Guido-Allen, D.A.

Hartenburg, D.S.

McCullough, P.A.

O'Neill, W.W.

Puchrowicz-Ochocki, S.B.

Speck, J.P.

Stevens, M.

Tobin, K.J.

Westveer, D.C.

Elsevier - Publisher Connector 

JACC February I(F)X 469A 
culer evl~l~l This iS cormstent with recent study showing protechve effect of 
immunizing LDL r~mptor-deflcmnt rab~ts with OxLDL, 
~ ClmulMory Effo¢l~ of Nl¢orandll After Flint [lose 
and Alter Repeated Dosing 
U, Thadam. ~ ot O~. .a .  O~ahorna C~, O~a,  USA 
N~'ofalld;! (NIC) Is a ru¢otmama:le d(~ivatw~ (n,[~_ H y ~ ]  racottnam~:~te 
~rate), which m'~pmv~ (~mae/~ gow and m an ami~chem¢ agent, 
but tm~ke mwahm ~ ¢*mn',~d not to be mmocmte¢l wrm de',~lormment of
!n a ~ l~nd ram~mlzed CroSsover Mud~ m 14 paf~mts with ~ 
emgm~ pectoe~, eltects o! t 0 mg NIC o~ placelpo (PL) on ,~%'tJfl bk~x) pm~swe 
(~P) ~d bean ra~ m ~alualed Mter ~ f l~  d0se ar~ a:'.-xer 2 weeks 
dose. Comlmmd Io ~ vames changu ~n sysfo~ (S) ard ~ c  (d) 
BP and ~ mm (HR) m the ~ p0s~0n aftsr !1~ first (~R~ ~ after 
~ : .~ ,a  ol I~1 emramt were: 
! l-imm~ 4 Hours aHou~ 
N~C e~. mC ~ ~C PL 
(S|BPIstDO~e -2~" -3 -tg' 0 t6" -4 
D~tt4 -it -4 5 ~t2 -3 
(D)BPt=Do~ .-t3" -~ -t3" -i -~2 -5 
Day t4 -7 -3 -7 -4 -4 -2 
(HR) tslDo~e 12 1 3 4 2 3 
O~et4 3 -2 -5 4 4 S 
Dala show h'lat r.~t dose ol 10 mg NIC emptied s~mficant clmtdalory 
eltects Ira- at leas1 up to 8 houm b~ me peak ~,',~ct and du~a~ o~ effec~ 
m~re ~ ammuam~ am~ re~ea~m ~.  Thos. ~ ~o pmra~ 
v~ew, ll~s sludy shows that c ~  torrance dm¢=k~ps fogom~g ~ 
eq~sme to ntcorandd. 
What Ro~e Ooes Uann.ol may In PnmmU.g 
Commst ~ ?  a ~ Ana~ts 
KJ. Tobm. P.A. McCultough. J.P. Speck. D.C. Westveer, OA. Guido-Nten. 
O.S. I"lmleNm~, S.B. ~ . -Ochod0,  W.W_ O'Nei,, M. Stmmns. 
Diwskm of Cardiovascular Medich'm, Her~. Ford a~d Vascuiar lnst;r~ 
Hemy Fo.rl Heat~ b~.  One Ford mac~ S~te 3C, Detro~ Mt 48202. 
USA 
Rece~ ~ have shown ltmt ~ use of mannttot may mcm~se renal o~t- 
ge~ demands, and deslm~, causing an osmot¢ diurems, may be ,n]u.ou~ to 
renal ~ after vascular contrast exposure. It's use. ~-=mfom, as a l~ro- 
phytact¢ agent to prevent contrast ~ t h y  after coronary 
remains controvers,~. As part of the PRINCE (Prmmr~r~n of Rad~K:ormast 
Induced Nephropathy Evaluat~0n) Tnal. palmnts ~ were ~ to a 
forced dmmsLs protocol (fumsemide I mg/kg WP and dopamme 3.g/kg/mm 
IV) and had a mean pulmooary capdla~ wedge pmssu~ <20 mmHg at the 
sta~ ot the procedure, received intravenous marmitol 12.5 oj1~g over 2 I'mum 
This administmtmn occurred clunng ~e conlrasl exposure and was foffo~ed 
by Ii~lrahon with 0.5 NS IV at a rato to match the urine oulput. As dictated by 
the protocol, those who were selected for mam,lol had a k~er mean PCWP. 
