Postoperative hyperglycemia and previously undiagnosed diabetes are associated with development of SSIs among cardiothoracic surgery patients. Screening for diabetes and hyperglycemia among patients having cardiothoracic surgery may be warranted to prevent postoperative and chronic complications of this metabolic abnormality.

1 Noradrenaline sensitivity and acetylcholine-induced relaxation were investigated in mesenteric resistance arteries of control and streptozotocin-induced diabetic rats. 2 The diabetic rats demonstrated enhanced vascular sensitivity to noradrenaline compared with age-matched controls (pEC50 5.99 ± 0.06 for diabetic rats, n = 25, versus 5.82 ± 0.03 for controls, n = 45, P < 0.05). 3 Significant impairment of acetylcholine-induced relaxation was observed in arteries from the diabetic animals compared with controls (pEC50 6.81 ± 0.17 for diabetic rats, n = 21, versus 7.54 ± 0.17 for controls, n = 45, P<0.001). 4 The difference between acetylcholine-induced relaxation in diabetic and control arteries remained in the presence of 10 gM indomethacin (pEC50 6.41 ± 0.11 for diabetic rats, n = 16, versus 7.59 ± 0.08 for controls, n = 20, P < 0.001). 5 The nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA, 1 mM) produced profound inhibition of acetylcholine-induced relaxation in diabetic arteries but partial inhibition in controls. The incomplete inhibition of acetylcholine-induced relaxation by L-NMMA in the control arteries was the result of ineffective inhibition of nitric oxide synthase since an alternative inhibitor, NG-nitro-Larginine methyl ester (L-NAME, 0.1 mM), led to similar inhibition to that seen in the diabetic arteries with L-NMMA. The endothelium-derived relaxing factor (EDRF)-mediated component of acetylcholineinduced relaxation determined by use of the nitric oxide synthase inhibitors was, therefore, apparently reduced in diabetic rats compared with control animals. 6 In further experiments L-NAME was found to enhance the response to noradrenaline in control rats but not in diabetic animals, suggesting that the abnormal response to noradrenaline in the diabetic animals was also due to reduced EDRF release. 7 Nitroprusside-induced relaxation (endothelium-independent) was similar in arteries from control and diabetic rats (pEC5o 7.61 ± 0.13 for diabetic arteries, n = 18, versus 7.68 ± 0.15 in the controls, n = 20, P not significant). 8 These results suggest that endothelial function is abnormal in mesenteric resistance arteries of streptozotocin-induced diabetic rats and that this is predominantly due to reduced EDRF release.

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1 Streptozotocin-induced diabetic rats (Wistar) were implanted with sustained release insulin pellets (release rate =4 u day-') or with placebo pellets (palmitic acid) from the onset of glycosuria. 2 Noradrenaline sensitivity, endothelium-dependent relaxation to acetylcholine and endotheliumindependent relaxation to sodium nitroprusside were assessed in mesenteric resistance arteries from the insulin-treated (IT) diabetic animals and compared to placebo-implanted (PI) diabetics and age-matched controls. 3 Arteries from PI-diabetic rats (8-10 weeks) demonstrated an enhanced maximal response to noradrenaline compared to controls, which was not prevented by insulin treatment (control 2.65 ± 0.17 mN mm'1, n = 18 arteries versus PI-diabetic 3.73 ± 0.40 mN mm-', n = 5, P <0.05; control versus IT-diabetic 4.02 ± 0.19 mN mm' , n = 22, P <0.001). Sensitivity to noradrenaline was similar between the three groups. 4 In the presence of the nitric oxide synthase inhibitor N0-nitro-L-arginine methyl ester (L-NAME), IT and PI arteries were more sensitive to noradrenaline than control arteries (pECm: control 5.75 0.08, n = 17, versus PI-diabetic 6.14 ± 0.09, n = 8, P <0.05; control versus IT-diabetic 6.38 ± 0.08, n = 20, P <0.001). 5 The maximum contractile response to depolarizing 125 mM K+ was significantly enhanced in IT-diabetic arteries but not PI-diabetic when compared to control arteries (maximum response: control 3.74±0.15mNmm-', n = 18, versus PI-diabetic 3.61 ±0.19mNmmnr, n = 11, NS; control versus IT-diabetic 4.66 ± 0.18 mN mm-', n = 22, P <0.001). 6 Endothelium-dependent relaxation to acetylcholine was profoundly impaired in the PI-diabetic arteries, but in the IT-diabetic arteries was not significantly different from controls (pECm: control 7.64 0.19, n = 17, versus PI-diabetic 6.07 ± 0.12, n = 8, P <0.001; control versus IT-diabetic 7.36 0.09, n = 22, NS). 7 Endothelium-independent relaxation to sodium nitroprusside was slightly but significantly impaired in the PI-diabetic arteries, but was not significantly different in the IT-diabetic arteries compared to controls (pEC50: control 7.78 ± 0.10, n = 13, versus PI-diabetic 7.31 ± 0.13, n = 13, P <0.05; control, versus IT-diabetic 7.64 ± 0.09, n = 16, NS).