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The heterogenity of chronic active hepatitis (CAH) HBs Ag-
RESISTF\NCE TO SPIRONOLF\CTONE IN NON F)ZHOTEROLE OF ENHPlNCED rlIr OSCITIC CIRRHOTICS: PROXIMPL SODIUM REABSORPTION. Cavesaro. P. ~no+l i . i. . Sacerdoti. G. Albino+ Department of Gatta University of Padua
F. Menon, 0. Merkel t 0. C. Hedicine. Clinical
verify if the The study was designed to reabamount ok proximal-fractional sodium may affect the response sorption (PFR Na) to spircnolactone in Aon a-rothemic ascitic We evaluated renal plasma flow cirrhotics. rate (GFRl, glomerular filtration (RPFl. (FE Nab. sodium fractional excretion distal fractional sodium reabsorption (DFR aldosterone (I’cIl in p 1a5ma Na, . PRPI. and 42 nscitlc cirrhotic5 with serum creatinine < 1.3 nag/d1 who then received spironolactont? at dOSO’1 up to 500 mg/day and in 25 ConCrols 111.10weve on the same iposodic diet. Non responders to spironolactone in 3 days1 (90 (bodv weiQht loss < 700 9 %, showed-a more reduced FE Na as a’result Of ; more increased PFR Na (D < 0.05). a more reduced DFR Na (p < O.O!Sl. and higher and PPI (p < values of PR6 0.051 than responders. No difference wari found in RPF and GFR. We conclude that the resistan ce to spiranolactone azothemic ascitic cirrhotics is ize to a yreatly enhanced PFR Na which limits the role of P& in renal sodium retention.
non
0.
An-.
M. ~?J~XSN.
Medicine. Rm&ni kspiti.
L.
wlligescuDept. of Intexnal
B.KhaEst. Ramra.
I,‘ol.cithin (LPC, is . ujor m*tabo1ita of p,,oqd,olipids tux'zxo..l, .nd proini1utory propati*s. sins9 th. liver plays . ujor rol. in UC r..o..l ..zd ~ms+s.ing, w. studied the Imp&o-biliacy wtabolisr of LPC in CClO-induc.d cirrhosis. Tuelrm ula, sirrhotio Wistar I.+S .nd d histology-prov+n, fitted jugular and biltary controls we*. c.tb.t.r‘ .,,d kqt under taurocholat, (1 Two mCi of 1-(ldclp*lmitoyl-LPC UWl/rilI, i...,. of radiostivity l'h, fat. I#.=. givm .‘ . bo1us. 1ir.r "pt.,‘. .nd ‘ubc.L1uI.r (plasm c1marancr, molm2ul.r biotransforootions .nd location, ?? ggregativo forms) was studied by combinmd ohro..towr.phis .nd r.diochais.1 ..thods. . prolor& pm ,BDC. in Results: 1) LPC has plasma in cirrhotis, dum rant:< to decreasad hapatic clearance and inmfficienl conrrrsion into lacithin: 2) both microsoul and cytocolic LPC mcylatioois much wlowmr in the cirrhotic than in ccuDul~tion occur‘ in tb. noru1 1iv*r; 3) LPPC?? the cirrhotic liver, largely .‘ . noa protein bound frwtion; ., th. s.l.cti;ity of LPC .c,l.&n observed in controls is PertiellFlost in cirrhosi#; 5) ??consiwt.nt frakion 02 LPC is conrertad into triglycoridw in cirrhosis,but controls. Thasd r...n derangaents of LPC metaboliu in the cirrhotic lirar ?rr ? 5. of pathogan*tic significance.
With..lbrmm-toxic
r.ts with
with comst.mt
cttosolis
‘trist
.ol.sul.r
not in
HEPATICAND INTESTINALOXIDATIVETISSUE DAMAGSAFTXk ISCHEWIAAND REPERFUSIW A.J. Auaustin. J. Wilr and J. Lut?, Dwpt. of Pbyriology, Universityof Yuerzburg, F. k. Gwraray The liver ir cmP8bmblrof 8cbievinghigh oxygen extrectionretiesand seems to hare 8 hiaher iscbuic tolcrrncrthan the prepositioned into&no. Concerning iscbemieand reperfusion,these tissuesshow ?? different way of rustrisingen oxidative Eurgw, most likelycausedby differrntfrer radicalsource,. This wes concludedfrom the fallowinaexperiments: Two modelsof irchmir were utilisrdwith mrlr wirtar rrtr: 1. Hwaenteric rrtrry occlusion [WQCI (45/90min irchemie[II): 150 min reperfurion[RI). 2. Subdirphrrgmrticrortic occlurion[AOC] (IS ?in ? [II: 45 min [Xl). After experimentslipid paroxide levwlr (LPO)in tissuewara drtrrminwdby the mrthod of Ohkwr et ?? l. (1979). 1. XOC: Aftrr 45/90 min of ischemieLPO of intastim increered
from 42.6
t 3 to 503/966
nmollg Not wright
(p
reperfusion
LPO in liver
increesed
from 133 i
12 to 499 t 56 (~(0.01). intestinal LPO rose to 1073 t 134 (P
slightly
dewed
by
hypoxie
and/or
non-
specific oxidases/Fonton and Iiabar - Weiss reaction might be predominantin the liver.
