Glucose infusion improves endogenous protein synthesis efficiency in multiple trauma victims.

Metabolic costs of excessive nutritional support in stressed patients have been increasingly recognized. The decreased endogenous protein synthesis efficiency (PSE) following major injury has been attributed to the predominant need of amino acid precursors for gluconeogenesis. The present study tested the hypothesis that provision of glucose alone, not to exceed the resting energy expenditure (REE), for the first 4 to 5 days after trauma would be enough to restore PSE and stimulate the injured body to accept full nutrition. Eight severely injured, adult, hypermetabolic, and highly catabolic patients admitted to the Trauma Intensive Care Unit (TICU) served as our subjects. Integrated measurements of whole body fuel-substrate kinetics were obtained for energy metabolism (indirect calorimetry), protein kinetics (primed constant infusion of 15N-glycine), and glucose kinetics (labeled glucose infusions). Two studies were conducted on each same subject, one in the early flow phase of injury (48 to 60 hours after trauma) and a second after 4 to 5 days of hypertonic glucose (4.1 +/- 0.5 mg/kg/min; 80% REE calories) infusion with electrolytes, trace elements, and minerals. Significant (P less than .05) increases in PSE (14%, 65% +/- 2% to 74% +/- 2%), plasma growth hormone and insulin levels, and respiratory quotient (RQ) (31%, 0.74 +/- 0.03 to 0.97 +/- 0.04), and decreases in endogenous glucose appearance rate (55%, 3.1 +/- 0.5 to 1.4 +/- 0.1 mg/kg/min), and negative N balance (48%, 219 +/- 26 to 114 +/- 15 mgN/kg/d) were observed. The results suggest that hypertonic glucose infusion alone may be sufficient for physiological adaptation in the immediate posttrauma days. This therapy restores normal PSE, which should protect the labile protein pool.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute right ventricular failure is caused by inadequate right ventricular hypothermia.

The hypothesis of this study was that inadequate right ventricular hypothermia contributes to the right ventricular dysfunction occasionally observed after cardiac operations. Dogs were placed on cardiopulmonary bypass, and 60 minute periods of hypothermic myocardial ischemia were imposed. Left ventricular temperature was always maintained at 15 degrees C and right ventricular temperatures were maintained at 15 degrees C (Group I, n = 8), 25 degrees C (Group II, n = 8), and 35 degrees C (Group III, n = 8). These temperatures were produced by infusion of hypothermic crystalloid cardioplegic solution and appropriate topical cooling and heating of the left and right ventricles, respectively. Multiple indices of ventricular function were obtained 15, 30, 45, and 60 minutes after bypass and compared to prebypass control values. In all Group I animals (left ventricular temperature = 15 degrees C, right ventricular temperature = 15 degrees C), postischemic indices of right ventricular function were not different from control values (p = NS). In Group II (left ventricular temperature = 15 degrees C, right ventricular temperature = 25 degrees C), two animals died 30 and 45 minutes after bypass, respectively, of right ventricular failure. In the other six animals in Group II, all indices of right ventricular function were significantly reduced (p less than 0.05) except for right ventricular systolic pressure. In Group III (left ventricular temperature = 15 degrees C, right ventricular temperature = 35 degrees C), two animals could not be weaned from cardiopulmonary bypass because of right ventricular akinesia. Six animals were weaned from bypass, but two died 15 minutes, one died 30 minutes, and one 45 minutes after bypass. Two animals lived 60 minutes, but all indices of right ventricular function were decreased. Failure to maintain right ventricular temperatures below 25 degrees C during 1 hour of cardiac ischemia in the dog can result in fatal right ventricular failure.