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yperinsulinemia is known to be associated with various cardiovascular risk factors, including high triglyceride concentrations, low high-density lipoprotein (HDL) cholesterol concentrations, high blood pressure (BP), and obesity. 1-3 However, there is some controversy about the role of insulin resistance (IR) in the regulation of BP. Several prospective studies have linked insulin concentrations to the incidence of hypertension [4][5][6] and it has been suggested that hyperinsulinemia and/or IR plays a role in the pathophysiology of hypertension. [7][8][9][10][11] But the association between insulin and hypertension remains contentious, 12 with a number of studies reporting no association between insulin and BP. 13,14 Moreover, to our knowledge a large study of the association between BP and IR has not been conducted in normal glucose tolerance Asians. Therefore, we decided to investigate the relationships between BP and IR using a homeostasis model (HOMA-IR) and further, to evaluate the association between body fat distribution and high BP in nondiabetic normoglycemic Koreans. Methods Subjects and MeasurementsThe total number of subjects involved was 53,477, all of whom presented for a routine health status check up at the Kangbook Samsung Hospital, College of Medicine in Sungkyunkwan University in 2002, and who were without specific medical complaints. Based on the results obtained, patients suspected of having acute inflammatory diseases, other malignancies and those taking BP-lowering medication were excluded. In addition we also excluded those taking antidiabetic agents and those with a fasting glucose over 110 mg/dl. Finally, 49,076 subjects (31,820 men; 17,256 women) were included in this study. Anthropometric indices of adiposity, metabolic variables (including fasting serum insulin and homeostasis model assessment (HOMA) index of insulin sensitivity), BP and several cardiovascular risk factors were measured. The BP was determined using a mercury manometer, between 08.00 h and 10.00 h, after the subject had been sitting upright for at least 10 min.When the systolic or diastolic BP exceeded 140 mmHg or 90 mmHg, it was re-measured twice after a rest and averaged. A high BP was defined as a SBP ≥140 mmHg or a DBP ≥90 mmHg.The body mass index (BMI: kg/m 2 ), the waist circumference and the waist -hip ratio were also measured. The subjects were asked questions concerning the risk factors for general cardiovascular disease (ie, past medical history, life style, such as alcohol consumption, smoking, and Background There is some controversy about the role of insulin resistance (IR) in the regulation of blood pressure (BP). Moreover, a large study of the association between BP and IR has not been conducted in normal glucose tolerance Asians. The present study investigated the relationships between IR, body mass index (BMI) and waist circumference and BP in normoglycemic Koreans. Methods and ResultsAnthropometric indices of adiposity, metabolic variables (fasting serum insulin and a homeostasis model assessment (H...

Activation of the peripheral nerve system by endotracheal intubation is accompanied by an increase in bispectral index (BIS). Esmolol produces a dose-dependent attenuation of the adrenergic response to endotracheal intubation. Desflurane increases sympathetic nerve activity and plasma norepinephrine relative to sevoflurane. The authors hypothesized that esmolol might blunt the BIS response to endotracheal intubation more during sevoflurane anesthesia than desflurane anesthesia. In this double blind, randomized study, after the induction of anesthesia, patients were mask-ventilated with either sevoflurane or desflurane (end-tidal 1 minimum alveolar concentration) and received normal saline or esmolol (0.5 mg/kg) 1 minute before intubation (sevoflurane-control, sevoflurane-esmolol, desflurane-control, and desflurane-esmolol groups, n=20/group). BIS, mean arterial pressure, and heart rate were measured before the induction of anesthesia (awake), before esmolol injection (time point -1), immediately before intubation (time point 0), and every minute for 5 minutes after tracheal intubation (time point 1 to 5). Compared with preintubation, esmolol attenuated the increase in BIS at 1 minute after intubation during sevoflurane anesthesia (5.1% for esmolol and 31.7% for control) but not during desflurane anesthesia (28.6% for esmolol and 30.8% for control). Mean arterial pressure and heart rate increased after intubation in all groups but the changes were greater in the control groups than the esmolol groups. In conclusion, a single dose of esmolol blunted the increase in BIS to tracheal intubation during sevoflurane but not desflurane anesthesia.