Hemodynamic responses to cocaine vary greatly between animals, and the vari
ability is related to the incidence of cocaine-induced cardiomyopathies and
hypertension. The variability in cardiac output and systemic vascular resi
stance responses to cocaine in individuals is correlated with the responses
to acute startle (air jet). This experiment was designed to determine whet
her responses to cocaine and to air jet are related to those evoked by a co
nditioned stimulus (tone preceding foot shock) and to an unconditioned stim
ulus (cold water). We verified the relationship in hemodynamic response pat
terns between cocaine and cold stress using selective receptor antagonists.
Rats were instrumented with a pulsed Doppler flow probe on the ascending a
orta for determination of cardiac output and with an arterial cannula for r
ecording arterial pressure and heart rate. After recovery, some rats were t
ested multiple times with four different stimuli: air jet (6 trials), 15-s
tone preceding 1-s foot shock (12 trials), cold water exposure (1 cm deep f
or 1 min, 4-12 trials), and cocaine (5 mg/kg iv, 4-6 trials) while hemodyna
mic parameters were recorded. Each stimulus was capable of eliciting a pres
sor response that was associated with variable changes in cardiac output. T
he cardiac output response to cocaine was correlated with the initial respo
nses to each stressor in individual rats. Responses evoked by cold stress w
ere most similar to those elicited by cocaine. Furthermore, nicardipine (25
mug/kg iv) or atropine methylbromide (0.5 mg/kg iv) pretreatment prevented
the cardiac output differences to acute cold stress, as noted after cocain
e administration. On the other hand, propranolol (1 mug/kg iv) exacerbated
both the decrease in cardiac output and the stress-induced increase in syst
emic vascular resistance as previously reported with cocaine. Therefore, th
e initial response to cold water exposure is a reliable method of evoking c
haracteristic hemodynamic response patterns that, as seen with cocaine, may
provide a suitable model for identifying the causes for predilection to st
ress-induced cardiovascular disease.