Ce. Atkins et al., ACUTE EFFECT OF HYDRALAZINE ADMINISTRATION ON PULMONARY-ARTERY HEMODYNAMICS IN DOGS WITH CHRONIC HEARTWORM DISEASE, American journal of veterinary research, 55(2), 1994, pp. 262-269
In an effort to better understand the role of vasodilators in the mana
gement of pulmonary hypertension associated with chronic heartworm dis
ease (HWD), pulmonary hemodynamic measurements were obtained from 7 ex
perimentally infected, anesthetized dogs before and after hydralazine
administration (mean dose, 1.96 mg/kg of body weight). Five dogs were
maintained on room air, while 2 were maintained on 100% oxygen during
the hydralazine study. The hemodynamic effect of hydralazine in dogs w
ith HWD was evaluated, using heart rate, cardiac index, mean pulmonary
artery pressure, mean arterial pressure, total pulmonary resistance,
total systemic resistance, total systemic resistance/total pulmonary r
esistance, left ventricular dP/dt(max) left ventricular end diastolic
pressure, and left and right ventricular double products ([mean arteri
al pressure x heart rate] and [mean pulmonary artery pressure x heart
rate], respectively). Responders were defined as those in which total
pulmonary resistance decreased greater than or equal to 20% without an
increase in mean pulmonary arterial pressure and in which heart rate
increase was less than or equal to 10%. Comparison was also made betwe
en maximal hemodynamic effect of hydralazine with that after 100% oxyg
en administration for 15 minutes to previously normoxemic dogs (n = 5)
. Significance was determined if P < 0.05, using the paired t-test. Hy
dralazine induced significant reductions in mean pulmonary and systemi
c arterial pressures and total pulmonary resistance, with no significa
nt change in heart rate, cardiac index, total systemic resistance, lef
t ventricular dP/dt(max) left ventricular end diastolic pressure, or r
ight and left ventricular double products. Four (57%) of the 7 dogs st
udied were considered responders. Pretreatment cardiac index, mean pul
monary artery pressure, and total pulmonary resistance did not allow d
ifferentiation of responders from nonresponders. However, pretreatment
right ventricular end diastolic pressure was significantly less in re
sponders than in nonresponders. Two dogs sustained hypotension after h
ydralazine administration, but no dogs had significant tachycardia. In
dogs with experimentally induced HWD, treatment with hydralazine had
significantly greater effect on cardiac index and mean pulmonary and s
ystemic arterial pressures and resistance than did administration of 1
00% oxygen. These data indicate that further study of vasodilators for
treatment of HWD-induced pulmonary hypertension may be warranted.