VENOUS RESISTANCE INCREASES DURING RAT ANAPHYLACTIC SHOCK

Anaphylactic shock is a sudden, life-threatening allergic reaction associated with severe hypotension. The increased venous resistance accounts for the anaphylactic hypotension in anesthetized dogs. However, the change in peripheral vascular resistances during anaphylactic hypotension in other animals such as rats is not known. We measured the mean circulatory filling pressure using the mechanical occlusion method of inflation of the right atrial balloon along with systemic arterial pressure (Psa), central venous pressure, and portal venous pressure. Cardiac output was also measured with the thermodilution method. From these hemodynamic variables, we calculated the total peripheral and venous (Rv) resistances during anaphylactic hypotension in anesthetized rats. These hemodynamic variables were compared with those in the hemorrhagic shock. After an intravenous injection of 0.6 mg antigen ovalbumin in sensitized rats, Psa decreased from 119 ± 4 to 43 ± 2 mmHg, cardiac output decreased from 84.5 ± 5.7 to 37.8 ± 2.1 mL min, central venous pressure decreased from 0.9 ± 0.1 to 0.1 ± 0.1 mmHg, and mean circulatory filling pressure also decreased from 6.0 ± 0.2 to 5.2 ± 0.3 mmHg. Thus, the Rv increased from 0.06 ± 0.05 to 0.15 ± 0.02 mmHg mL−1 min−1, but total peripheral resistance did not significantly change. Portal venous pressure also increased from 5.6 ± 0.5 to 21.5 ± 0.9 mmHg. Hematocrit markedly increased from the baseline values of 43% ± 1% to 55% ± 1% at 15 min after antigen. During hemorrhagic shock, Psa decreased in the manner similar to anaphylactic shock; however, Rv did not significantly change, and portal venous pressure decreased. In conclusion, in rat anaphylactic shock, a substantial increase in Rv presumably due to hepatic venoconstriction may decrease venous return, resulting in systemic hypotension.