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Baroreflex Sensitivity Impairment During Hypoglycemia Diabetes Volume 65, January 2016 209 Ajay D. Rao,1,2 Istvan Bonyhay,3 Joel Dankwa,1 Maria Baimas-George,1 Lindsay Kneen,1 Sarah Ballatori,3 Roy Freeman,3 and Gail K. Adler1 Baroreflex Sensitivity Impairment During Hypoglycemia: Implications for Cardiovascular Control Diabetes 2016;65:209–215 | DOI: 10.2337/db15-0871 Studies have shown associations between exposure to of cardiovascular benefit(4–7). These results raise the hypoglycemia and increased mortality, raising the pos- possibility that exposure to hypoglycemia has adverse sibility that hypoglycemia has adverse cardiovascular and unknown effects that persist after hypoglycemia effects. In this study, we determined the acute effects resolves and may oppose cardiovascular benefits of im- of hypoglycemia on cardiovascular autonomic control. proved glycemic control (8,9). Seventeen healthy volunteers were exposed to exper- Prior exposure to hypoglycemia impairs the hormonal imental hypoglycemia (2.8 mmol/L) for 120 min. Car- and muscle sympathetic nerve activity (MSNA) response fl COMPLICATIONS diac vagal barore ex function was assessed using the to subsequent hypoglycemia (10), the hormonal responses fi modi ed Oxford method before the initiation of the to subsequent exercise (11), and autonomic control of hypoglycemic-hyperinsulinemic clamp protocol and dur- cardiovascular function (12). After exposure to hypogly- ing the last 30 min of hypoglycemia. During hypoglycemia, cemia, induced by the hypoglycemic-hyperinsulinemic compared with baseline euglycemic conditions, 1)baro- clamp protocol, individuals exhibit decreased baroreflex reflex sensitivity decreases significantly (19.2 6 7.5 vs. 32.9 6 16.6 ms/mmHg, P < 0.005), 2) the systolic blood sensitivity (BRS), decreased MSNA response to transient pressure threshold for baroreflex activation increases hypotension, and decreased norepinephrine response to significantly (the baroreflex function shifts to the right; orthostatic stress compared with prior exposure to 120 6 14 vs. 112 6 12 mmHg, P < 0.005), and 3)the euglycemic-hyperinsulinemic conditions. These changes maximum R-R interval response (1,088 6 132 vs. in autonomic cardiovascular control are present in the 1,496 6 194 ms, P < 0.001) and maximal range of the euglycemic state 16 h after hypoglycemic exposure (12). R-R interval response (414 6 128 vs. 817 6 183 ms, P < Thetimeofonsetforthesechangesisnotestablished. 0.001) decrease significantly. These findings indicate The baroreflex plays a central role in maintaining reduced vagal control and impaired cardiovascular ho- cardiovascular homeostasis. Impaired baroreflex function meostasis during hypoglycemia. is associated with increased mortality in patients with diabetes, hypertension, and cardiovascular disease (13– 15). Thus, hypoglycemia-induced changes in autonomic Rigorous glycemic control is the cornerstone of diabetes cardiovascular control could contribute to the mortality management; however, this results in increased episodes associated with hypoglycemia (7,8,16). of iatrogenic hypoglycemia (1). Multiple community- and The modified Oxford test is the gold standard for hospital-based studies have shown an association between characterizing the baroreflex. By assessing baroreflex exposure to hypoglycemia and increased mortality (2,3). function across a wide range of clinically relevant blood Furthermore, results of several large-scale clinical trials pressures, this test defines the full hemodynamic range of investigating the outcome of intensive glycemic control baroreflex engagement. The modified Oxford method has have shown increased cardiovascular mortality or a lack not been used to assess BRS during hypoglycemia. The 1Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Received 25 June 2015 and accepted 28 September 2015. ’ Brigham and Women s Hospital, Harvard Medical School, Boston, MA R.F. and G.K.D. contributed equally to this work. 2Section of Endocrinology, Diabetes and Metabolism, Department of Medicine, © 2016 by the American Diabetes Association. Readers may use this article as Temple University School of Medicine, Philadelphia, PA long as the work is properly cited, the use is educational and not for profit, and 3Department of Neurology, Beth Israel Deaconess Medical Center, Harvard the work is not altered. Medical School, Boston, MA Corresponding author: Roy Freeman, [email protected]. 