Abdominal
ischemia and reperfusion evoke reflex excitation of the cardiovascular system and generate
reactive oxygen species. We have shown previously that the
reactive oxygen species hydrogen peroxide (H2O2) elicits reflex excitation of the cardiovascular system after serosal application to abdominal organs. However, it is not known if
ischemia-sensitive afferents respond to
reactive oxygen species or if scavengers such as
dimethylthiourea (
DMTU) inhibit the response of these afferents to
ischemia or reperfusion. Therefore, to provide more information on the neurophysiological mechanisms underlying the activation of these afferents, we studied their responses to H2O2 applied to the receptive field during recordings of single-unit activity of
ischemia-insensitive or -sensitive abdominal visceral C fiber afferents in anesthetized cats. Additionally, we recorded single-unit activity of
ischemia and reperfusion-sensitive afferents before and
after treatment with
DMTU (10 mg/kg), which scavenges H2O2 and
hydroxyl radicals or the
iron chelator deferoxamine (
DEF, 10 mg/kg), which inhibits
hydroxyl radical formation. Application of 44 mumol H2O2 to afferent endings increased the discharge frequency in nine of 11
ischemia-sensitive units, from 0.01 +/- 0.01 to 0.67 +/- 0.16 impulses per second. In contrast, only one of 10
ischemia-insensitive C fibers responded to H2O2 application. In an additional 13
ischemia-sensitive C fibers,
DMTU significantly (p < 0.05) attenuated
ischemia-induced increases in discharge frequency from 0.42 +/- 0.18 to 0.24 +/- 0.1 impulses per second (
ischemia versus
DMTU +
ischemia, respectively). In eight additional C fibers, we found that reperfusion after 5 minutes of
ischemia was associated with an increase in discharge activity from a baseline activity of 0.02 +/- 0.01 to 0.44 +/- 0.07 impulses per second.
DMTU significantly attenuated the reperfusion-induced increases in discharge frequency from 0.08 +/- 0.04 to 0.18 +/- 0.06 impulses per second.
DEF significantly (p < 0.05) attenuated the increased discharge activity from 0.39 +/- 0.07 to 0.10 +/- 0.04 impulses per second (
ischemia versus
DEF +
ischemia, respectively) in an additional 11
ischemia-sensitive C fibers. In contrast,
iron-saturated
DEF did not attenuate
ischemia- and reperfusion-induced increases in impulse activity. Thus,
ischemia-sensitive but not
ischemia-insensitive abdominal visceral afferents respond to H2O2. Furthermore,
ischemia- and reperfusion-sensitive afferents decreased their impulse activity to a repeated period of
ischemia or reperfusion after
DMTU or
DEF treatment. These data suggest that
reactive oxygen species, particularly H2O2 and
hydroxyl radicals, activate abdominal visceral C fibers in the cat during brief periods of
ischemia and reperfusion.