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Risk factors of atherosclerosis and saphenous vein endothelial function
C Sessa1, M D Morasch, M Friedland
1Department of Vascular Surgery, Wayne State University, Detroit, USA.
Insights
Saphenous vein endothelial function is impaired by atherosclerosis risk factors like diabetes and smoking. These factors can cause veins to release contracting factors, impacting cardiovascular health.
Area of Science:
- Vascular Biology
- Cardiovascular Research
- Endothelial Function
Background:
- Impaired vasomotor function is implicated in atherosclerosis pathophysiology.
- Endothelial dysfunction may affect bypass graft patency.
- Investigated atherosclerosis risk factors' influence on saphenous vein endothelial function in cardiovascular disease patients.
Purpose of the Study:
- To evaluate the in vitro effect of atherosclerosis risk factors on saphenous vein endothelial function.
- To assess the contractile and relaxant responses of saphenous veins to various vasoactive agents.
Main Methods:
- Studied 45 saphenous vein rings (intact and denuded endothelium).
- Administered norepinephrine (NE), acetylcholine (Ach), histamine (H), and serotonin (5-HT).
- Analyzed responses in relation to patient risk factors (diabetes, smoking, hypertension).
Main Results:
- Norepinephrine caused increased contraction in diabetics, smokers, and hypertensive patients.
- Acetylcholine response varied; relaxation was reduced in hypertensive and diabetic patients.
- Histamine induced relaxation then contraction, with greater contraction in diabetics.
- Serotonin caused contraction, unaffected by endothelial removal.
- Evidence suggests endothelium-derived contracting factor (EDCF) release.
Conclusions:
- Saphenous veins can secrete a contracting factor, particularly in patients with atherosclerosis risk factors and diabetes.
- Mechanisms regulating the balance of endothelial relaxing and contracting factors require further investigation.
- The source of vasoconstrictor substances from endothelial cells needs elucidation.
Background:
Impaired vasomotor function has been suggested as playing a role in the pathophysiology of atherosclerosis and it may also affect the late patency of bypass grafts. We evaluated, in vitro, the influence of risk factors of atherosclerosis on saphenous vein endothelial function in patients with cardiovascular diseases.
Methods:
Forty-five saphenous vein rings with intact (E+) and denuded endothelium (E-) were studied. The following drugs were used: norepinephrine (NE), acetylcholine (Ach), histamine (H) and serotonine (5-HT).
Results:
Contraction to norepinephrine (n=15) showed a maximal tension of 783+/-115 percent that was increased in diabetics, smokers, and patients with hypertension. There was a wide range of response to acetylcholine in rings with intact endothelium (n=25), (mean relaxation 16.4+/-1.7 percent, ranging from -22.2 percent to 45 percent) with relaxation (26+/-1.1 percent) and contraction (-11+/-1.2 percent); relaxation was reduced in patients with hypertension and in diabetics (7.4+/-2.6 percent vs non diabetics 24.4+/-1.73 percent; p<0.01). Five of the 12 veins from diabetics exibited contraction (10+/-1.48 percent). Histamine (n=15) caused moderate relaxation at low doses (25+/-2.46 percent) followed by contraction at higher concentrations (184+/-5.7 percent). This was greater in diabetics (193+/-6.8 percent vs non diabetics 157+/-5.3 percent; p=0.045) while in preparations without endothelium (n=10) only relaxation was obtained (45+/-2.89 percent). Contraction (242+/-7.4 percent) was observed in response to serotonine (n=15) that was not affected by endothelial removal. In this study saphenous vein: (1) exhibited a wide range of responses to acetylcholine; (2) evoked marked contraction to norepinephrine and serotonine; (3) elicited contraction in response to histamine that was endothelium-dependent, suggesting the production or the release of an endothelium-derived-contracting-factor (EDCF).
Conclusions:
Saphenous vein is able to secrete a contracting factor in patients with risk factors of atherosclerosis and above all diabetes. The mechanisms that regulate the balance between the relaxing and contracting factors and how the endothelial cells become the source of the substances with vasoconstrictor activity remain to be determined.