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SUMMARY. We banded the left pulmonary artery in rats to investigate, in the same animal, the effect of both increased and decreased flow on the lung vasculature and to determine how these hemodynamic states modify the structural changes produced by a 2-week exposure to hypobaric hypoxia. In unanesthetized rats, pressures were recorded from the main pulmonary artery and aorta via indwelling catheters, cardiac output was calculated by the Fick principle, and pulmonary and systemic vascular resistance estimated. Technetium-99m macroaggregated albumin was injected and radionuclide activity counted separately over the right and left lungs as a measure of flow. At postmortem, right and left ventricles of the heart were weighed and the lungs injected to permit analysis of arteriograms and morphometric assessment of structural changes in the pulmonary vascular bed. Flow in the left lung was reduced to one-fifth normal in rats with left pulmonary artery bands. In "room air" rats, pressure proximal to the left pulmonary artery band and in the right lung was slightly higher than in nonbanded controls, but not as high as in nonbanded or banded hypoxic rats. Changes in flow and pressure in both lungs of "room air" rats with left pulmonary artery bands were associated with a mild degree of extension of muscle into peripheral pulmonary arteries normally nonmuscular, medial hypertrophy of normally muscular arteries, and reduced arterial density. These three structural changes were present in both lungs of "hypoxic" rats but were much more severe. High flow in the right lungs of "hypoxic rats" with left pulmonary artery bands worsened only the degree of extension. Decreased flow and pressure in the left lungs of these animals prevented both the extension and the medial hypertrophy of hypoxia, but not the severe reduction in arterial density. It seems that the latter may occur as a direct response to low oxygen tension, whereas extension and medial hypertrophy are influenced by altered flow and pressure, respectively. (Circ Res 52: 432-441, 1983) IN previous studies, we observed that rats, during a 2-week exposure to chronic hypoxia, develop a progressive rise in pulmonary artery pressure associated with structural changes in the pulmonary vascular bed (Rabinovitch et al., 1979). The structural changes consist of extension of muscle into peripheral arteries normally nonmuscular, increased medial wall thickness of normally muscular arteries, and reduced arterial density relative to alveolar. In the present study, we banded the left pulmonary artery in the rat to determine for the first time in the same animal how increased flow (to the right pulmonary vascular bed) and decreased flow (to the left) might alter the structural remodeling of chronic hypoxia. Methods Animals StudiedTwenty-four adult male Sprague-Dawley rats (mean weight 336 ± 33 g) were used; 15 were selected randomly to be kept in room air (room air rats) and 11 to be exposed to chronic hypobaric hypoxia (air at 380 torr) for 2 weeks (hypoxia rats). Seven of the 15 ro...

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1. Acute renal failure was induced in conscious rate by subcutaneous injection of glycerol. 2. Expansion of the extracellular space by infusion of 150 mmol/l sodium chloride (saline) partly protected the animals against acute renal failure. 3. This protective effect of saline infusion disappeared when the animals were treated with indomethacin. This effect could be reversed by the addition of prostaglandin (PGE2) to the saline infusion. 4. We suggest that prostaglandins may be involved in mediating the protection afforded by saline infusion against acute renal failure due to glycerol.

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Abstract. The haemodynamic and renal effects of synthetic prostaglandin A2 (PGA2) have been studied in 10 hypertensive subjects during a) a short lasting infusion of hypotensive doses of 3–9μg/kg min. of PGA2; b) a continuous infusion starting with subdepressive doses and extended with hypotensive doses.—The rapid hypotensive effect observed with high doses was accompanied by an increase in cardiac output and renal blood flow without significant changes in the peripheral vascular bed. Hepatic blood flow was decreased. These observations show a preferential renal redistribution of cardiac output. During the administration of subdepressive doses of PGA., a marked renal effect was observed, consisting in an increase in free water clearance and diuresis with no significant modifications of general haemodynamics. The natriuretic effect was much less pronounced suggesting that PGA2 is not a specific natriuretic hormone.—The haemodynamic and renal effects of endogenous PGs may play an important role in renal functions and in blood pressure regulation.

SummaryOne hundred 125I-sodium iothalamate and endogenous creatinine clearances in 36 subjects were compared with standard inulin clearance measurements. There was a very close correlation of the urine/plasma ratios between any two of the three clearances studied, hence both labelled iothalamate and creatinine can be relied upon for the estimation of the glomerular filtration rate in clinical practice. The mean ratio of 125I-sodium iothalamate to inulin clearance was 1.01 and that of creatinine to inulin 1.03. It is concluded that the clearance of 125I-sodium iothalamate can be substituted for the clearance of inulin in clinical determinations of the glomerular filtration rate but that in centres without radioisotope facilities the endogenous creatinine clearance can be used instead.

1. Renal venous prostaglandin concentrations (PGA, PGE and PGF) were determined, together with renal plasma flow, urinary output and blood pressure changes, before and after infusion of sodium chloride solution (saline) in four normotensive and three hypertensive subjects. 2. No changes in blood pressure and in glomerular filtration rate were observed. 3. Saline infusion induced a significant increase in renal venous PGA and PGE, and also in total and non-cortical renal plasma flow and urinary output. There was an insignificant increase in renal venous PGF. 4. These findings show that prostaglandin release after saline infusion is associated with changes in renal blood flow and suggest that the natriuretic and diuretic effect of saline could be the result of prostaglandin release.