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clinical practice. Hemodynamically significant MR in dogs with MMVD can lead to cardiac remodeling, including left ventricular eccentric hypertrophy, enlargement of the left atrium (LA), and dilation of the pulmonary veins. 4 Cardiac enlargement

Open access
in American Journal of Veterinary Research

developed, such as the main PA-to-aorta (AO) ratio and right PA distensibility index, which are noninvasive, straightforward to use, and not affected by Doppler ultrasonographic alignment restrictions. 7 , 8 In recent studies, 9 – 11 the pulmonary vein (PV

Open access
in American Journal of Veterinary Research

Abstract

Objective

To test the possible role of endothelial cells in mediating fade of norepinephrine-induced constriction and the effect of heartworm infection on these responses.

Design

Rings of pulmonary vein from control and heartworm-infected dogs were constricted with norepinephrine (10−5.5 M) and followed over 65 minutes. Time profiles were established by measuring active tension every 2 minutes for the first 10 minutes, then every 5 minutes for 15 minutes, then every 10 minutes for 40 minutes. Time profiles were done in pulmonary vein rings with and without endothelial cells, and in the presence and absence of N-nitro-L-arginine methyl ester (L-NAME; nitric oxide synthase inhibitor), mefenamic acid (cyclooxygenase inhibitor), or methylene blue (guanylate cyclase inhibitor).

Animals

12 noninfected control and 11 heartworm-infected dogs.

Results

Pulmonary vein constricted with norepinephrine spontaneously loses tension (fades) over time. Fade was not different between control and heartworm-infected dogs. In pulmonary vein from control dogs, methylene blue decreased fade while L-NAME and mefenamic acid did not. In pulmonary vein from heartworm-infected dogs, L-NAME and methylene blue significantly decreased fade, but mefenamic acid did not.

Conclusion

Nitric oxide, but not cyclooxygenase products, mediates fade of norepinephrine-induced constriction in pulmonary vein from heartworm-infected dogs. In control dogs, neither nitric oxide nor cyclooxygenase products appear to be involved in fade. We conclude that in canine pulmonary vein, fade of norepinephrine-induced constriction is mediated, in part, by endothelial cells.

Clinical Relevance

Altered production of endothelium-derived relaxing factors may be important in the pathogenesis of heartworm disease.

Free access
in American Journal of Veterinary Research

lesion of EIPH is remodeling of small-diameter pulmonary veins (venous remodeling). 5 Venous remodeling is characterized by collagen deposition in walls and smooth muscle hypertrophy of veins resulting in thickening of walls and narrowing of lumens. 7

Full access
in American Journal of Veterinary Research

vascular changes can be detected on radiography in cats with L-CHF. 11 , 13 A previous study revealed dilation of the pulmonary vein and artery dilation in approximately 50% and 70% of the cats, respectively, with L-CHF caused by various diseases including

Open access
in American Journal of Veterinary Research

cardiac apex to the dorsal point of intersection of the heart and diaphragm. h = Diameter of the cranial pulmonary artery measured perpendicular to the long axis of the vessel at the level of the third rib. i = Diameter of the cranial pulmonary vein

Full access
in American Journal of Veterinary Research

Abstract

Objective

To test the effect of heartworm infection on agonist-induced constriction of canine pulmonary artery and vein in vitro.

Procedure

Cumulative concentration-response relations to norepinephrine, serotonin, histamine, prostaglandin F2α, and the thromboxane A2 analog U-44069 were determined, using isolated rings of pulmonary artery and vein from control and heartworm-infected dogs. To determine the role of endothelial cells in histamine constriction, some rings were denuded of endothelial cells in both artery and vein.

Animals

Noninfected control and heartworm-infected dogs.

Results

There was no difference in constriction response to norepinephrine, serotonin, prostaglandin F2α, or U44069 of pulmonary artery or vein from control or heartworm-infected dogs. Histamine-induced constriction of pulmonary artery from heartworm-infected dogs was not different from control values, however, when endothelial cells were removed from control, but not heartworm-infected pulmonary artery, histamine-induced constriction was enhanced. Histamine-induced constriction of pulmonary vein from heartworm-infected dogs was significantly depressed, compared with that of control pulmonary vein. However, removal of endothelial cells in pulmonary vein from heartworm-infected, but not control dogs significantly increased constriction.