F. Menon, 0. Merkel t 0. C. Hedicine. Clinical
verify if the The study was designed to reabamount ok proximal-fractional sodium may affect the response sorption (PFR Na) to spircnolactone in Aon a-rothemic ascitic We evaluated renal plasma flow cirrhotics. rate (GFRl, glomerular filtration (RPFl. (FE Nab. sodium fractional excretion distal fractional sodium reabsorption (DFR aldosterone (I’cIl in p 1a5ma Na, . PRPI. and 42 nscitlc cirrhotic5 with serum creatinine < 1.3 nag/d1 who then received spironolactont? at dOSO’1 up to 500 mg/day and in 25 ConCrols 111.10weve on the same iposodic diet. Non responders to spironolactone in 3 days1 (90 (bodv weiQht loss < 700 9 %, showed-a more reduced FE Na as a’result Of ; more increased PFR Na (D < 0.05). a more reduced DFR Na (p < O.O!Sl. and higher and PPI (p < values of PR6 0.051 than responders. No difference wari found in RPF and GFR. We conclude that the resistan ce to spiranolactone azothemic ascitic cirrhotics is ize to a yreatly enhanced PFR Na which limits the role of P& in renal sodium retention.
non
0.
An-.
M. ~?J~XSN.
Medicine. Rm&ni kspiti.
L.
wlligescuDept. of Intexnal
B.KhaEst. Ramra.
I,‘ol.cithin (LPC, is . ujor m*tabo1ita of p,,oqd,olipids tux'zxo..l, .nd proini1utory propati*s. sins9 th. liver plays . ujor rol. in UC r..o..l ..zd ~ms+s.ing, w. studied the Imp&o-biliacy wtabolisr of LPC in CClO-induc.d cirrhosis. Tuelrm ula, sirrhotio Wistar I.+S .nd d histology-prov+n, fitted jugular and biltary controls we*. c.tb.t.r‘ .,,d kqt under taurocholat, (1 Two mCi of 1-(ldclp*lmitoyl-LPC UWl/rilI, i...,. of radiostivity l'h, fat. I#.=. givm .‘ . bo1us. 1ir.r "pt.,‘. .nd ‘ubc.L1uI.r (plasm c1marancr, molm2ul.r biotransforootions .nd location, ?? ggregativo forms) was studied by combinmd ohro..towr.phis .nd r.diochais.1 ..thods. . prolor& pm ,BDC. in Results: 1) LPC has plasma in cirrhotis, dum rant:< to decreasad hapatic clearance and inmfficienl conrrrsion into lacithin: 2) both microsoul and cytocolic LPC mcylatioois much wlowmr in the cirrhotic than in ccuDul~tion occur‘ in tb. noru1 1iv*r; 3) LPPC?? the cirrhotic liver, largely .‘ . noa protein bound frwtion; ., th. s.l.cti;ity of LPC .c,l.&n observed in controls is PertiellFlost in cirrhosi#; 5) ??consiwt.nt frakion 02 LPC is conrertad into triglycoridw in cirrhosis,but controls. Thasd r...n derangaents of LPC metaboliu in the cirrhotic lirar ?rr ? 5. of pathogan*tic significance.
With..lbrmm-toxic
r.ts with
with comst.mt
cttosolis
‘trist
.ol.sul.r
not in
HEPATICAND INTESTINALOXIDATIVETISSUE DAMAGSAFTXk ISCHEWIAAND REPERFUSIW A.J. Auaustin. J. Wilr and J. Lut?, Dwpt. of Pbyriology, Universityof Yuerzburg, F. k. Gwraray The liver ir cmP8bmblrof 8cbievinghigh oxygen extrectionretiesand seems to hare 8 hiaher iscbuic tolcrrncrthan the prepositioned into&no. Concerning iscbemieand reperfusion,these tissuesshow ?? different way of rustrisingen oxidative Eurgw, most likelycausedby differrntfrer radicalsource,. This wes concludedfrom the fallowinaexperiments: Two modelsof irchmir were utilisrdwith mrlr wirtar rrtr: 1. Hwaenteric rrtrry occlusion [WQCI (45/90min irchemie[II): 150 min reperfurion[RI). 2. Subdirphrrgmrticrortic occlurion[AOC] (IS ?in ? [II: 45 min [Xl). After experimentslipid paroxide levwlr (LPO)in tissuewara drtrrminwdby the mrthod of Ohkwr et ?? l. (1979). 1. XOC: Aftrr 45/90 min of ischemieLPO of intastim increered
from 42.6
t 3 to 503/966
nmollg Not wright
(p
reperfusion
LPO in liver
increesed
from 133 i
12 to 499 t 56 (~(0.01). intestinal LPO rose to 1073 t 134 (P
slightly
dewed
by
hypoxie
and/or
non-
specific oxidases/Fonton and Iiabar - Weiss reaction might be predominantin the liver.