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 ± 5mL · min^-1 · 100 g^-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 ± 5mL · min^-1 · 100 g^-1) and SHR (84 ± 4mL · 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 a 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.