To evaluate the use of a Na/H exchanger (NHE-1) inhibitor as a cardioprotective adjunct therapy to low-volume resuscitation in two different rat models of traumatic hemorrhagic shock.
These findings suggest that the differential expression of NOS, cytokines, and endothelin-1 in different organs are associated with the development of vascular hyporeactivity after hemorrhagic shock and may account, at least in part, for the vascular bed diversity observed.
Hemorrhagic shock-induced vascular hyporeactivity in the rat: relationship to gene expression of nitric oxide synthase, endothelin-1, and select cytokines in corresponding organs.
Our study results suggest that hypothermia may exert its neuroprotective effects by reducing markers of apoptotic pathway, particularly Caspase-3 on TBI and HS.
We found that hemorrhagic shock alone or in combination with intestinal ligation caused not only morphological damage to ileal mucosa, but also induced BT and promoted release of TNF-alpha, IL-6, and IL-10 in serum and lymph.
Meanwhile, the relationship of the mRNA/protein expression of connexins 37, 40, and 43(Cx40 and Cx43) to the changes of vascular reactivity after hemorrhagic shock and the effect of antisense oligodeoxynucleotide of Cx40 or Cx43 on vascular calcium sensitivity and vascular reactivity were investigated.
Hepatic transcription factor activation and proinflammatory mediator production is attenuated by hypertonic saline and pentoxifylline resuscitation after hemorrhagic shock.
In contrast, HS-induced mucosal inflammation and apoptotic cell death in the duodenum, jejunum, and colon were far less than those observed in ileum as judged by the levels of expression of TNF-alpha, iNOS, activated caspase 3, and Bcl-2.
Upregulation of mitochondrial respiratory complex IV by estrogen receptor-beta is critical for inhibiting mitochondrial apoptotic signaling and restoring cardiac functions following trauma-hemorrhage.