Effect of arsenical drugs on in vitro vascular responses of pulmonary artery from heartworm-infected dogs

Daria S. Maksimowich From the Departments of Physiology (Maksimowich, Kaiser), Pathology (Bell), and Microbiology (Williams), Michigan State University, East Lansing, MI 48824-1101.

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Thomas G. Bell From the Departments of Physiology (Maksimowich, Kaiser), Pathology (Bell), and Microbiology (Williams), Michigan State University, East Lansing, MI 48824-1101.

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 DVM, PhD
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Jeffrey F. Williams From the Departments of Physiology (Maksimowich, Kaiser), Pathology (Bell), and Microbiology (Williams), Michigan State University, East Lansing, MI 48824-1101.

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Lana Kaiser From the Departments of Physiology (Maksimowich, Kaiser), Pathology (Bell), and Microbiology (Williams), Michigan State University, East Lansing, MI 48824-1101.

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Abstract

Objective

To test the effect of thiacetarsamide and melarsomine on vascular responses in isolated rings of pulmonary artery from heartworm-infected dogs.

Animals

18 heartworm-infected dogs.

Procedure

Isolated rings of pulmonary artery from heartworm-infected dogs were randomly treated with thiacetarsamide (30 μg/ml) or melarsomine dihydrochloride (30 μg/ml) for 30 minutes; untreated rings from the same dog served as control. Cumulative dose-response relations to norepinephrine, nitroglycerin, and methacholine were determined.

Results

Norepinephrine-induced constriction was not altered by treatment with either thiacetarsamide or melarsomine. Treatment with thiacetarsamide depressed nitroglycerin-induced relaxation, compared with values for untreated control rings and rings treated with melarsomine. Treatment of rings with thiacetarsamide or melarsomine depressed methacholine-induced relaxation, compared with values for untreated rings. Histologic examination of rings indicated that treatment with thiacetarsamide or melarsomine resulted in loss of endothelial cells.

Conclusion

Endothelial cell loss as a direct drug effect may be responsible for impaired endothelium-dependent relaxation in pulmonary artery from heart-worm-infected dogs. Thiacetarsamide appears to have additional effects on vascular smooth muscle, which may explain why fewer complications are observed in dogs treated with melarsomine.

Clinical Relevance

Melarsomine may be a safer drug than thiacetarsamide and could be a better treatment for dogs with heartworm infection. (Am J Vet Res 1997;58:389–393)

Abstract

Objective

To test the effect of thiacetarsamide and melarsomine on vascular responses in isolated rings of pulmonary artery from heartworm-infected dogs.

Animals

18 heartworm-infected dogs.

Procedure

Isolated rings of pulmonary artery from heartworm-infected dogs were randomly treated with thiacetarsamide (30 μg/ml) or melarsomine dihydrochloride (30 μg/ml) for 30 minutes; untreated rings from the same dog served as control. Cumulative dose-response relations to norepinephrine, nitroglycerin, and methacholine were determined.

Results

Norepinephrine-induced constriction was not altered by treatment with either thiacetarsamide or melarsomine. Treatment with thiacetarsamide depressed nitroglycerin-induced relaxation, compared with values for untreated control rings and rings treated with melarsomine. Treatment of rings with thiacetarsamide or melarsomine depressed methacholine-induced relaxation, compared with values for untreated rings. Histologic examination of rings indicated that treatment with thiacetarsamide or melarsomine resulted in loss of endothelial cells.

Conclusion

Endothelial cell loss as a direct drug effect may be responsible for impaired endothelium-dependent relaxation in pulmonary artery from heart-worm-infected dogs. Thiacetarsamide appears to have additional effects on vascular smooth muscle, which may explain why fewer complications are observed in dogs treated with melarsomine.

Clinical Relevance

Melarsomine may be a safer drug than thiacetarsamide and could be a better treatment for dogs with heartworm infection. (Am J Vet Res 1997;58:389–393)

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