Eight‐fold differences in STaH were detected among 15 inbred rat strains (Klemcke et al., Shock 29:748, 2008) suggesting genetic effects on STaH. In that study, blood volumes (BV) for all strains were assumed to be 5.83 % of body weight and 55% of that BV was removed. We also showed that differences in STaH might reflect strain‐dependent differences in BV (Klemcke et al., FASEB J 23: 801.1, 2009). To address this hypothesis, each rat of 5 inbred rat strains was hemorrhaged based on its own BV measured using Evans Blue dye 24 hr prior to hemorrhage and its STaH determination. BV varied (P <0.01) among Brown Norway (BN/Mcwi; n = 14; 7.43 ± .10 ml/100 g body weight, mean ± SEM), Salt Sensitive (S; n = 10; 7.08 ± .15), Fawn Hooded Hypertensive (FHH; n=10; 6.74 ± .08), Lewis (LEW; n=10; 6.74 ± .08), and DA (n=10; 6.74 ± .08) rat strains. With equal hemorrhages (47.1 ± .05 % of measured BV), STaH did not differ among rat strains (155 ± 12 min; P = 0.95). When considering both studies it is apparent that: 1) Strain‐related differences in BV contributed to differences in STaH in our 1st study; 2) In FHH rats 1.3% more of total BV was removed in the current study, yet they survived 1.5 hr longer; and 3) In LEW rats identical BV were removed in both studies, yet currently LEW rats survived 1 hr longer. Such observations suggest that Evans Blue dye and/or blood sampling for BV determinations might be preconditioning stimuli that improve STaH in some rat strains.