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European Heart Journal Advance Access originally published online on February 3, 2005
European Heart Journal 2005 26(5):464-471; doi:10.1093/eurheartj/ehi113
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© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions{at}oupjournals.org

Haematocrit, type 2 diabetes, and endothelium-dependent vasodilatation of resistance vessels

Andrea Natali1,2,*, Elena Toschi1,2, Stephanie Baldeweg3, Arturo Casolaro1,2, Simona Baldi1,2, Anna Maria Sironi1,2, John S. Yudkin3 and Ele Ferrannini1,2

1Department of Internal Medicine, Via Roma 67, 56100 Pisa, Italy
2CNR Institute of Clinical Physiology, University of Pisa, Pisa, Italy
3Department of Medicine, University College, London, UK

Received 10 May 2004; revised 23 November 2004; accepted 2 December 2004; online publish-ahead-of-print 3 February 2005.

* Corresponding author. Tel: +39 050 992814; fax: +39 050 553235. E-mail address: anatali{at}ifc.cnr.it

Aims In conditions such as type 2 diabetes, hypertension, and smoking, in which haematocrit (Hct) tends to be higher, endothelial function is impaired. In vitro, haemoglobin neutralizes nitric oxide very effectively. Whether red blood cells participate in the regulation of endothelial function in vivo has not been established.

Methods and results Clinical and haematological parameters and forearm blood flow responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were measured in 84 type 2 diabetic patients and 19 control subjects. Diabetics showed blunted dose–response curves to both SNP and ACh. In diabetics, across quartiles of Hct, ACh blood flow responses were progressively lower (881±96, 652±81, 513±54, 307±46%, P</0.0001), and maximal SNP responses tended to be lower (706±72, 578±61, 607±69, 499±53%, P=0.06) despite similar age, body mass index, glycated haemoglobin (HbA1c), blood pressure, serum total and HDL-cholesterol levels, indices of insulin sensitivity, and markers of inflammation. After normalizing the ACh response for the SNP response (ACh/SNP ratio), a progressive reduction across Hct quartiles (1.54±0.23, 1.22±0.15, 0.93±0.09, 0.66±0.09, P<0.0001) was still observed, with patients in the III and IV quartile showing a blunted response compared with controls (1.44±0.08). Both in diabetics and controls, the ACh/SNP ratio was reciprocally related to Hct (r=–0.46 and r=–0.66, respectively, P<0.002 for both). This association was independent of comorbidities, gender, metabolic control, plasma lipids, or concomitant treatments, was stronger in the subjects with preserved endothelium-dependent dilatation, and was unchanged when haemoglobin replaced Hct.

Conclusion Both in diabetics and non-diabetics, haematocrit is inversely related to small vessel endothelium-dependent dilatation. Thus, in addition to blood rheology, a direct negative effect on nitric oxide availability might explain the link between high Hct and cardiovascular disease.

Key Words: Endothelium • Nitric oxide • Haemoglobin • Haematocrit


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