Balanced salt solution in the treatment of hemorrhagic shock. Studies in dogs.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to C R Baxter.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Radioimmunoassays for 5(S), 12(R)-dihydroxyeicosa-6, 14-cis, 8,10-trans-tetraenoic acid (leukotriene B4, LTB4) and 5(S)-hydroxy-6(R)-L-gamma-glutamyl-L-cysteinyl-glycinyleicosa-7,9- trans, 11,14-cis-tetraenoic acid (leukotriene C4, LTC4) have been used to quantify the concentrations of these arachidonic acid metabolites in plasma (12 patients) and blister fluid (6 patients) of burned patients. The results of this study demonstrate that, in general, burn plasma LTB4, and LTC4 were not elevated; however, in individual cases, transient high levels of leukotrienes were observed. Correlation between leukotriene "peaks" and the clinical course could not be established. High levels of LTB4 and LTC4 in burn blister fluid suggest their participation in local inflammatory reactions.
Transient hypertriglyceridemia occurs in patients with severe thermal injury, and some patients have a low clearance of exogenous triglyceride (TG) from plasma. This suggests an impaired lipolysis. In the current study, we measured the levels of apolipoproteins required for clearance of endogenous and/or exogenous TG. Twenty-five thermal injury patients (18 men and 7 women) having an average of 52% +/- 6% (SE) total burn surface area were followed for a period of nine weeks. The levels of plasma lipids and apolipoproteins C-II, C-III, E, and A-I were measured after a 12-hour "fast," ie, prior to the parenteral administration of fat emulsion. The levels of plasma cholesterol and apolipoproteins C-II, C-III, and A-I were low. Plasma TG levels, however, were not abnormally elevated, while apo E levels were within normal range. The results indicate that thermally injured patients have reduced levels of apoproteins necessary for TG metabolism. This condition may predispose to intolerance of exogenous TG.
The lipolytic capacity of patients with severe and moderate thermal injury was assessed in vivo by determining the rate of clearance of chylomicrons. Twelve patients, two women and ten men, age 34 +/- 12 years, had burns varying from 28% to 84% of total burn surface area (TBSA). Seven patients had an average burn size of 63% TBSA. They were hypocholesterolemic and normotriglyceridemic during parenteral alimentation that excluded fat emulsion. But when Lyposil was infused intravenously (150 mg/kg/hr for a period of eight hrs), plasma triglyceride (TG) levels increased. Most of the triglyceride was in the form of chylomicrons, which had a prolonged residence time in plasma. Patients with moderate thermal injury (mean % TBSA 38% +/- 9%) had normal TG levels before fat infusion. When Liposyl was infused intraduodenally (170 mg/kg/hr), the plasma TG levels remained normal and the chylomicron half-life was very short. These observations suggest that patients with severe thermal injury may have reduced lipolytic capacity, especially during parenteral administration of fat emulsion.
Isolated coronary perfused guinea pig hearts were used to determine if aging alters left ventricular (LV) intrinsic contractile response to unresuscitated burn shock. We first compared control hearts from both young (N = 10) and aged (N = 10) guinea pigs. Compared with young control hearts, aged control hearts showed significantly lower left ventricular performance (LVP) (84.2 +/- 1.6 v 76.0 +/- 1.5; P less than 0.003), +dP/dtmax (1417.5 +/- 52.4 v 1048 +/- 48.7; P less than 0.001), and -dP/dtmax (1079 +/- 79 v 916 +/- 27; P less than 0.001) at a left ventricular end-diastolic pressure (LVEDP) of 10 mmHg. A 43% +/- 2% third-degree burn (Walker model) was studied in 20 young and 10 aged guinea pigs. The aged burn hearts showed significantly lower LVP (57.1 +/- 2.1 v 65.5 +/- 2.0; P less than 0.01) and +dP/dtmax (1026 +/- 66.4 v 1219 +/- 59.9; P less than 0.001) at an LVEDP of 10 mm Hg. In addition, LV function curves for the aged burn hearts were shifted downward and to the right of curves obtained from the young burn hearts (P less than 0.05). Contractile defects in the aged group were neither related to altered beating frequency nor to maximally effective increases in diastolic stretch. While increased extracellular calcium concentration (from 1 to 8 millimolar [mM]) increased LVP, +dP/dtmax, and -dP/dtmax in a dose-dependent manner in both young and aged burn hearts, absolute values of measured contractile performance were consistently less in the aged hearts compared with the young hearts at identical calcium concentrations. Finally, we examined the effects of thermal injury on contractile function within the aged group. Peak LVP and maximal rate of relaxation were uniformly decreased in all burn hearts compared with control aged hearts. The +dP/dtmax was not significantly altered by burn in this age group (burn: 1026 +/- 66; control: 1048 +/- 49). This study suggests that severe myocardial contractile changes resulting from a major thermal insult in subjects with already compromised hearts is likely a significant limiting factor in the response to burn shock.
