Effect of hemorrhagic shock on renal release of prostaglandin E

Pa, Johnston; Ee, Selkurt

doi:10.1152/ajplegacy.1976.230.3.831

Cited by 31 publications

(11 citation statements)

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“…In previous studies, HH has been found to increase renal prostaglandin synthesis and release (14). Similarly, in the present study HH was found to increase renal medullary prostaglandin concentration.…”

Section: Resultssupporting

confidence: 88%

The Role of Renal Nerves and Prostaglandins in Control of Renal Hemodynamics and Plasma Renin Activity during Hypotensive Hemorrhage in the Dog

Henrich¹,

Anderson²,

Berns³

et al. 1978

J. Clin. Invest.

109

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A B S T R A C T The effects of hypotensive hemorrhage (HH) on renal hemodynamics and plasma renin activity (PRA) during prostaglandin (PG) synthesis inhibition were examined in three groups ofdogs. In each group of animals arterial blood pressure was lowered by a 30% decrement. In the first group of eight control animals, HH was not associated with a significant change in glomerular filtration rate (GFR, 42-36 ml/min, NS); renal blood flow (RBF) declined significantly, from 234 to 171 ml/min, P < 0.05. In the second group of eight animals, pretreated with RO 20-5720 (RO, 2 mg/kg), a competitive inhibitor of PG synthesis, HH was associated with a significant fall in GFR (43-17 ml/min, P < 0.001) and RBF (195-89 ml/min, P < 0.001). In the third group of eight animals, pretreatment with indomethacin (IN, 10 mg/kg), a chemically dissimilar PG inhibitor, HH was also associated with a significant fall in GFR (38-8 ml/min, P < 0.001) and RBF (150-30 ml/min, P < 0.001). Renal denervation attenuated this renal ischemic effect of HH in the presence of PG inhibition. In the RO group, GFR (34 vs. 17 ml/min, P < 0.005) and RBF (145 vs. 89 ml/min, P < 0.025) were significantly greater in denervated vs. innervated kidneys during HH. Similarly, in animals treated with IN, a significantly higher GFR (28 vs. 8 ml/min, P < 0.005) and RBF (101 vs. 30 ml/min, P < 0.005) occurred in denervated as compared to innervated kid- neys during HH. With HH, the increase in PRA in the control group (3.34-11.68 ng/ml per h, P < 0.005) was no different than that observed in the RO group (4.96-18.9 ng/ml per h, P < 0.001) or IN group (4.71-17.8 ng/ml per h, P < 0.001). In summary, the present results indicate that renal PG significantly attenuate the effect of HH to decrease GFR and RBF. Furthermore, renal denervation exerts a protective effect against the enhanced renal ischemic effects which occur in the presence of PG inhibition during HH. Finally, PG inhibition does not alter the effect of HH to cause anl increase in PRA.

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Section: Resultssupporting

confidence: 88%

The Role of Renal Nerves and Prostaglandins in Control of Renal Hemodynamics and Plasma Renin Activity during Hypotensive Hemorrhage in the Dog

Henrich¹,

Anderson²,

Berns³

et al. 1978

J. Clin. Invest.

109

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“…Support for this interpretation comes from the observation that PGE-like material in the renal vein of the dog is increased by hypoperfusion (25)(26)(27). Under these conditions in the dog, inhibition of cyclooxygenase markedly increases RVR (26)(27)(28).…”

Section: Discussionmentioning

confidence: 96%

Prostaglandins mediate the vasodilatory effect of mannitol in the hypoperfused rat kidney.

