r abrupt nitrous oxide administration in a canine model of critical coronary stenosis induces regional myocardial dysfunction that is worsened by halothane. Anesth Analg 1988;67:81422. 71rr existence of a dose-resporise retntion betzueerr nitrous oxide concentration and regional dysfunction in cornprorriised myocardium, nnd uhether or not Iialothane-iriduced rnyocardial depression alleviated this regional dysfunction ions examined. Nitrous oxide 7uas administered to eight d o p ulitli experimentally induced left anterior descending c-orunary artery (LAD) criticol stenusis during fentanyl (ZOO p,y/kg bolus plus 1.5 pgkf'.iriiri-l) anesthesia. Tzoo modes of nitrous oxide administration zuere ernployed:,yrndziat iiri steps of 20'70 inspired, i.c., O%, 20%, 40%, and 60% inspired) arid abrupt (0-60% inspired). Regional myocardial function was assessed by soriornicrornetry. Repenal dysfunction in the compromised myocnrdium, in the furrn of postsystolic sllortenirzg (PSSI, increased aboue baselinc kzds during 40% (4.2 t 2.3% to 12.1 i 3.9%, P < 0.05) and 60% (4.2 i 2.3% to 12.5 t 3.6%, P < 0.05) inspired nitrous oxide (gradual administration) and also during abrupt 60% nitrous oxide administration (6.4 i 2.6% to 9.9 t 3.2%, P < 0.05). After abrupt 60% inspired nitrous oxide administration, halothane (0.7% inspired) ions introduced and caused decreases in mean arterial pressure (206.1 2 4.5 mm Hg to 76.2 2 5.5 mm Hg, P < 0.05) and peak LV dPldt (1700 * 250 mm Hglsec to 1100 2 ZOO mm Hglsec, P < 0.05). Halothane caused a rrinrked increase in PSS (9.9 i 3.2% to 30.8 k 12.6%, P < 0.05). T h i s nitrous oxide administration caused regional dysfunction in myocardium supplied by a critically narrozoed LAD whether administered gradually or abruptly arid at coricentrations as lotu as 40% inspired. The addition of halothane to decrease myocardial oxygen demand resulted in marked zuorsening, rather than alleviation, of regional ryocardial dysfunction.