately afterthe return
(Fig. 1). The negative correlation between contraction to normal environmental pressure (P < 0.05), but after
frequencyand pressurewashighlysignificant(i\ = -0.940, 30 min of recovery the heart rate had rebounded and
PRESSURE EFFECTS IN B THERMYDRON
Table I pressures of 55 and 62 MPa, respectively. Variability of
eHxepaorsturraele(6<2>/MByPtah)ogartateharetehetremmpyedrraotnurbeesforeamiafterhyperbaric t=he17.i5n4t,erPbe<at0.i0n1te(rcvoamlpaarlseod tionctrheeas2e8dMPsiagnciofinctarnotlly(Fi(g.F
3). After 30 min ofrecovery at 28 MPa, the ventricular
/H(min ') contraction pattern became much moreregular,although
a diastolic notch not present in the control recording be-
Temperature(C) Control Recovery
came evident (Fig. 2), and the standard deviation ofthe
5(6) 40.5 0.8 15.2 4.0* interbeat intervals was markedly reduced (Fig. 3). Crabs
10(3) 60.7 4.8 43.3 13.0 in thisgroup were returnedto normobaric holdingvessels,
20(6) 92.2 5.5 104.2 9.6 but all died within 24 h ofexperimental use.
Crabswereallowed 30minafterreturntonormal pressurebeforethe Above 55 MPa the interbeat interval ofcrabs tested at
recoveryvalueswereobtained. Valuesareshownasthemean 1 SEM; 20Cbecame increasingly variable (Fig. 3) and there was
samplesizein parentheses. evidence of a systolic plateau in some animals (Fig. 2).
* Valuesignificantlydifferent from control(P<0.01. ANOVAR). However, all animals examined at this temperature
maintained organized cardiac activity, and they regained
theirinitial ventricularcontraction pattern as soon asthey
was not significantly different from the control value were returned to normal environmental pressure. All an-
(Table I). imals in this group survived, apparently healthy, for at
At 20C, the change in heart ratewith increasing pres- least 48 h after experimental use.
sure was much less dramatic than at the lower tempera-
tures. The ratedecreased only49%, reachinga minimum Discussion
of 47.3 5.9 min"1 at 62 MPa (Fig. 1). There was a
significant correlation between heart beat frequency and During preparation at ambient sea-level pressure the
pressure (rs = -0.706, n = 60, P < 0.01), but significant crabs appeared healthy and responsive, although all
changes from the control rate occurred only above 55 showed the marked lack of coordination typical of this
MPa (F = 20.38, P < 0.01). As soon as the pressure was specieswhen depressurized (Mickel andChildress. 1982a).
lowered, heart beat frequency rebounded above pre-ex- Toleranceofrepeated decompression forextended periods
5C
posure values and remained elevated for at least 30 min and survival at sea level at for up to 5 days have also
(Table I). been reported (Mickel and Childress, 1982a), suggesting
that the short hypobaric exposure required for instru-
Contraction pattern mentation of the crabs did not irreversibly affect their
physiological state.
The relationship between ventricular contraction pat- The relationship between temperature and heart beat
tern and experimental pressure was also dependent on frequency at the normal environmental pressure for B.
temperature. Generally, the systolic spikes became less thermydron is directly comparable to that observed in
defined and the interbeat interval tended to vary more as shallow-living invertebrates (deFur and Mangum, 1979).
pressure was increased. These effects were more pro- At higher pressures this relationship changed markedly,
nounced at lower temperatures (Figs. 2, 3). Crabs tested with heart rate first becoming more, then less dependent
at 5C showed increased variability in ventricular con- on temperature in the 5 to 10C range. Between 10 and
traction waveform at pressures as low as 34 MPa; vari- 20C, the dependency of heart beat frequency on tem-
ability continued to increase until about 55 MPa, when perature remained more or less constant over the entire
ventricular contractions became extremely sporadic or pressure range.
ceased. At 62 MPa. the standard deviation ofthe interbeat The effect of high hydrostatic pressure on membrane
intervals increased significantly compared to the control lipids is to decrease fluidity by increasing the order ofthe
value (F = 20.14, P < 0.01; Fig. 3). Following return to hydrophobic acyl chains within the membrane (Wann
normal environmental pressure there was little increase and Macdonald, 1980; Somero, 1992). This packing of
in the uniformity of ventricular contraction and all the acyl chains may both change the ion permeability of
crabs died within 1 h ofdecompression, suggesting that the membrane and limit the diffusion ofmembrane pro-
the effects ofhyperbaric exposure are irreversible at this teins(Cossins and Macdonald, 1989). In addition, fusion
temperature. ofneurotransmittervesicleswiththepostsynapticterminal
At 10C. the ventricular contraction pattern began to ofnerve fibers may be disrupted (Wann and Macdonald.
degenerateatpressuresabove41 MPa(Fig. 2). The higher 1980). leading to failure of postsynaptic activation (see
chart speed used at this temperature allows resolution of below). Thecombinedtendenciesoflowtemperatureand
biphasic contraction peaks and ventricular fibrillation at high pressure to order membrane lipids may becountered
212 C. N. AIRRIESS AND J. J. CHILDRESS
5 C 10 C 20 C
Pressure
Depth (m)
(MPa)
2711
28
4072 41
5432 55
6112 62
2711 28
30s 10 s 10 s
Figure 2. Chart records showing ventricular contraction in three individual Bylhograea thermydron
dunng progressive hyperbanc exposure at 5, 10. and 20C. The 28 MPa records at the bottom ofthe
illustration were obtained following 30 min ofrecovery at normal environmental pressure forthisspecies.