Conclusion

Heartworm infection alters histamine-induced constriction responses of pulmonary artery and vein. These changes may reflect high circulating histamine concentrations in heartworm-infected dogs, compared with that in controls. Increased circulating histamine concentrations in vivo could bring about decreased sensitivity of histamine receptors or decreases in the number of receptors expressed.

Clinical Relevance

Mast cells and histamine may be important factors in altered endothelium-mediated responses associated with heartworm disease. (Am J Vet Res 1997;58:394–397)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To determine whether endothelial cell (EC) von Willebrand factor (vWf) is uniformly distributed in canine blood vessels.

Design

Content of EC vWf from vascular segments was evaluated in Haütchen preparations, using immunohistochemistry. EC from femoral arteries and veins and jugular veins were grown in culture, and the intracellular content and constitutive release of vWf from these cells were measured. The amount of vWf mRNA in the cultured EC was determined.

Animals

Vascular segments for Hautchen preparations and EC for culture were obtained from 5 and 10 clinically normal, mixed-breed dogs, respectively.

Procedures

Appropriate vascular segments were removed, fixed, processed for immunohistochemistry, using a monospecific polyclonal antibody to canine vWf, and Haütchen preparations were made. Intracellular and constitutive released vWf was measured, using an ELISA, and vWf mRNA was measured by Northern blot analysis.

Results

Intact endothelial linings from femoral veins, jugular veins, vena cava, and pulmonary veins stained more intensely than femoral arteries, carotid arteries, aorta, and pulmonary veins. Constitutive release and intracellular content of vWf in cultured EC from femoral veins was about 30 times higher than that from femoral arterial EC, which was barely detectable. Similar differences were seen in amounts of mRNA.

Conclusions

There is marked diversity in EC vWf in canine vasculature that may result from differences in vWf mRNA.

Clinical Relevance

Low amounts of vWf in canine systemic arterial EC may contribute to thromboresistance of canine arteries. (Am J Vet Res 1996; 57:750–755)

Free access
in American Journal of Veterinary Research

Abstract

Objective—To characterize structural changes in pulmonary vessels of dogs with dirofilariosis.

Animals—8 dogs with dirofilariosis and 2 unaffected control dogs.

Procedure—Pulmonary artery pressure was measured in affected dogs, and dogs then were euthanatized. Scanning electron microscopy was used to examine vascular corrosion casts of pulmonary vasculature. Tissue sections of pulmonary vasculature were evaluated by use of histologic examination.

Results—Pulmonary artery pressure was higher in dogs with severely affected pulmonary vessels. In tissue sections, dilatation, as well as lesions in the tunica intima and proliferative lesions resulting in constriction or obstruction, were frequently observed in branches of the pulmonary artery. Numerous dilated bronchial arteries were observed around affected pulmonary arteries. Hyperplastic venous sphincters were observed in small pulmonary veins and venules. In corrosion casts, affected pulmonary lobar arteries had dilatation, pruning, abnormal tapering, constriction, and obstruction. In small arteries and arterioles, surface structures representing aneurisms and edema were seen. Bronchial arteries were well developed and extremely dilated, and they formed numerous anastomoses with pulmonary arteries at all levels, from the pulmonary trunk to peripheral vessels. Capillaries in the lungs were dilated with little structural change. Small pulmonary veins and venules had irregular annular constrictions that were caused by hyperplastic smooth muscle cells of venous sphincters.

Conclusions and Clinical Relevance—Scanning electron microscopy of microvascular casts delineated links between the bronchial and pulmonary circulations in dogs with dirofilariosis. Results of scanning electron microscopy provided a structural explanation for the development of pulmonary circulatory disturbances and pulmonary hypertension in dogs affected by dirofilariosis. (Am J Vet Res 2002:63:1538–1544)

Full access
in American Journal of Veterinary Research

seen on the lateral projections (white arrowhead); no left atrial enlargement is appreciated on the dorsoventral projection. The pulmonary veins are radiographically normal where visualized. There is incidentally a small smoothly margined expansion of

Open access
in Journal of the American Veterinary Medical Association