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Biomedical subjects

A P Robin

Publications and source records attributed to A P Robin.

28 records · Page 2Linked to original sources
PubMed1981

Lipoprotein lipase activity in surgical patients: influence of trauma and infection.

Hypertriglyceridemia commonly accompanies clinical sepsis and may be caused by increased hepatic production or decreased clearance of triglyceride from the bloodstream. In contrast, enhanced lipid clearing capacity is usually seen after uncomplicated trauma. The purpose of the study was to determine the role of lipoprotein lipase (LPL) in effecting the above changes. Enzyme activity was assayed in skeletal muscle and adipose tissue biopsy samples from 11 normal subjects and from 17 injured and 11 infected surgical patients. Normal subjects after 4 days of 5% dextrose infusion (D5) showed a significant decrease in adipose tissue LPL activity but no change in skeletal muscle activity. Trauma patients after several days of D5 had higher activity in adipose tissue and higher plasma insulin levels than diet-matched control subjects but showed no change in skeletal muscle activity. Infected patients with high plasma triglyceride levels had significantly decreased LPL activity in both tissues. A linear relationship was found between insulin concentration and adipose tissue LPL activity in normal subjects. We conclude that: (1) low tissue LPL activity in sepsis may result in diminished lipid clearance and contribute to hypertriglyceridemia, (2) after trauma, changes in tissue LPL activity as well as other factors such as altered hemodynamics play a role in determining in vivo lipid clearance, and (3) adipose tissue LPL activity is related to the plasma insulin concentration in normal subjects.

Adipose Tissue↗
PubMedDate not supplied

Total parenteral nutrition during acute pancreatitis: clinical experience with 156 patients.

Over a 3-year period, 156 of 815 patients admitted to a single institution with acute pancreatitis received total parenteral nutrition (TPN) for 2,572 patient days. Seventy had "simple" acute pancreatitis (group I) and 86 (group II) developed local complex disease (pseudocyst, abscess, or necrotic gland). In groups I and II, respectively, days without oral intake (NPO) were 13.6 +/- 1.5 (SEM) and 24.0 +/- 2.1 (p less than 0.005), hospital days were 19.8 +/- 1.7 and 35.8 +/- 3.2 (p less than 0.005), and duration of TPN was 10.9 +/- 1.0 and 21.0 +/- 2.3 days (p less than 0.005). Thirty-three patients in group I and 53 in group II required exogenous insulin. Alteration of standard formulas was necessary in 87 patients, but cessation of therapy was necessary in only one instance. Twenty catheters were removed for suspected sepsis with only 3 confirmed cases. Fat-based formulas were well tolerated in 15% of patients. During TPN, body weight rose from 95.0 +/- 2.4% to 97.4 +/- 4.3% of ideal in group I and remained at 90.5 +/- 1.8% in group II. Albumin rose from 3.36 +/- 0.10 to 3.50 +/- 0.08 g/dl in group I and from 3.01 +/- 0.07 to 3.35 +/- 0.07 g/dl in group II. The entire cohort differed from 10 randomly chosen patients who did not receive TPN in terms of days NPO (2.8 +/- 0.3) and hospital days (5.5 +/- 0.6). Variables associated with prolongation of hospital stay and time NPO were number of prognostic criteria, local complex disease, and underlying chronic pancreatitis only in select groups. We conclude that during acute pancreatitis, TPN can be administered safely but with careful monitoring and we recommend early aggressive therapy in the subgroups noted above and when underlying malnutrition exists. In the borderline patient, TPN may be administered by peripheral vein until the severity of disease is manifest.

Acute Disease↗
PubMedDate not supplied

Plasma clearance of fat emulsion in trauma and sepsis: use of a three-stage lipid clearance test.