At5C,thecontractionwaveformbecamelessdistinctandinterbeatvariabilityincreasedwith higherpressure.
Totalacardiaoccurredatpressureshigherthan 55 MPa. andcontractionsremaineddisorganizedfollowing
returntonormalpressure.Hyperbancexposurewasbettertoleratedincrabstestedat 10C,butextrasystolic
spikes and ventricular fibrillation were evident at higher pressures. Recovery was more complete at this
temperature than at 5C, although thecontraction frequency remained depressed. Compared tothe other
twoexperimentaltemperatures,theeffectsofincreased pressureoncontraction frequency andwaveformat
20Cwereminimal. After30minofrecovery,thecontractionpatternhadreturnedtonormalandtheheart
rate had rebounded abovecontrol values.
within the lifetime ofan organism by increasing the ratio and duration ofspontaneous burst discharges from these
of unsaturated to saturated fatty acids composing the motoneurons maybe modulated byoutput from thesmall
membrane bilayer(Cossinsand Macdonald, 1989). In or- pacemakercellsatthe posterioroftheganglion (Hartline,
ganisms lr ;ng in the high pressure-high temperature en- 1967), although it has been suggested that fine control of
vironment o 'he hydrothermal vents, the effects ofhigh burst characteristics is achieved by interaction between
pressure on ; hrane fluidity may be partiallycompen- the large and small CG cells (Sullivan and Miller, 1984).
sated, requiri>: 'ver proportion ofunsaturated mem- In the gastropod Helix, increased hydrostatic pressure re-
braneconstitUL 'neveoptimal membraneviscosity. duces the firing rate of postsynaptic cells (Wann et al.,
The beat ofth<_ ^an heart is neurogenic (Alex- 1979), possibly due to a reduction in excitatoryjunctional
androwicz, 1932), gc;-i d by burstdischarges from the potential (ejp) amplitude arising from decreased neuro-
cardiacganglion (CG)o, ts innerdorsalwall. Thestriated transmitter release at higher pressures. Although pace-
muscle ofthe myocardium is polyneuronally and poly- maker cell burst frequencies may increase in response to
synaptically innervated byprocessesfrom thelarge motor increased pressure (Wann and Macdonald, 1980), there
CG
neurones ofthe (Alexandrowicz. 1932). This inner- areseveral potential sitesforpostsynaptic failurebetween
vation, alongwith tight electrotonic couplingbetween in- the pacemaker cells ofthe crustacean CG and the myo-
dividual muscle fibers, ensures rapid spread ofexcitation cardium.
throughout the myocardium, resulting in strong, coor- Mickel and Childress (1982a) showed that both the re-
dinated contraction ofthe ventricle with each burst from duction in heart beat frequency and the degeneration of
theCG (Kuramotoand Kuwasawa, 1980). The amplitude EKG organization brought about by decreasing pressure
PRESSURE EFFECTS IN B THERMYDRON 213
3.0 and (or) myocardial excitation in the neuromuscular sys-
tem ofthe heart.
S 2.5 The failure ofcrabs subjected to a pressure of62 MPa
O at 5C to recover fully from treatment suggests that dis-
2.0 ruption ofthe phospholipid membranes at this pressure-
M
temperature combination is so complete as to be irre-
S versible. The slower rate of recovery of crabs tested at
1.5 10C and the complete recovery ofanimals in the 20C
group indicates that the higher temperatures precluded
1.0 complete disruption ofthe membrane systemsand further
V supports the involvement ofmembrane properties rather
0.5 than enzyme kinetics in the observed cardiac responses
to changes in pressure.
0.0 Shedding of proteins from cell membranes begins at
Con2t8rol 62 Reco2v8ery pressures above 30 MPa (Deckmann el ai, 1985), and is
anotherpossible explanation forthe irreversible effectsof
Pressure (MPa) hyperbaricexposure observed in B. thermydron. Substan-
sucFciegsusirvee3c.ontrAavcetriaognesosftatnhedavredntrdiecvlieatoifoBnytohfotghreaeianttehrvearlmsydbreotnwebeefnor1e0, tmiualcrhelehaisgeheorfpirnteesgsruarlesme(ambboruatne100proMtPeai)n,s ohcocwuervsero,nlyanadt
during, and after hyperbaric exposure at 5, 10. and 20C. Interbeat protein release is enhanced by higher temperatures
variability increased markedly in crabs exposed to 62 MPa pressure at (Deckmann et a!.. 1985). These findings are in contrast
both 5 and 10C (F = 20.14. P < 0.01 and F = 17.54. P < 0.01, to the present data, which show more deleterious effects
respectively):however, variabilityremained much higherafterreturnto ofincreased pressure at lower temperatures.
