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Titolo:
CORONARY VASOCONSTRICTION AFTER PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY IS ATTENUATED BY ANTIADRENERGIC AGENTS
Autore:
GREGORINI L; FAJADET J; ROBERT G; CASSAGNEAU B; BERNIS M; MARCO J;
Indirizzi:
UNIV MILAN,OSPED MAGGIORE,CTR FISIOL CLIN & IPERTENS,CLIN MED GEN,VIAFRANCESCO SFORZA 35 I-20122 MILAN ITALY CLIN PASTEUR,UNITE CARDIOL INTERVENT TOULOUSE FRANCE
Titolo Testata:
Circulation
fascicolo: 2, volume: 90, anno: 1994,
pagine: 895 - 907
SICI:
0009-7322(1994)90:2<895:CVAPTC>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-FLOW VELOCITY; ADRENERGIC-RECEPTOR BLOCKADE; MYOCARDIAL-ISCHEMIA; CONSCIOUS DOGS; SUBSELECTIVE MEASUREMENT; BALLOON ANGIOPLASTY; VASODILATOR RESERVE; ARTERIES INVIVO; ENDOTHELIUM; SEROTONIN;
Keywords:
ANGIOPLASTY; SYMPATHETIC NERVOUS SYSTEM; NEURAL REFLEXES; VASOCONSTRICTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
65
Recensione:
Indirizzi per estratti:
Citazione:
L. Gregorini et al., "CORONARY VASOCONSTRICTION AFTER PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY IS ATTENUATED BY ANTIADRENERGIC AGENTS", Circulation, 90(2), 1994, pp. 895-907

Abstract

Background Vasoconstriction occurs after percutaneous transluminal coronary angioplasty (PTCA) along the dilated vessel, The vasomotor changes, initiated by the mechanical stretch of the stenotic region, are thought to be due to various mechanisms but whether the sympathetic nervous system plays a role in this phenomenon remains unknown. Methods and Results Quantitative angiography (ARTREK) was performed in 45 patients undergoing an epicardial vessel PTCA for a stenosis of 76+/-1% (1)in basal conditions, (2) after PTCA, and (3) 30 minutes after PTCA (vasoconstriction). In 14 control patients, the same measurements were obtained up to 60 minutes after PTCA. Coronary diameters were measured along the PTCA vessel at the narrowest stenosis level and at a level peripheral to stenosis. In 36 patients two diameters were also measuredat a proximal segment and at a distal segment along a nonmanipulated vessel. Thirty minutes after PTCA the dilated segment underwent a -31+/-2% (mean+/-SEM, ANOVA, P<.05) reduction in diameter when compared with PTCA values, and the segment peripheral to stenosis showed a reduction of -17+/-2% (P<.05). In all patients a significant vasoconstriction also was observed along the control vessel (proximal segment, -14+/-3%; P<.05 versus basal; and distal segment, -17+/-2%). At the time of maximal vasoconstriction (30 minutes after PTCA), the patients (treatment groups) received (1) 18 mu g/kg IC phentolamine (Phe, n=7), (2) 14mu g/kg IC yohimbine (YO, n=7), (3) 16 mu g/kg IC propranolol (Pro) followed by 18 mu g/kg IC phentolamine (Pro+Phe, n=7), and (4) 0.2 mg/kg IC bretylium (Bre, n=10). In 14 patients (control groups) an intracoronary injection of warm saline was given. After drug injections, angiograms were repeated at 5-minute intervals for 20 minutes and ended after a 300-mu g intracoronary trinitro-glycerin injection. At stenosis level, Phe and Bre counteracted vasoconstriction, inducing a dilatation of +19+/-3% and +22+/-6%, respectively, while Pro+Phe caused a dilatation of +16+/-9% above the PTCA values (P<.05 versus PTCA). YO only partially reversed vasoconstriction (from -33+/-4% to -12+/-4%, P=NS versus PTCA). At peripheral-to-stenosis level, vasoconstriction was abolished by Phe (+26+/-7%, P<.05 versus basal), while it was still present after Pro+Phe (-23+/-2%) and Pre (-18+/-4%). In addition, Phe and Bre dilated the control vessel at the proximal segment (+17+/-6% and +8+/-4%, respectively, P<.05 versus basal), while YO and Pro+Phe only counteracted vasoconstriction (from -15+/-3% to +7.6+/-1% and from -16+/-3% to +4+/-5%, respectively, P=NS versus basal). At the distal segmentonly Phe produced a vasodilatation of +23+/-1%; YO counteracted constriction (from -16+/-2% to +9+/-6%, P<.05 versus basal), whereas after Pro+Phe and Bre, the vasoconstriction persisted. Conclusions The mechanical stretch and ischemia caused by balloon inflation induced vasoconstriction mediated by alpha-adrenergic receptors (mainly alpha(1)), overcoming a beta-mediated dilatation. The use of different antiadrenergic drugs showed that Phe counteracts post-PTCA vasoconstriction, and the simultaneous use of alpha- and beta-receptor blocking agents (Pro+Phe and Bre) reveals the presence of a peripheral, predominant beta-mediated dilatation. The presence of vasoconstriction also along the control vessels not branching from the stretched ramus provides evidence for the existence of neural sympathetic vasoconstrictor reflexes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 03:02:16