The role of prostaglandins in Na retention of porta-cava shunted rats

Soggia, Giovanni; Olmeo, N.; Satta, Andrea; Faedda, Rossana; Branca, G. F.; Anania, V.; Desole, Maria Speranza; Bartoli, E

doi:10.1016/s0031-6989(84)80071-5

Cited by 2 publications

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“…If it is the splanchnic pooling that causes Na reten tion, then it should be considered consistent with it that Na retention precedes the formation of ascites. This is supported by experiments from our lab: we created a portocaval anastomotic network in rats in the presence of an intact liver: in these animals Na retention occurred only during indomethacin administration, indicating that the blood volume trapped within the anastomosis had activated a homeostatic Na-retaining mechanism: when the antagonist, Na excreting action of prostaglan dins was abolished, Na retention ensued [28], This extra volume retained by the kidney, aimed at normalizing the blood volume, must also over-expand the volume pooled in the splanchnic area. Therefore, the overall plasma volume must increase at an early stage of LC.…”

Section: Discussionmentioning

confidence: 72%

Importance of Liver Interstitial Pressure on Sodium Retention

Satta

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Branca

et al. 1988

Nephron

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Experiments were performed on 23 dogs to assess the effect of splanchnic pooling on renal hemodynamics and Na retention. When the thoracic duct pressure was raised to 40 cm H₂O (HTDP), liver interstitial pressure rose from 9.0 ± 0.4 to 19.8 ± 1.1 cm H₂O. Simultaneously, glomerular filtration rate (GFR) and renal plasma flow fell in the left kidney from 16.3 ± 1.7 to 9.6 ± 1.3 and from 73.7 ± 12.2 to 44.3 ± 9.8 ml · min^-1, respectively (p < 0.01). U_Na · V fell to 59 ± 9% of control value (p < 0.01). Plasma antidiuretic hormone (ADH) rose from 29.5 ± 7.7 to 46.9 ± 9.2 pg·ml^-1 (p < 0.05). When a portocaval shunt (PCS) was opened in 10 dogs during HTDP after the first set of experimental measurements, splanchnic pressure fell from 17.2 ± 1.1 to 11.5 ± 1.2 cm H₂O, attended by a return towards control of GFR. ADH fell significantly to 16.5 ± 8.1 during PCS, and to 9.7 ± 1.5 pg · ml^-1 during a last, postexperimental control period. Instead, U_Na V remained unchanged at the low levels measured during HTDP alone. When the HTDP was released in the 17 dogs without, and the 10 dogs with PCS, all variables became indistinguishable from control, except for U_Na V, which remained reduced, even in 4 aldosterone-escaped animals. No significant change in any of these variables occurred in 6 sham-operated control animals. These data demonstrate that it is possible to increase interstitial liver pressure through the lymph duct. Renal hemodynamics is impaired and causes Na retention because of the activation of mechanisms sensitive to the fall in ‘effective’ central volume. Na retention outlives the hemodynamic effects, which are quickly reversible, suggesting that it may be either independent of the fall in GFR or maintained by mechanisms independent of hemodynamics.

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Section: Discussionmentioning

confidence: 72%