normal pressure in crabstestedatthelowertemperature. The interbeat Despite the changes in heart beat frequency and ven-
interval also increased significantly in response to hyperbaric exposure
aatn2d0reCco(vFer=y8m.o42r,ePc<om0p.l0e1t)e.atlhtahnouagth5theorch1an0gCe.wEarsromrucbahrslerssepdrreasmeanttic1 atrtiicounlairncoBntrtahcetrimoyndpraotnt,ertnhiassssopceicaiteesd swihtohwsprresesmuarrekavabrlie-
SEM. tolerance toward pressure changes at all temperatures
tested. At 5C. thelowesttemperature used inthepresent
study, there were no significant differences in heart rate
were less pronounced at lowertemperatures. The change and noobviouschangesincontraction patternatpressures
in heart rate accompanying decompression was, in fact, u5pCto 41 MPa. Previous results from the same species at
hnIenigglchioegnritbrtlaeesmtap,tetr5haetCuprr(eeMssiecrnketedlusctaeunddythecClheisalerdvlreyersidtsey,moo1nf9s8bt2rraaa;dtyeFcisag.rtdhi1a)at. bweatvweefseohnromw0e.od1nlnayondasti3gp4nriefMsiscPaunartesapnrleedssssdutirsheraunepftf6ei.co9tnMoonPfahteha(erMtiEcrKkaetGle
arsessuolctiiantgedfrdiosmorhgyapneirzbaatriiocn eofxptohseurceontarsawcetlilonaswalviemiftortmh.e aprnedssCuhrieldrraenssg,e o1f9862.a9),togi4v1inMgPB.atfhoerrampypdarroenntalytonloerramballe
If the primary effects of pressure variation on cardiac physiological function. Atthe highertemperaturestested,
the pressure range for stable cardiac function is shifted
function were enzymatically mediated, then one would
towardhigherpressures, butthe magnitudeofthetolerable
expect that temperature changes would have comparable range remains similar. The tolerance of B. thermydron
effects on cardiac function under both hypo- and hyper- for such broad ranges ofpressure at any temperature im-
baric conditions. Conversely, if the system affected by plicates adaptations that decrease membrane compressi-
psurreess(uwrheicchhaldleecnrgeeasiessltihpeidv-ibsacsoesdi.tythoefnphaodsepchroelaispeidinmpermes-- abinlditySoamnedrios c(o1n9s8i9s)teanntdwtihtehfbinodtihngtsheofprBeedhiacntieotnalo.f(G1i9b9b2s)
branes)wouldbecompensatedbyatemperature reduction that species found at greater depths show greater com-
(causing an increase in membrane viscosity), whereas in- pensation fortheeffectsofpressure. A reduction in mem-
creased pressure would be counteracted bya temperature brane compressibility compared with shallower-living
increase. The latter type of pressure-temperature inter- species would preserve the integrity and function ofcell
action has now been shown to occur in response to both membranes and their associated proteins, making this
hypo- and hyperbaric exposure in B. thermydron, impli- deep-sea crab less susceptible to the deleterious effects of
catinga homeoviscous mechanism in which phospholipid changes in environmental pressure.
membrane fluidity is affected by external pressure distur-
bance. Superfluous ventricular contraction spikes and Acknowledgments
prolonged plateaus suggest that disturbed membrane The authorsthank thecaptains andcrewsofR/VJohn
transport leads to the failure ofneurotransmitter release }'. Vickers and R/V Atlantis II, and the pilots of DSV
214 C. N. AIRRIESS AND J. J. CHILDRESS
Alvin: without them these studies could not ha\e been Hartline. D. K. 1967. Impulseidentificationandaxon mappingofthe
conducted. Special th:1 iks are also due to Dr. G. Somero nineneuronsin thecardiacganglion ofthe lobsterHomarusamer-
for hiscounsel on effects ofpressure on enzyme func- icanus. J. Exp. Biol 47: 327-340.
tion, and L. G .Jezky for her assistance and support Kurammyootcoa.rdT.i.umanodfKt.heKulowbastsearw.aP.an1u9l8i0n.isjGaapnognliicuosn.icJ.acCtoimvapt.ioPnhvosfiotlh.e
during the experimental portion ofthis work. Financial B 139: 67-^6.
support was provided by NSF grants OCE-9012076 and Macdonald. A. G.. and I. Gilchrist. 1980. Effects of hydraulic de-
OCE-9301374aswellasby NSERCand AHFMR fellow- compression and compression on deep sea amphipods. Comp.
ships to CNA. Biochem Physiol 67A: 149-153.
Macdonald. A. G.. and I. Gilchrist. 1982. The pressure tolerance of
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