When dogs are subjected to an anastomosis between a large systemic artery and one of the pulmonary arteries, the subsequent progress of events is related to the diameter of the fistula.If this is large, exceeding about 5 mm., there is usually a rapid onset of fatal cardiac failure, as in the animal described by Ekstrom et al. (1951-52) and in 16 of the 21 dogs reported on by Muller et al. (1953) who anastomosed the aorta with a pulmonary artery.When the communication is small, usually 3 mm.or less in diameter, as it frequently is when the subclavian artery is employed in the anastomosis, the animals survive with a normal or only slightly raised blood pressure in the pulmonary artery, and vascular changes do not occur in the small pulmonary arteries.In a third group where the diameter of the fistula is intermediate in size, the animals survive with pulmonary hypertension, and vascular changes occur (Muller et al., 1953; Ferguson and Varco, 1955).The structural changes described are usually medial hypertrophy and intimal fibrosis, histological features characteristic of an early grade of hypertensive pulmonary vascular disease in the human lung (grades 1 to 3 on the basis of the criteria of Heath and Edwards, 1958).The severe structural changes characterized by generalized and complex local forms of vascular dilatation, which are pathognomonic of the late stages of hypertensive pulmonary vascular disease associated with congenital cardiac septal defects in man (grades 4 to 6), do not appear to have been reported in dogs with artificial aorto-pulmonary anastomosis and generalized pulmonary hypertension.However, vascular changes comparable to these, confined to the left upper lobe, in dogs subjected to an end- to-end anastomosis between the left subclavian artery and the pulmonary artery to this lobe have been reported by Dammann et al. (1957).In these animals there was pulmonary hypertension only in the restricted area of lung served by the anastomosis, while the blood pressure in the main pulmonary artery was normal, so that the hmodynamic conditions cannot be considered as analogous to those found in human disease.Hence up to the present it has not really been estab- lished that the complete progression of structural changes seen in human hypertensive pulmonary vascular disease can be experimentally produced in the dog exposed to comparable physiological conditions.In fact the frequency of the severe lesions in man, in contrast to the rarity of them in dogs, suggests that a factor of time in addition to elevation of blood pressure in the pulmonary artery is necessary for their development.The purpose of this communication is to demonstrate that higher grades of hypertensive pul- monary vascular disease can occur after the experimental production of an aorto-pulmonary anastomosis and generalized pulmonary hypertension.The presence of severe pulmonary vascular changes in one of three dogs subjected to this procedure is reported.The additional etiological factor is discussed later.The relation between the histological appearance of the pulmonary arteries of these dogs and that of the pulmonary arteries in man in patent ductus arteriosus is also discussed, bearing in mind that the hemodynamic abnormalities were acquired in the experimental animals but have been present from birth in human disease.
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Heath et al. (1959) studied this question.