14.4 vs. 26.1 mmHg. p = 0.0009. The mean baseline serum c1"eatimne (Cr) 
was 2.2 ± 0.38 vs. 2.59 ± 0.94 in the mannttokexpased (groc~ 1, n = 22) vs. 
the mannitol-unexposed (group 2. n = 76), p = 0.05. Groups 1 and 2 were 
othe~rise sin~lar with respect to confotmdem including diabetic status and 
contrast volume received. The mean induced urine flow rates were 167.62 
± 58.00 vs. 133.20 ± 55.63 mYmin/over 24 hours, p = 0.02, in groups 1 and 
2 r e ~ .  The resultant mean Cr at 48 houm after contrast exposure 
was 2.72 ~ 1.19 vs. 3.11 ± 1.21 mg/dl, p = 0.22, and the mean ~ 1  
increase in Cr was 0.61 ± 0.98 vs. 0.58 ± 0.72 mg/dl, p = 0.88, respectrvely. 
Conclusions: Despite its use in patients with mote favorable renal funchon 
and hemodyrmmic profiles, the controlled, pmspectnte IV administration of 
mannitol was not effectwe in preventing renal injury despite augmentato'~ of 
a forced diuresis with other agents. 
~ A Randomized "t~ial of  Prevention Measures in 
Patients at High Risk for Contrast Nephropathy: 
Initial Results of  the PRINCE Study 
M. Stevens, P.A. McCuilough, K.J. Tobin, J.P. Speck, D.C. Westveer, 
O.A, Guido-Allen, D.S. Hartenburg, S.B. Puchrowicz-Ochocki, W.W. O°Neig. 
Division of Cardiovascular Medicine, Henry Ford and Vascular Institute, 
Henry Ford Heaffh System, One Ford Place, Suite 3C, Detroit, M1482~.,2o • 
USA 
Recent studies from series of PTCA and CABG patients indicate that baseline 
renal o~furctmn m an indelmndem IXe<~cfor f monal~ after ~ ~,-~,. 
cl.res. We have pmv~usly tmown a gra0~l mlatmmm~ w~ me ¢ ~  ol 
renal failure and ~ Im:~l~y of m-homital death m Im,mn~ un(~ 
Io0p ~urel¢~, mannitol) have 8ho.~ no clear ~ ~ I 
of patmm= m r~m, We Nt  out t ~ ttm the ~ .,~t a fo¢=¢1 ¢~nm 
a~er me con.a~ e~Do~um w~h a ~ of me~ ~mu~ m~u~ m 
a mduce~ ~me c~ re.al U~r~ ,n ~ ~mm~ w e ~ m  
0,9 mg/~, The ~m~Im were ~,~lar with rL~xcl to age, W~l~ ~:~¢ 
edent 0t i~ml  vMctll~r ¢lileMe, The f0R~Kl ~tmm~ fwct~e¢l m 
um~ flow rallm, 1~3 ~ ~4 vs. I~3 ~ SS ml/hr, O~e 1he ~4 h~um gtef ¢o11~11t 
exposure (p ~ 0.001), Thrum ~ m ~ tugil~lt ~ ~ ~ fl(mH1d 
the s r~J  memase m ~ Cr, 03 ~ 0.6 v~ O.g ± 0,9 mQ~l m me lowest 
,n ~he ~ace~o a~m re~ ~ w,~ a. ~ ~ .avr.g meam.~d 
d ~ pem~ begmm~ at the mn ol am~gmp~ o~ ~me~m 
to ~ a unne go~ ra~e of ~, 145 m~hr m me 24 houm aftra me pm¢e~m, 
Heart Failure: Beta Antagonists 
Wednesday, Apnl 1, 1998, Noon-2:00 p.m. 
Georgia Wodd Congress Center. West Exhibit Hall Level 
Presentation Hour. 1:00 p.m.-2:00 p.m. 
Canmdl~l  Inhibits EndoUtelln-1 B lo lyn lheMI  In 
Cu~med Human Coronary Ar~ry ~ l  
EH G~i~,~, G. ~ , / L M .  Romanic, R.R. Ruff~o, Jr.. ~ 
ot Ca,~,~asc~ar P~n~aco~j~, ~ B=~c,~,~ Ptwmz¢e=,¢a~, 
