Ae. Toet et al., REDUCED SURVIVAL AFTER ISOPRENALINE DOPAMINE IN D,L-PROPRANOLOL INTOXICATED RATS/, Human & experimental toxicology, 15(2), 1996, pp. 120-128
1 Respiratory and cardiovascular failure are principle toxic effects o
f beta-blocker overdose. Respiratory arrest is the primary cause of de
ath in beta-blocker intoxicated rats. 2 The effect of beta-adrenocepto
r agonists on respiratory and cardiovascular failure in beta-blocker o
verdose was investigated in a model of acute d,l-propranolol (30 mg kg
(-1) h(-1)) intoxication in spontaneously breathing rats. 3 Neither th
e aselective, hydrophilic beta-agonist isoprenaline (10, 25, 50 mu g k
g(-1) min(-1)), nor the beta(1)-selective, lipophilic beta-agonist fle
robuterol (1,3,10 mu g kg(-1) min(-1)) and the beta(2)-selective, lipo
philic beta-agonist clenbuterol (10, 25, 50 mu g kg(-1) min(-1)) had a
ny beneficial effect on cardiovascular and respiratory variables or su
rvival time in d,l-propranolol intoxicated spontaneously breathing rat
s. 4 Isoprenaline (10 mu g kg(-1) min(-1)) had no favourable effect on
haemodynamic and respiratory variables in artificially ventilated d,l
-propranolol intoxicated rats either. 5 Addition of dopamine to isopre
naline resulted in a significant reduction of survival time, primarily
caused by a decrease in mean arterial blood pressure, in artificially
ventilated d,l-propranolol intoxicated rats. Addition of glucagon to
isoprenaline did not affect survival time. 6 Artificial ventilation is
the most important supportive measure in d,I-propranolol intoxication
in the rat.