Cardiovascular actions of XXXX or @entity1508 in @entity3485 @entity1707 .

@entity1707 @entity308 @entity296 @entity3727 @entity1508 @entity548 @entity190 @entity64 @entity26 @entity18089 @entity880 @entity3485 @entity3810 @entity1063 @entity65
During normovolemia, @entity3810 causes mild sympathetic stimulation and direct @entity296 ; these effects offset each other, resulting in only minimal cardiovascular changes. To test the hypothesis that during @entity3485 this balance would change and @entity308 predominate, 10 @entity1707 were made @entity3485 (30% @entity190 ) and then were given 70% @entity3727 (0.25 MAC in @entity1707 ) or an equipotent concentration of @entity1508 , an agent that does not cause sympathetic stimulation. The alternate anesthetic was given to the same @entity3485 @entity1707 on another day. Five minutes after induction of anesthesia during @entity3485 , both @entity3727 and @entity1508 caused significant, physiologically important deterioration of compensation for @entity548 . @entity1508 decreased systemic vascular resistance (SVR); @entity3727 was more variable in its action, and SVR did not decrease significantly. Both agents caused similar decreases in cardiac output, mean aortic blood pressure, @entity64 volume, @entity26 consumption, and left ventricular minute work, despite increases in plasma epinephrine concentration and plasma @entity18089 activity. No differences were found between groups for any of these variables (P greater than 0.05). Plasma @entity1063 concentration increased only in the @entity3727 group and was greater in that group than in the @entity1508 group. The @entity65 for @entity548 was expressed metabolically by similar decreases in the two groups in partial pressure of @entity26 of mixed venous blood and by increases in blood @entity880 concentration. Thirty minutes after induction of anesthesia, with stable end-tidal anesthetic concentrations, both groups had some cardiovascular, but no metabolic, recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