K~ng o~ P~. ,~.  R~ 19406. USA 
It has been m¢~,~-y ~ed thai CHF pa~e~s mm~d ~ car~lo l  have 
s~j~mr~y _r,~,___,c.~__ cmmmm~g ,~-~I  (ET-~) ~ as compared to 
~mm~ed mments. The m~c~ms m p~sma ET-I k.,e*s cormmnmU 
~th a ~ ~ ~ in va~m~ immmemm uud to mea- 
sure the ~ ~ ~ of head P=tiiurB. ~ ,  the f1~ch~-~i~.T~ 
for the ciecmase rn ET-1 was not known Tt-¢=~fore, rne f,,-=s~ s~,~'y was 
des-~g~..d to ~ me d~mct effects of cen~d~m* on ET-I 
5~S in ct.d~fed ~ corollary ~f1~ erl~0~hellal ~ (HCAECs). HCAECa 
were tmaP~J w~h canmd~lol 15 rmn Ire'lot o file ado~itlon of see.~n and ET-1 
levels were measured in the ~.~.~;;~..,,~,.~ mlmlnJ, m 24 hr later. ~ Ira> 
a ~ !  ml~mn of r, emm-med~ 
of ET-I bmsyne~ms ,~th an tC~ = i uM. Pm1~roE'r-1 mRNA e~easmn 
was also mhil~ted by carvedlol maln~nL Oe~r p -adnmo,~v~v a~ago~sls 
such as proprar~ol (10 uM) o~ ce~pm~ol (10 uM) did no~ effect ET.1 
thess. Fu'~e~mmo~, me amh~,~ant IXObUO~ (10 uM) ~ not enect ET-1 
product~n, fo'~muno-hisfochE~cel analys~ of HCAECs silo demonstmtsd 
b~at cenmd~of mh;b;h~3 ET-1 ~ .  These data ~te  thal cenm~Iof 
o~rec~ mhil~s me Im)syne~,s of ET-I in HCAECs, and this effect may 
con1~Imle to its ~,a;.-.;~lat mg and anlqamlifmaftve actions. Fmlhermom. these 
effects may contnbum to the ab~ltty of cantedilof to improve dtnlcal outcome 
in CHF paftents. 
~ Ooes Canmdllol Inhibit Aorlal  Smooth Muscle Cell 
Prol l femtlon? 
P. Mohacsi', K. PI0Ss ~ , HU. Tschanz ~ , S. Gasoflefl I , R. Asm~, 
G. Spon~. ' C ~  U,",tt~t~," ~ Bert,., Gerrp~.t~/; 21.q'Mffu'te of
Biochemistry.. Untversdy of Basel, Germany: ~Boehnnger-Man~ll~m, 
Marmheim. Germany 
Canmdilol [C] is a multiactiog ant]hypertenshte drug recently also apf~oved 
for the treatment of heart failure and combines ~- with a~.bloCking and an- 
tioxidant activities. It was shown that C protects the vasculalum from chronic 
pathological processes such as ischemia, atherosck~osts and remodelling 
that is observed in the cardiovascular system after pressure overload and 
shear stress. To evaluate the antiproliferatwe activity of C on human aofffc 
vascular smooth muscle ceils [SMC], we tested the influence of C and of 
diff ~ ~_nt agents whc'h contnbute to C's activity. SMC were cultured under 
serum free conditions and either treated for 6 hm wffh different cor~-,,;,~- 
tions of C, C's metabofite BM 91.0228 IBM] [without ~.blocldng, but 30.fold 
C 
E 
F 


What role does mannitol play in preventing contrast nephropathy? a prospective analysis 

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What role does mannitol play in preventing contrast nephropathy? a prospective analysis

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