Acute effect of hydralazine administration on pulmonary artery hemodynamics in dogs with chronic heartworm disease

Clarke E. Atkins From the Department of Companion Animal and Special Species Medicine, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606 (Atkins, Keene) and the Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706 (McGuirk).

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Bruce W. Keene From the Department of Companion Animal and Special Species Medicine, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606 (Atkins, Keene) and the Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706 (McGuirk).

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Sheila M. McGuirk From the Department of Companion Animal and Special Species Medicine, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606 (Atkins, Keene) and the Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706 (McGuirk).

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Takashi Sato From the Department of Companion Animal and Special Species Medicine, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606 (Atkins, Keene) and the Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706 (McGuirk).

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Summary

In an effort to better understand the role of vasodilators in the management of pulmonary hypertension associated with chronic heartworm disease (hwd), pulmonary hemodynamic measurements were obtained from 7 experimentally 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 with 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 resistance, left ventricular dP/dtmax, left ventricular end diastolic pressure, and left and right ventricular double products ([mean arterial pressure × heart rate] and [mean pulmonary artery pressure × heart rate], respectively). Responders were defined as those in which total pulmonary resistance decreased ≥ 20% without an increase in mean pulmonary arterial pressure and in which heart rate increase was ≤ 10%. Comparison was also made between maximal hemodynamic effect of hydralazine with that after 100% oxygen administration for 15 minutes to previously normoxemic dogs (n = 5). Significance was determined if P < 0.05, using the paired t-test.

Hydralazine induced significant reductions in mean pulmonary and systemic arterial pressures and total pulmonary resistance, with no significant change in heart rate, cardiac index, total systemic resistance, left ventricular dP/dtmax, left ventricular end diastolic pressure, or right and left ventricular double products. Four (57%) of the 7 dogs studied were considered responders. Pretreatment cardiac index, mean pulmonary artery pressure, and total pulmonary resistance did not allow differentiation of responders from nonresponders. However, pretreatment right ventricular end diastolic pressure was significandy less in responders than in nonresponders. Two dogs sustained hypotension after hydralazine 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 systemic arterial pressures and resistance than did administration of 100% oxygen. These data indicate that further study of vasodilators for treatment of hwd-induced pulmonary hypertension may be warranted.

Summary

In an effort to better understand the role of vasodilators in the management of pulmonary hypertension associated with chronic heartworm disease (hwd), pulmonary hemodynamic measurements were obtained from 7 experimentally 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 with 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 resistance, left ventricular dP/dtmax, left ventricular end diastolic pressure, and left and right ventricular double products ([mean arterial pressure × heart rate] and [mean pulmonary artery pressure × heart rate], respectively). Responders were defined as those in which total pulmonary resistance decreased ≥ 20% without an increase in mean pulmonary arterial pressure and in which heart rate increase was ≤ 10%. Comparison was also made between maximal hemodynamic effect of hydralazine with that after 100% oxygen administration for 15 minutes to previously normoxemic dogs (n = 5). Significance was determined if P < 0.05, using the paired t-test.

Hydralazine induced significant reductions in mean pulmonary and systemic arterial pressures and total pulmonary resistance, with no significant change in heart rate, cardiac index, total systemic resistance, left ventricular dP/dtmax, left ventricular end diastolic pressure, or right and left ventricular double products. Four (57%) of the 7 dogs studied were considered responders. Pretreatment cardiac index, mean pulmonary artery pressure, and total pulmonary resistance did not allow differentiation of responders from nonresponders. However, pretreatment right ventricular end diastolic pressure was significandy less in responders than in nonresponders. Two dogs sustained hypotension after hydralazine 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 systemic arterial pressures and resistance than did administration of 100% oxygen. These data indicate that further study of vasodilators for treatment of hwd-induced pulmonary hypertension may be warranted.

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