The effects of calcium-blocking agents on sympathetic responses to acute haemorrhagic shock in dogs

Pollard, BJ; Fletcher, I.R.; Tait, Alan R.; Knight, Paul R.; Spek, A. F. L. Van Der

doi:10.1016/0300-9572(89)90135-4

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Conclusion: Modulation Of Pmn1

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2005

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“…Immune modulation by DHP drugs would therefore pose a significant practical challenge because suppression of cardiovascular function could worsen hemodynamic instability in the presence of shock. 16,17 Structurally novel N-substituted DHPs have been developed, however, that are manyfold more potent as SOCE inhibitors than are prior related drugs. 15 If drugs of this class were shown to inhibit immune cell calcium entry at doses with little or no effect on cardiovascular function, it would suggest that they might be of therapeutic value in the control of postshock inflammation.…”

Section: Conclusion: Modulation Of Pmnmentioning

confidence: 99%

Store-Operated Calcium Channel Inhibition Attenuates Neutrophil Function and Postshock Acute Lung Injury

Lee

Feketeova

et al. 2005

The Journal of Trauma: Injury, Infection, and Critical Care

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Modulation of PMN Ca2+ entry by means of selective SOCE channel inhibition attenuates PMN inflammatory responses in vitro. In vivo, SOCE channel blockade attenuates trauma and hemorrhagic shock-induced PMN priming and lung injury without gross evidence of hemodynamic side effects. The relative specificity of SOCE channel blockade for "nonexcitable" cells such as PMNs may make it a valuable form of chemoprophylaxis for the inflammatory consequences of hemorrhagic shock in trauma patients.

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Section: Conclusion: Modulation Of Pmnmentioning

confidence: 99%