Based on our earlier work, a 2.5-fold increase in insulin secretion should completely inhibit hepatic glucose production through the hormone's direct effect on hepatic glycogen metabolism. The aim of the present study was to test the accuracy of this prediction and to confirm that gluconeogenic flux, as measured by three independent techniques, was unaffected by the increase in insulin. A 40-min basal period was followed by a 180-min experimental period in which an increase in insulin was induced, with euglycemia maintained by peripheral glucose infusion. Arterial and hepatic sinusoidal insulin levels increased from 10 ؎ 2 to 19 ؎ 3 and 20 ؎ 4 to 45 ؎ 5 U/ml, respectively. Net hepatic glucose output decreased rapidly from 1.90 ؎ 0.13 to 0.23 ؎ 0.16 mg ⅐ kg ؊1 ⅐ min ؊1 . Three methods of measuring gluconeogenesis and glycogenolysis were used: 1) the hepatic arteriovenous difference technique (n ‫؍‬ 8), 2) the [ (1) showed that hepatic glucose production (HGP) can be inhibited by selective increases in the arterial or portal vein insulin concentration. In response to a 14-U/ml increase in arterial insulin (no change in portal insulin), a Ͼ50% reduction in net hepatic glucose output (NHGO) was observed. Likewise, a 14-U/ml increase in portal insulin (no change in arterial insulin) also resulted in a Ͼ50% reduction in NHGO. In addition, the above studies showed that insulin acted directly on the liver, with a rise in hepatic sinusoidal insulin quickly inhibiting HGP by reducing net hepatic glycogenolysis. The indirect effect of insulin on HGP, on the other hand, resulted from a decrease in gluconeogenic flux rate caused by a reduction in the flow of gluconeogenic amino acids and glycerol to the liver and diversion of carbon derived from glycogenolysis to lactate rather than glucose. The reduction in HGP in this group was also, in part, the result of a decrease in net hepatic glycogenolysis, which occurred as a result of a slight rise in the hepatic sinusoidal insulin level, which, in turn, occurred as a result of the rise in hepatic artery insulin. It took 1 h to detect a significant indirect effect of insulin on HGP.Sindelar et al.(1) created selective changes in the arterial or portal insulin level by infusing somatostatin to inhibit insulin secretion and replacing insulin by infusion through a peripheral and/or portal catheter. Stimulation of pancreatic insulin secretion, on the other hand, results in an increase in both portal and arterial levels of the hormone. Therefore, in the present study, our aim was to determine if a two-to threefold increase in insulin, occurring simultaneously in portal and peripheral blood, would inhibit HGP primarily through an effect on glycogen metabolism. Although Sindelar et al. (1) reported that portally delivered insulin did not affect gluconeogenic flux, their estimate of the latter relied solely on the measurement of the net hepatic uptake (arteriovenous [AV] difference) of gluconeogenic precursors. In the present study, we combined the hepatic AV difference technique, along...

Current monitoring technologies are unable to detect early, compensatory changes that are associated with significant blood loss. We previously introduced a novel algorithm to calculate the Compensatory Reserve Index (CRI) based on the analysis of arterial waveform features obtained from photoplethysmogram recordings. In the present study, we hypothesized that the CRI would provide greater sensitivity and specificity to detect blood loss compared with traditional vital signs and other hemodynamic measures. Continuous noninvasive vital sign waveform data, including CRI, photoplethysmogram, heart rate, blood pressures, SpO2, cardiac output, and stroke volume, were analyzed from 20 subjects before, during, and after an average controlled voluntary hemorrhage of ∼1.2 L of blood. Compensatory Reserve Index decreased by 33% in a linear fashion across progressive blood volume loss, with no clinically significant alterations in vital signs. The receiver operating characteristic area under the curve for the CRI was 0.90, with a sensitivity of 0.80 and specificity of 0.76. In comparison, blood pressures, heart rate, SpO2, cardiac output, and stroke volume had significantly lower receiver operating characteristic area under the curve values and specificities for detecting the same volume of blood loss. Consistent with our hypothesis, CRI detected blood loss and restoration with significantly greater specificity than did other traditional physiologic measures. Single measurement of CRI may enable more accurate triage, whereas CRI monitoring may allow for earlier detection of casualty deterioration.

Vital signs historically served as the primary method to triage patients and resources for trauma and emergency care, but have failed to provide clinically-meaningful predictive information about patient clinical status. In this review, a framework is presented that focuses on potential wearable sensor technologies that can harness necessary electronic physiological signal integration with a current state-of-the-art predictive machine-learning algorithm that provides early clinical assessment of hypovolemia status to impact patient outcome. The ability to study the physiology of hemorrhage using a human model of progressive central hypovolemia led to the development of a novel machine-learning algorithm known as the compensatory reserve measurement (CRM). Greater sensitivity, specificity, and diagnostic accuracy to detect hemorrhage and onset of decompensated shock has been demonstrated by the CRM when compared to all standard vital signs and hemodynamic variables. The development of CRM revealed that continuous measurements of changes in arterial waveform features represented the most integrated signal of physiological compensation for conditions of reduced systemic oxygen delivery. In this review, detailed analysis of sensor technologies that include photoplethysmography, tonometry, ultrasound-based blood pressure, and cardiogenic vibration are identified as potential candidates for harnessing arterial waveform analog features required for real-time calculation of CRM. The integration of wearable sensors with the CRM algorithm provides a potentially powerful medical monitoring advancement to save civilian and military lives in emergency medical settings.

Currently available triage and monitoring tools are often late to detect life-threatening clinically significant physiological aberrations and provide limited data in prioritizing bleeding patients for treatment and evacuation. The Compensatory Reserve Index (CRI) is a novel means of assessing physiologic reserve, shown to correlate with central blood volume loss under laboratory conditions. The purpose of this study was to compare the noninvasive CRI device with currently available vital signs in detecting blood loss. Study subjects were soldiers volunteering for blood donation (n = 230), and the control group was composed of soldiers who did not donate blood (n = 34). Data collected before and after blood donation were compared, receiver operator characteristic curves were generated after either donation or the appropriate time interval, and areas under the curves (AUCs) were compared. Compared with pre-blood loss, blood donation resulted in a mean reduction of systolic blood pressure by 3% (before, 123 mmHg; after, 119 mmHg; P < 0.01). The CRI demonstrated a 16% reduction (before, 0.74; after, 0.62; P < 0.01). Heart rate, diastolic blood pressure, and oxygen saturation remained unchanged. The AUC for change in CRI was 0.81, 0.56 for change in heart rate, 0.53 for change in systolic blood pressure, 0.55 and 0.58 for pulse pressure and shock index, respectively. The AUCs for detecting mild blood loss at a single measurement were 0.73 for heart rate, 0.60 for systolic blood pressure, 0.62 for diastolic blood pressure, 0.45 for pulse oximetry, and 0.84 for CRI. The CRI was better than standard indices in detecting mild blood loss. Single measurement of CRI may enable a more accurate triage, and CRI monitoring may allow for earlier detection of casualty deterioration.

Degradation of the visual system can lead to a dramatic reduction of mobility by limiting a person to his sense of touch and hearing. This paper presents the development of an obstacle detection system for visually impaired people. While moving in his environment the user is alerted to close obstacles in range. The system we propose detects an obstacle surrounding the user by using a multi-sonar system and sending appropriate vibrotactile feedback. The system aims at increasing the mobility of visually impaired people by offering new sensing abilities.