210 BRS Impairment During Hypoglycemia Diabetes Volume 65, January 2016 purpose of this study was to test the hypothesis that Hypoglycemic-Hyperinsulinemic Clamp Protocol impairment in baroreflex cardiovascular control begins As previously described, participants received a primed during hypoglycemia. We therefore assessed baroreflex continuous intravenous infusion of regular insulin at function using the modified Oxford method before and 80 mU/m2 body surface area/min for ;150 min (all partic- during a hypoglycemic-hyperinsulinemic clamp protocol ipants received Humulin R [Eli Lilly, Indianapolis, IN], in healthy participants. except one who received Novolin R [Novo Nordisk, Princeton, NJ]). Twenty percent dextrose was infused RESEARCH DESIGN AND METHODS intravenously to achieve blood glucose of 2.8 mmol/L Study Population (50mg/dL)for120min(17).Bloodsampleswerewith- Healthy men and women, aged 18 to 40 years, were drawn through an indwelling intravenous catheter recruited from the greater Boston area. Exclusion placed in a retrograde fashion in the participant’s wrist/ criteria included evidence of any medical illness hand that rested in a warm box (150°F) throughout the on history or physical examination, BMI .30 kg/m2, procedure. Plasma glucose was assessed every 5 min using tobacco use, substance abuse, pregnancy, lactation, men- a bedside glucose analyzer (YSI 2300 STAT Plus Glucose & opause, abnormalities on electrocardiogram, or abnor- Lactate Analyzer; YSI, Yellow Springs, OH). Blood was mal blood electrolyte, liver function test, complete collected for analysis of insulin at baseline and during blood count, or urinalysis values. The study protocol the insulin infusion. (NCT01394627) was approved by the Partners Insti- Baroreflex Assessment tutional Review Board, and all subjects provided writ- Cardiac vagal baroreflex function was assessed using the ten informed consent. modified Oxford method (18) at baseline and during the Diet and Activity last 30 min of the hypoglycemic clamp (Fig. 1). After a Participants stopped over-the-counter medications 2 weeks baseline measurement of blood pressure and heart rate before admission and refrained from vigorous exercise using an automated oscillometric blood pressure monitor from 1 week before admission to the Center for Clinical (Dinamap; Critikon, Inc., Tampa, FL), participants received Investigation at Brigham and Women’sHospital.Partic- intravenous bolus injections of 100 mg sodium nitroprusside, ipants consumed an isocaloric diet (125 mmol/day Na+, followed 60 s later by 150 mg phenylephrine hydrochloride as 125 mmol/day K+,20mmol/dayCa2+) lacking foods previously described (12). This procedure causes a decrease in high in monoamines beginning 4 days before and con- systolic blood pressure (SBP) of ;15 mmHg below baseline tinuing throughout the admission. A hypoglycemic- SBP, followed by an increase of ;15 mmHg above baseline. hyperinsulinemic clamp procedure was performed in the R-R interval and beat-to-beat blood pressure were measured morning, with participants having been supine and fasting using the Finometer (FMS, Amsterdam, the Netherlands). since midnight. Baroreflex assessments were performed in duplicate. The Figure 1—Timing of the baroreflex assessment (modified Oxford) relative to the plasma glucose levels (mean 6 SD) during the hypoglycemic-hyperinsulinemic clamp protocol. The straight line represents the target glucose level (2.8 mmol/L). diabetes.diabetesjournals.org Rao and Associates 211 Figure 2—Baroreflex function from a representative subject measured by the modified Oxford method during baseline euglycemia (circles) and hypoglycemia (triangles). Data points represent the corresponding values of SBP and cardiac interval (R-R) during the pharmacologically induced blood pressure change. For baroreflex assessment, R-R is plotted as a function of SBP between the lowest and the highest SBP values. The linear portion (arrows) of the sigmoid function describes BRS (see RESEARCH DESIGN AND METHODS). During hypoglycemia, BRS is decreased, maximal R-R interval is decreased, and the sigmoidal baroreflex function curve shifts to the right. minimum and maximum R-R intervals were used to define increased serum insulin from baseline levels of 29 6 the range of heart rate response during the baroreflex 11 pmol/L to 731 6 290 pmol/L. Figure 1 shows plasma function assessment. BRS was determined by the slope glucose levels during the clamp procedure and timing of the relation between the R-R interval and SBP. The of the modified Oxford test. The average plasma glu- threshold of baroreflex function was defined as the SBP cose during the 120 min of hypoglycemia was 2.8 6 at which the R-R interval started to increase after reaching 0.1 mmol/L. fi its minimum value during the modi ed Oxford test. The Baroreflex Assessment Before and During fl fi saturation point of barore ex function was de ned as Hypoglycemia the SBP at which the R-R interval reached its maximum Blood pressure and heart rate were assessed before the value (Figs. 2 and 3). modified Oxford procedures at baseline, when subjects Statistical Analysis were euglycemic, and during the hypoglycemic
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