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150 OSB{KKEx ET AL<br />
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Cot 1 Cot 3<br />
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http://legacy.library.ucsf.edu/tid/fpe59c00/pdf<br />
Cot 4<br />
An<br />
-/L<br />
Cot 5 ~a Cot 6<br />
e P./PCr ,<br />
• PCr/0.TP<br />
Cot7 nleRwSBP<br />
- ~ccccxsrcas =f - F .^ asa stffc }<br />
FlG. 5 . Metabolic and meAunrral respnmrs to araje anenal-trnout shunts L41'SI in sr .en pn. Data<br />
tle pesented as pr+KnLigt changt from cnntrul (Su Y, J. 3- and 6 genenllv had an mctrase ,n HR x SBP<br />
during rmpoutlon of thunr tondmonf Cars 2 . l and 7 genrmlh had a dernaac m HR x SBP dunng<br />
impovuon nf .hunt eondniom The meut+obc pnameten IP,/PCr and PL-r/ATPI Parallel rhanges on mt .<br />
duniul panmeten tHR x SRPI: that is, am mivease in HR N SBr,canmmed .nlh am mmase in P{PCr<br />
end d.ertase in PCr/ATP nuos A derrease in HR x SBP is generally auwnaud ..iM a sl,ght ,nneau .<br />
drnrate. on rw change tn O,/P('r arM a 9rgln derrtau, mrrease, or no change on PCR!ATP ranos . P, .<br />
Inorgamr phosphate: PCr. phouphoc¢aone: ATP, denoune ttiphmPhn2 HR. hean ratr. and SBP-slxobr<br />
blood pnssure .<br />
HR x SBP relationship appeared to be quite stable : i.e. . there was minimal change in<br />
P/PCr for any change in the HR x SOP (Fig . 6) . The PCr/ATP vs HR x SOP r41ationship<br />
also appeared to be quite stable . with very little change in PCr/ATP with a<br />
change in HR x SBP (Fig. 7/.<br />
Evaluation of comMned cat data . for the entire volume loading time . demonslrated<br />
that PCr/ATP almosl always decreased (even if the decrease oas sometimes small)<br />
after opening of the AV shums. regardless of the HR x SBP /esponse (Fig . 8). In<br />
addition. P,/PCr generally increased in conjunction with a decrease in PCr/ATP for<br />
all points of time throughout acu7e volume loading (Rg . 9) . When changes in P,/f°Cr<br />
were eorrelated with changes in HR x SBP for all points in time for the entire grolap .<br />
there appeared to be a trend towald linearity (Fig . 10) t+'ith P,/PCr increasing as 11R<br />
x SOP increased .<br />
DISiL351O.`t<br />
There are a number of hypotheses concerning the tissue events which may lead In<br />
myroeardial eell damage and/or death (-'8--i1): ischemia . hypoxia . acidemia. oxygen<br />
PUBLICATIQNS<br />
10347656<br />
I<br />
028399