Total parenteral nutrition (TPN) is now widely available, but there is a relatively little data relating to the optimal substrate support in different types of patients. In critically ill patients who require parenteral nutrition, underlying metabolic alterations will influence the capacity for substrate utilization; in them, fat emulsion may serve as a useful energy source but may also have deleterious effects. The intravenous fat tolerance test has been widely used as a measure of the capacity of the organism to clear exogenous fat from the bloodstream. We have devised and employed a three-stage lipid clearance test using Intralipid-10% as a substrate. The rates of infusion are such that first order kinetics are followed during the first two stages yielding fractional removal rates, and zero order kinetics are followed during the third infusion yielding maximal clearance rates. Six injured and 6 infected patients displayed a greater capacity for lipid clearance than 13 normal subjects. Four injured patients who also had received multiple transfusions failed to show this response. Fractional removal rates were influenced by injury and infection to a greater extent than maximal clearance rates. Models are presented utilizing enzyme saturation kinetics and treating endogenous triglyceride as a competitive inhibitor (for the enzyme-substrate system of lipoprotein lipase-Intralipid triglyceride). The importance of employing enzyme saturation kinetics in the interpretation of lipid clearance tests is noted. The calculated apparent Michaelis-Menten constant for Intralipid triglyceride during the lipid clearance test is 521 +/- 38 (SEM) micromole/liter. In vitro systems utilizing Intralipid triglyceride as a substrate have yielded values in this range.

Adult↗
PubMedDate not supplied

Adipose tissue response to insulin following injury.

Derangements of posttraumatic glucose metabolism have long been recognized, with observed changes implicating abnormal action of insulin on target tissues. Insulin is important as well in fat metabolism, and "resistance" to insulin's effects on lipid metabolism after injury has been demonstrated. Although fat-derived fuels are the body's major energy source during starvation and after injury, most studies of posttraumatic insulin "resistance" have focused on carbohydrate metabolism. This study investigated adipose tissue response to insulin in vitro in rats subjected to starvation and/or trauma. Relationships between various parameters, including adipocyte size and weight, plasma glucose, insulin, and glycerol, and basal and insulin-suppressed lipolytic rates, were also studied. Results observed include a decrease in adipocyte size and an increase in basal lipolysis in both starved and traumatized rats, with both decreased sensitivity (T greater than S) and responsiveness (S greater than T) to insulin. These results support the concept that adipocytes of injured animals retain the ability to respond to insulin but lipolytic rates at maximal suppression are still quite high as compared to fed controls. Only minor differences were observed between starved animals and those with starvation and superimposed trauma.

Adipose Tissue↗
PubMedDate not supplied

Intravenous fat emulsion acutely suppresses neutrophil chemiluminescence.

The immediate effect of intravenous fat emulsion on neutrophil oxidant release was studied. Opsonized nonencapsulated S. aureus was used to stimulate neutrophil activity. Luminol enhanced chemiluminescence was followed over 15 min and recorded as peak output (P; mV), integral under the curve (I; V-sec) and rate of increase (R; mV/sec). Eighteen chronically ill patients receiving glucose based total parenteral nutrition were studied before and after a 4- to 6-hr test infusion of 500 ml of 10% fat emulsion. P decreased from 719 +/- 46 to 461 +/- 42 mV (p less than 0.001), I decreased from 169 +/- 17 to 111 +/- 12 V-sec (p less than 0.001) and R decreased from 6.9 +/- 1.0 to 4.0 +/- 0.6 mV/sec (p less than 0.001). Preincubation of normal whole blood with fat emulsion in vitro did not adversely affect chemiluminescence (11 studies), nor did incubation of normal neutrophils with patient postinfusion plasma (10 studies). We conclude that fat emulsion infusion acutely suppresses neutrophil chemiluminescence. The suppression is not a direct effect of the fat emulsion per se and is not due to inhibitory substances in the plasma following infusion.

Adult↗
PubMedDate not supplied

Metabolic consequences of hypercaloric glucose infusions.

Recent studies have demonstrated that an altered pattern of substrate mobilization and fuel utilization exists in patients who are acutely ill secondary to either injury or infection. These studies have important implications regarding the nutritional support of these patients. This review addresses some of the metabolic sequelae of total parenteral nutrition with hypertonic glucose as the primary source of non-protein calories. The consequences of administering glucose calories in excess of energy requirements are considered. The patterns of gas exchange, fuel utilization and fuel storage in nutritionally depleted and hypermetabolic patients are discussed with specific reference to fat metabolism. Administration of glucose in hypercaloric quantities may produce a respiratory as well as a metabolic stress. The former appears to be related to a ventilatory stimulus associated with an increased rate of carbon dioxide production. In acutely ill patients, this response is magnified and there is also a considerable rise in oxygen consumption and free norepinephrine excretion. It is this group of patients which shows the most profound elevation in minute ventilation. The metabolic pathways and regulatory mechanisms which may be involved are discussed. A scientific approach to substrate administration in acutely ill patients can be taken only after these patterns of metabolic responses have been fully elucidated.

Carbon Dioxide↗