Why the study?
Does hypertension produced by the Goldblatt technic alter blood volume, cardiac size, and renal function in dogs?
Does hypertension produced by the Goldblatt technic alter blood volume, cardiac size, and renal function in dogs?
The Goldblatt technique successfully induced sustained hypertension in a majority of the experimental dogs, providing a model to study associated physiological changes.
Answers are grounded in this paper and cite their sources.
Establishes Goldblatt renal artery constriction model in dogs; leaves open translation to human hypertension mechanisms and management.
Freeman and Page found no significant changes in plasma volume during a period of hypertension experimentally produced by the Goldblatt technic, in 3 dogs, 2 of which were completely sympathectomized. We have followed the changes in plasma, cell and total volume by the dye method of Gibson and Evans, in 5 female dogs, none of which were sympathectomized, during periods of hypertension produced by the Goldblatt technic, varying from 1 to 10 months, in an attempt to correlate observed changes in blood volume with changes in mean arterial pressure, renal function and cardiac size as determined by X-ray. Control mean arterial pressure was established by an average of 12 determinations by femoral puncture over a period of 1 month prior to operation. In the operative procedure the renal artery clamp was completely closed and then released 1 to 11/2 turns. Constriction of the right renal artery was effected in each animal first, followed by constriction of the left renal artery at a subsequent operation 2 weeks later. Recovery from the surgical procedure was uneventful in all except Dog 23 in which, following the constriction of the left renal artery uremia developed. Following the complete release of the clamp on the left renal artery this animal survived but a chronic azotemia persisted. Renal function was estimated by determinations of phenolsulphonephthalein excretion and blood urea nitrogen. Control mean arterial blood pressures were normal in all dogs. Following constriction of the right renal artery, there was no change in pressure in 1 dog, a transient rise in 1 dog and sustained increase of from 30 to 501 mm Hg in 3 dogs.
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Gibson et al. (1938) studied this question.
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