Why does inflammation persist: a dominant role for the stromal microenvironment?
We have now demonstrated that prenatal inflammation suffices to induce deferred glutamatergic synaptic dysfunction in adult.
Many chemical mediators are known to be released from the site of inflammation.
However, not all patients progress as quickly and, as the inflammation resolves, the arterial wall becomes thickened and tender with the pulse still present.
Similar inflammation around pulmonary arterial and pulmonary venous vessels was noted in contralateral lung lobes but not in sham-operated control rats.
This inflammation consisted essentially of polymorphous cells (18 cases out of 24).
The responses to ischemia and reperfusion also involves an inflammatory response, and inflammation involves interactions between circulating neutrophils and the endothelium.
These circulating factors would promote vascular inflammation and endothelial dysfunction, and result in insulin resistance and hypertension as described above.
