Although intravenous (iv) injection of
potassium cyanide (KCN) activates the arterial chemoreflex, it has been questioned whether cytotoxic
hypoxia reproduces a physiological stimulus such as hypoxic
hypoxia (low inspired O2 tension). Thus, the goal of the present study was to compare the cardiovascular responses elicited by
intravenous injection of KCN to those caused by hypoxic
hypoxia in awake rats before and after bilateral
ligature of carotid body arteries. We tested the hypothesis that hypoxic
hypoxia activates the cardiovascular chemoreflex just as KCN does, causing an increase in arterial pressure and
bradycardia. Intact adult Wistar rats received an
intravenous injection of KCN (160 microg/kg) and were exposed to hypoxic
hypoxia (7-5% O2 breathing) for 10-15 s at random while mean arterial pressure (MAP) and heart rate (HR) were measured. After the experiments, the animals were submitted to bilateral
ligature of carotid body arteries or
sham operation and the protocol was repeated on the subsequent day. Before surgery, all rats showed an abrupt rise in arterial pressure accompanied by a marked
bradycardia in response to KCN or hypoxic
hypoxia, with a very similar pattern. After surgery, these responses persisted only in the
sham-operated group and were totally abolished in the
ligature group. In conclusion, our data show that KCN is an appropriate stimulus to activate arterial chemoreflex because its cardiovascular responses are comparable to those induced by hypoxic
hypoxia. Thus, the use of KCN as a tool to evaluate different aspects of the complex pattern of cardiovascular, respiratory, and behavioural responses to chemoreflex activation seems to be physiologically acceptable.