Johnston¹,

Bernard²,

Perrin³

et al. 1981

J. Clin. Invest.

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A B S T R A C T We have previously reported that mannitol strikingly increases blood flow to rat kidnevs hypoperfused at 35-40 mm Hg. This vasodilator effect is not due to volume expansion or alterations in plasma osmolality. We have tested the hypothesis that the vasodilatory effect of mannitol in the ischemic rat kidney is mediated by one of the vasoactive renal hormone systems: renin-angiotensin, kallikrein-kinin, or prostaglandins.Rats were infused with 5% mannitol in 0.9% saline to 3-5% of body weight. In agreement with our previous studies, RBF increased 1.3+0.1 ml/min despite maintenance of perfusion pressure at 35-40 mm Hg.The cyclooxygenase inhibitors, meclofenamate and indomethacin had no effect on renal blood flow (RBF) in hypoperfused kidneys. However, in rats pretreated with these inhibitors, expansion with mannitol increased RBF by only 0.37+0.02 ml/min, 28% of the response in the untreated group (P < 0.001). Infusion of prostacyclin (PGI2) into the renal artery during reduced perfusion resulted in an increase in RBF of 1.0+0.1 ml/min. Subsequent expansion with mannitol increased RBF by only 0.5±0.1 ml/min more, less than one-half of the effect of mannitol in a concurrent group of rats not treated with PGI2.Unlike PGI2, prostaglandin E2 had only a minimal vasodilator effect during hyperperfusion. Imidazole, an inhibitor of thromboxane synthesis, did not alter RBF or renal vascular resistance during hypoperfusion.Treatment of rats during hypoperfusion with the angiotensin-converting enzyme (kininase II) inhibitor teprotide increased RBF by 1.1±0.3 ml/min. However,

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“…In trauma patients, inhibitory activities affecting neutrophil chemotaxis, lymphocyte reactivity, and neutrophil chemiluminescence have been identified in the sera. [39][40][41][42] The nature of the inhibitory activity in trauma patients' sera is at present unknown. It is not clear whether it is a newly synthesized product, a protein, or a substance of a different nature.…”

Section: Discussionmentioning

confidence: 99%

“…This is a most powerful endogenous immune suppressant for T-cell and macrophage responsiveness. 26,42 Finally, PGE2 induces the release of the potent antiinflammatory cytokine IL-10, which has been found to contribute to endotoxin hyporesponsiveness in vitro, 43 and which is the functional suppressor in plasma patients with meningococcal sepsis. 44 Conversely, the use of IL-10 antibodies restored PGE2-induced monocyte suppression.…”

Section: Discussionmentioning

confidence: 99%

Postoperative serum attenuates LPS‐induced release of TNF‐α in orthopaedic surgery

Reikerås

Sun

Wang

et al. 2007

Journal Orthopaedic Research

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Studies with ex vivo stimulation of whole blood samples from injured patients have revealed a diminished production capacity for a broad range of secretory products, including inflammatory cytokines. Recent interest has focused on the release of mediators in serum that depress the cell-mediated immune response following trauma. The involvement of the lipid mediator prostaglandin E2 (PGE2) has been assumed because it is a potent endogenous immunosuppressor. In the present study, we tested the hypothesis that inhibitory substances circulating in the patient's serum after a major musculoskeletal trauma might impair leukocyte function by evaluating the effect of such serum on cytokine release in a whole blood model. Six females and three males undergoing elective total hip replacement were included in the study. Ex vivo LPS-induced TNF-a and IL-10 were measured in whole blood sampled preoperatively and added serum taken before, at the end of operation, and at postoperative days 1 and 6 with saline as negative control. LPS induced significant releases of TNF-a and IL-10 in whole blood. Addition of preoperative, postoperative, and day-1 postoperative serum did not alter the LPS-induced release of TNF-a as compared to saline. In the presence of serum from postoperative day 6, however, the expression of TNF-a was significantly reduced as compared to saline and preoperative serum (p ¼ 0.021 and 0.008, respectively). Neither of the serum samples altered the release of IL-10. PGE2 was significantly (p ¼ 0.008) increased in serum at postoperative day 6 as compared to preoperative levels. In conclusion, these data show that at day 6 after major orthopaedic surgery, the patient serum contained activity that inhibited ex vivo LPS-induced TNF-a release. The potent TNF-a inhibitory activity found at day 6 after injury correlated with increased levels of PGE2 and indicates cellmediated hyporesponsiveness to a second stimulus. ß

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Effect of hemorrhagic shock on renal release of prostaglandin E

Cited by 31 publications

References 0 publications

The Role of Renal Nerves and Prostaglandins in Control of Renal Hemodynamics and Plasma Renin Activity during Hypotensive Hemorrhage in the Dog

The Role of Renal Nerves and Prostaglandins in Control of Renal Hemodynamics and Plasma Renin Activity during Hypotensive Hemorrhage in the Dog

Prostaglandins mediate the vasodilatory effect of mannitol in the hypoperfused rat kidney.

Postoperative serum attenuates LPS‐induced release of TNF‐α in orthopaedic surgery

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