TY - JOUR
T1 - Quantitative monitoring of brain function, vital signs, and hormonal response during acute insulin-induced hypoglycemia
AU - Chalew, S. A.
AU - Sakamoto, R. N.
AU - McCarter, R.
AU - Hanukoglu, A.
AU - Kowarski, A. A.
AU - Matjasko, J.
PY - 1989/10
Y1 - 1989/10
N2 - Acute insulin-induced hypoglycemia provokes changes in central nervous system activity and release of counterregulatory hormones. The clinical relationship between central nervous system activity, hormone secretion, and vital signs has not to our knowledge been previously reported. We used computerized electroencephalographic (CEEG) analysis to monitor 5 nondiabetic subjects during acute insulin-induced hypoglycemia (0.75 U/kg intravenous push). Their glucose nadir was 38±6 mg/dl (mean ± 1 SD). A three-phase pattern of change in CEEG power in response to hypoglycemia was observed: phase 1 was characterized by an increase in total CEEG power (natural log of activity = 9.1±1.3 μV2) over baseline (8.7±1.2 μV2) in the theta, delta, and beta frequency bands. This phase preceded and coincided with the glucose nadir. During phase 2, power in all frequency bands fell significantly below baseline. A nadir in CEEG power (8.0±1.6 μV2) occurred 40 to 55 minutes after insulin injection as glucose levels were rising. During phase 3 there was a return to baseline in CEEG power and frequency spectra. Heart rate increase just before phase 1; peak heart rate (91±8 beats/min) coincided with peak CEEG power and was significantly higher than basal rate (71±11, P<0.05). A significant increase in respiratory rate occurred during phase 1 of the CEEG and persisted through phase 2. A significant decrease in mean blood pressure (nadir = 73±6 mm Hg) below preinsulin blood pressure (81±8 mm Hg, P<0.05) coincided with the nadir of CEEG power in phase 2. Blood pressure returned to basal levels during phase 3. Peak plasma epinephrine (652±207 versus 46±30 pg/ml), norepinephrine (500±219 versus 273±107 pg/ml), and pancreatic polypeptide levels (1,023±689 versus 114±24 pg/ml) were all significantly elevated over respective basal concentrations (P<0.05). Peak hormone levels occurred during CEEG phase 2. This study demonstrates a temporal association of changes in CEEG power, vital signs, and hormonal secretion. These techniques may be applicable for further investigation of the clinical neuroendocrinology of the response to acute hypoglycemia.
AB - Acute insulin-induced hypoglycemia provokes changes in central nervous system activity and release of counterregulatory hormones. The clinical relationship between central nervous system activity, hormone secretion, and vital signs has not to our knowledge been previously reported. We used computerized electroencephalographic (CEEG) analysis to monitor 5 nondiabetic subjects during acute insulin-induced hypoglycemia (0.75 U/kg intravenous push). Their glucose nadir was 38±6 mg/dl (mean ± 1 SD). A three-phase pattern of change in CEEG power in response to hypoglycemia was observed: phase 1 was characterized by an increase in total CEEG power (natural log of activity = 9.1±1.3 μV2) over baseline (8.7±1.2 μV2) in the theta, delta, and beta frequency bands. This phase preceded and coincided with the glucose nadir. During phase 2, power in all frequency bands fell significantly below baseline. A nadir in CEEG power (8.0±1.6 μV2) occurred 40 to 55 minutes after insulin injection as glucose levels were rising. During phase 3 there was a return to baseline in CEEG power and frequency spectra. Heart rate increase just before phase 1; peak heart rate (91±8 beats/min) coincided with peak CEEG power and was significantly higher than basal rate (71±11, P<0.05). A significant increase in respiratory rate occurred during phase 1 of the CEEG and persisted through phase 2. A significant decrease in mean blood pressure (nadir = 73±6 mm Hg) below preinsulin blood pressure (81±8 mm Hg, P<0.05) coincided with the nadir of CEEG power in phase 2. Blood pressure returned to basal levels during phase 3. Peak plasma epinephrine (652±207 versus 46±30 pg/ml), norepinephrine (500±219 versus 273±107 pg/ml), and pancreatic polypeptide levels (1,023±689 versus 114±24 pg/ml) were all significantly elevated over respective basal concentrations (P<0.05). Peak hormone levels occurred during CEEG phase 2. This study demonstrates a temporal association of changes in CEEG power, vital signs, and hormonal secretion. These techniques may be applicable for further investigation of the clinical neuroendocrinology of the response to acute hypoglycemia.
KW - Brain: electroencephalography
KW - Hormones: concentrations
KW - Measurement techniques: electroencephalography
KW - Metabolism: hypoglycemia
KW - Monitoring
UR - http://www.scopus.com/inward/record.url?scp=0024424120&partnerID=8YFLogxK
U2 - 10.1007/BF01618252
DO - 10.1007/BF01618252
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C2 - 2681552
AN - SCOPUS:0024424120
SN - 0748-1977
VL - 5
SP - 229
EP - 235
JO - Journal of Clinical Monitoring
JF - Journal of Clinical Monitoring
IS - 4
ER -