Intensity of halothane- and hypercapnia-induced cerebral hyperemia is strain-dependent in rats

Cerebrovascular responses to physiologic and pharmacologic stimuli vary between laboratories using different strains of the same species. We tested whether the cerebral blood flow (CBF) response to 1% halothane or hypercapnia is strain-dependent in rats. Age-matched adult male (n = 14 of each strain) Wistar, Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR) were anesthetized with pentobarbital and mechanically ventilated. Under baseline conditions blood flow to cerebrum (microspheres) in WKY (66 +/- 5 mL.min-1.100 g-1) was less than (P < 0.05) in Wistar (88 +/- 5 mL.min-1.100g-1) and SHR (83 +/- 5 mL.min-1.100 g-1). Blood flow to brainstem was greater (P < 0.05) in Wistar (106 +/- 8 mL. min-1.100 g-1) than in WKY (71 +/- 5 mL.min-1. 100 g-1) and SHR (84 +/- 4 mL.min-1.100 g-1). In the halothane protocol (n = 8 each strain), administration of 1% halothane, during normocapnia, increased blood flow to the cerebrum in WKY (64 +/- 6 to 120 +/- 12 mL.min-1.100 g-1, P < 0.05) and SHR (78 +/- 6 to 115 +/- 8 mL.min-1.100 g-1, P < 0.05) but not Wistar rats (88 +/- 8 to 102 +/- 5 mL.min-1.100 g-1, not significant). Discontinuing halothane caused blood flow to return to baseline values. In the hypercapnia protocol (n = 6 each strain), exposure to 3% CO2 (to achieve a PaCO2 of 50-55 mm Hg) and 6% CO2 (to achieve a PaCO2 of 60-70 mm Hg) caused blood flow to the cerebrum to increase in Wistar (87 +/- 11 to 112 +/- 15 to 162 +/- 23) to similar amount as observed in WKY (69 +/- 7 to 115 +/- 13 to 162 +/- 23 mL.min-1. 100 g-1) but less than that observed in SHR (89 +/- 7 to 174 +/- 24 to 237 +/- 28 mL.min-1.100 g-1). These data demonstrate that the cerebral hyperemic response to vasodilator stimuli is strain-dependent in rats.