Regulation of peripheral blood flow in Complex Regional Pain Syndrome: clinical implication for symptomatic relief and pain management

Background. During the chronic stage of Complex Regional Pain Syndrome (CRPS), impaired microcirculation is related to increased vasoconstriction, tissue hypoxia, and metabolic tissue acidosis in the affected limb. Several mechanisms may be responsible for the ischemia and pain in chronic cold CPRS. Discussion. The diminished blood flow may be caused by either sympathetic dysfunction, hypersensitivity to circulating catecholamines, or endothelial dysfunction. The pain may be of neuropathic, inflammatory, nociceptive, or functional nature, or of mixed origin. Summary. The origin of the pain should be the basis of the symptomatic therapy. Since the difference in temperature between both hands fluctuates over time in cold CRPS, when in doubt, the clinician should prioritize the patient's report of a persistent cold extremity over clinical tests that show no difference. Future research should focus on developing easily applied methods for clinical use to differentiate between central and peripheral blood flow regulation disorders in individual patients

Effect of ACE inhibitors on endothelial dysfunction: Unanswered questions and implications for further investigation and therapy

Experimental studies have suggested that angiotensin-converting enzyme (ACE) inhibitors may have an important role in blocking the progression of and/or reversing endothelial dysfunction. The extrapolation of these experimental studies to the clinical situation has, however, been disappointing. Studies of forearm-mediated endothelial vasodilatation in patients with hypertension with captopril, enalapril, and cilazapril have been negative. The finding of the Trial in Reversing Endothelial Dysfunction (TREND) that the administration of quinapril to normotensive patients with coronary artery disease in part restores endothelial-mediated coronary vasodilation, as assessed by intracoronary administration of acetylcholine, has important implications for future therapy and raises several important questions. The differences in the TREND and previous studies of ACE inhibitors on endothelial dysfunction may be due to mechanistic differences in endothelial dysfunction in patients with coronary artery disease and hypertension. Although in general there has been a good correlation between endothelial dysfunction as assessed by forearm flow and coronary endothelial dysfunction as assessed by acetylcholine, these vascular beds may be affected differently by therapeutic interventions, especially with an ACE inhibitor, which may affect sheart stress and angiotensin II formation in different vascular beds differently. Third, one needs to question whether the effect of quinapril on coronary endothelial dysfunction is a class effect or unique to quinapril. It will be necessary to test the effectiveness of other ACE inhibitors on coronary endothelial dysfunction in humans before concluding that the beneficial effects of quinapril are due to a class effect.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44542/1/10557_2004_Article_BF00051113.pd