Thermal injury was produced in rabbits to determine (1) whether hypertriglyceridemia was inducible by thermal injury and, if so, (2) what was its time course and (3) how were the levels of apolipoproteins B, E, and A-I affected. In this study, seven New Zealand-specific pathogen-free male rabbits were inflicted with a burn to 27% of the total body surface area; another seven rabbits underwent a sham procedure. Plasma triglyceride levels rose markedly in the thermally injured group, and the hypertriglyceridemia persisted for ten days. Total plasma apolipoprotein B levels increased markedly by three days postburn and remained elevated for a period longer than the hypertriglyceridemia. In contrast, apolipoprotein E levels slowly increased, reaching a peak by day 10, and declined thereafter. Plasma levels of apolipoprotein A-I increased rapidly and remained elevated for two months. Thus, hypertriglyceridemia and concomitant changes in levels of apolipoproteins B, E, and A-I could be induced in rabbits by thermal injury. Plasma triglyceride levels were elevated for some time and then returned to normal, whereas apolipoprotein levels remained elevated for a longer time. These abnormalities may impair normal lipid transport in the postburn phase.
Explore the source record for details and available documents.
The release of oxygen free radicals from ischemic myocardium has been implicated as a causative factor of cardiac dysfunction after thermal injury. In this study, isolated coronary perfused guinea pig hearts were used to determine if free radical scavengers improve left ventricular (LV) intrinsic contractile response to burn shock. Parameters measured included peak isovolumic LV pressure (LVP) and maximal rate of LVP rise (+dP/dtmax) and fall (-dP/dtmax) at a constant preload. Control animals were immersed in body temperature water and divided into four groups: Group 1, untreated N = 10; Group 2, control animals treated with unbound superoxide dismutase (SOD), N = 5; Group 3, control animals treated with ficoll-SOD, N = 5; and Group 4, control animals treated with PEG-SOD, N = 5. Scald burn equivalent to 45% of total body surface area was produced in 64 animals. Fluid resuscitation was initiated immediately after burn in all animals, and animals were then divided into seven burn experimental groups. In Group 5, 10 animals were treated with fluid alone, lactated Ringer's, 4 mL/kg/% burn. Burned animals in Group 6 (N = 10) received a reduced volume of Ringer's 2 mL/kg/% burn plus unbound-SOD, 50 mg/kg; 10 animals in Group 7 received this volume of Ringer's plus ficoll-SOD, 50 mg/kg. In groups 8, 9, and 10 animals were given fluid, lactated Ringer's, 2 mL/kg/% burn plus varying doses of PEG-SOD (Group 8: N = 9, 1,000 U; Group 9: N = 10, 6,000 U; Group 10: N = 5, 12,000 U). In Group 11 (N = 10), animals received SOD-PEG, 6,000 U, plus catalase, CAT-PEG, 6,000 U, given with 4 mL/kg/% burn lactated Ringer's solution. Hypotension, hypothermia, and hemoconcentration were similar in all animals after thermal injury, regardless of treatment regimen. Burn hearts showed significantly lower LVP, +dP/dt max, and -dP/dt max than control hearts (P less than 0.05). Compared to controls, coronary pressure and coronary vascular resistance were significantly higher in all treated burn groups. There was no significant difference in heart rate or time to peak pressure or time to maximal contraction or relaxation among the groups. Left ventricular function curves for burned hearts were shifted downward and to the right of curves obtained from control hearts (P less than 0.01), regardless of scavenger treatment. PEG-SOD, 6,000 U, improved left ventricular contractility (+dP/dt) at maximal levels of end-diastolic pressure but deficits in left ventricular pressure and relaxation persisted.(ABSTRACT TRUNCATED AT 400 WORDS)
Explore the source record for details and available documents.