Assessment of vasomotor endothelial function inpatients with diabetes mellitus type l at different stages ofdiabetic nephropathy

Abstract


Aim. To study a vasomotor endothelial function in patients with diabetes mellitus (DM) type 1 at different
stages of diabetic nephropathy (DN).
Material and methods. Twenty six patients with DM type 1(11 males and 15 females, mean age
25.9 ±4.3 years, mean history of DM 12.9 + 3.4 years) entered the study. They were divided into 4
groups: group 1 -without renal affection, group 2 - with microalbuminuria (MAU), group 3 - with
proteinuria (PU), group 4 - with chronic renal failure (CRF). The control group consisted of 7
healthy volunteers. Endothelium-dependent vasodilation (EDVD) was studied in the test with reactive
hyperemia provoked by 4-5 min occlusion of the brachial artery by pneumocollar and subsequent assessment
of arterial diameter changes after decompression using high-resolution ultrasound dopplerography.

Results. Reactive hyperemia resulted in dilation of the artery in all the examinees. This dilation was
maximal on second 30 after removal of the collar in the controls, group 2, 3 and 4 and reached
9.2 ± 2.9, 9.63 ± 3.62, 7.25 ± 5.23 and 4.42 ± 4.05%, respectively. Resting blood flow velocity was
similar in all the groups and rose maximally by 95-150%. To estimate EDVD of the brachial artery
more precisely, the coefficient of endothelial sensitivity to shift tension was calculated. It made up
0.084 ± 0.04 (control group), 0.0825 + 0.08 (group 1), 0.138 ± 0.07(group 2), 0.067 ± 0.05 (group
3) and 0.052 ± 0.04 (group 4).
Conclusion. At the earliest stage of DN (stage MAU), EDVD is not affected as maximal vasodilation
of the brachial artery and endothelial sensitivity to shift tension do not differ from the control values.
This means that the stage of MAU is reversible in early treatment, but PU and CRF are not reversible
stages associated with depletion of endothelial cells and loss of sensitivity to changing hemodynamic
conditions.

About the authors

M V Shestakova

I R Yarek-Martynov

N S Ivanishina

I I Dedov

References

  1. Standi Е., Balletshofer В., Dahl В. et al. Predictors of 10-year macrovascular and overall mortality in patients with NIDDM: the Munich General Practitioner Project. Diabetologia 1996; 39: 1540-1545.
  2. Stern M. P. Diabetes and cardiovascular disease. The "common soil" hypothesis. Diabetes, 1995; 44: 369-374.
  3. Quyyumi A. A. Endothelial function in health and disease: new insights into the genesis of cardiovascular disease. Am. J. Med. 1998; 105: 32S-39S.
  4. Johnston M. Т., Creager S. J., Scales K. M. et al. Impaired endothelium-dependent vasodilation in patients with insulin-dependent diabetes mellitus. Circulation 1993; 88: 2510-2516.
  5. Stehotiwer С. D., Lambert J., Donker A. J., van Hinsbergh V. W. Endothelial dysfunction and pathogenesis of diabetic angiopathy. Cardiovasc. Res. 1997; 34: 55-68.
  6. Laight D. W., Carrier M. J., Anggard E. E. Endothelial cell dysfunction and the pathogenesis of diabetic macroangiopathy. Diabetes Metab. Res. Rev. 1999; 15: 274-282.
  7. Chan N. N., Vallance P., Colhoun H. M. Nitric oxide and vascular responses in Type 1 diabetes. Diabetologia 2000; 43; 137-147.
  8. Cohen R. A. Nitric oxide bioavailability and diabetic endothelial cell dysfunction. In: Tooke J., ed. Vascular disease in diabetes. Servier, France; 2001: 87-106.
  9. Chappey O., Wautier A. F., Boval В., Wautier J. L. Endothelial cells in culture: an experimental model for the study of vascular dysfunctions. Cell Biol. Toxicol. 1996; 12: 199-205.
  10. Born G., Schwartz C., eds. Vascular endothelium: physiology, pathology, and therapeutic opportunities. Stuttgart: Schattauer; 1997.
  11. Celermajer D. S., Sorensen K. E., Gooch V. M. et al. Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Lancet 1992; 340 (8828): 1111-1115.
  12. Марцинкевич Г. И., Ким В. Н., Ковалев И. А. и др. Эндотелийзависимые вазомоторные реакции и их неинвазивная оценка с использованием функциональных проб у лиц с факторами риска развития атеросклероза. Кардиология 2000; 12: 56-58.
  13. Quyumi A. A., Dakak N., Mulkany D. et al. Nitric oxide activity in the atherosclerotic human coronary circulation. Atherosclerosis 1997; 29: 308-317.
  14. Cooke J. P., Rossitch E. J., Andon N. A. et al. Flow activates an endothelial potassium channel to release an endogenous nitrovasodilator. J. Clin. Invest. 1991; 88: 1663-1671.
  15. Smith P., Карта J. A., Jacobs M. S. et al. Endothelium-dependent vascular relaxation in patients with type 1 diabetes. Diabetes 1993; 42: 148-153.
  16. London G. M., Marchais S. J., Guerin A. P. et al. Arterial structure and function in endstage renal disease. Nephrol. Dial. Transplant. 2002; 17: 1713-1724.
  17. Дедов И. И., Шестакова M.B. Диабетическая нефропатия.: Универсум Паблишинг; 2000.
  18. Biegelsen E. S., Loscalzo J. Endothelial dysfunction and atherosclerosis. J. Coron. Artery Dis. 1999; 10: 241-256.

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