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Biomedical subjects

T Lund

Publications and source records attributed to T Lund.

At least 145 records · Page 8Linked to original sources
PubMed1989

Microvascular exchange during burn injury: III. Implications of the model.

The present work investigates the implications of the predictions of a dynamic mathematical model of microvascular exchange following a nonresuscitated burn injury in a rat (Bert et al.: Circulatory Shock 28:199-219, 1989). Transport coefficients, transmicrovascular pressures, and the resultant fluid and protein fluxes were examined in order to assess their quantitative importance to the dynamic behavior of small (10% body surface area) and large (40% body surface area) burns. Edema accumulation in the injured tissue is dependent not only on events occurring in that tissue but is influenced strongly by interaction with the plasma and the noninjured tissue compartments.

Animals↗
PubMed1989

Thermal skin injury: I. Acute hemodynamic effects of fluid resuscitation with lactated Ringer's, plasma, and hypertonic saline (2,400 mosmol/l) in the rat.

Heart rate (HR), central venous pressure (CVP), mean arterial pressure (MAP), and cardiac index (CI) were measured in anesthetized rats subjected to a 40% body surface area full-thickness scald burn. Postburn intravenous fluid therapy with lactated Ringer's (5 ml/hr), plasma (2.5 ml/hr), or very hypertonic saline (2,400 mosmol/l) (0.75 ml/hr) was compared to unburned or burned, untreated controls. HR and CVP were not influenced significantly by thermal injury. MAP decreased steadily in the untreated group from 110 mmHg to 80 mmHg at 3 hr postburn. In the fluid-treated groups MAP did not change significantly. During the first 15 min postburn, CI was reduced to 58-71% of control values (P less than 0.01). CI increased during Ringer's and plasma infusion to 74-80% of control values (P less than 0.02 vs. unburned). Despite infusion therapy, hematocrit increased from 48 to 52%, clearly less than in the unresuscitated group (increase from 48 to 58%). Theoretically, the 2,400 mosmol/l saline would expand extracellular volume by five to six times the infused volume. Still, CI was reduced by 55% at 3 hr postburn in the hypertonic saline as well as in the burned, untreated group (P less than 0.001 vs. unburned). The low CI was mainly due to a reduced stroke volume.

Animals↗
PubMed1989

Thermal skin injury: II. Effects on edema formation and albumin extravasation of fluid resuscitation with lactated Ringer's, plasma, and hypertonic saline (2,400 mosmol/l) in the rat.

Pentobarbital anesthetized rats were subjected to a 40% body surface area full-thickness scald burn. Intravenous fluid therapy was given as lactated Ringer's (5 ml/hr), plasma (2.5 ml/hr), or very hypertonic saline (2,400 mosmol/l) (0.75 ml/hr) and compared to unburned or burned, untreated controls. At 3 hr postburn, skin water and albumin content and extravasation of radiolabelled albumin were determined. Water content in injured skin increased by 35-78% (least in the untreated group, most in the plasma group) compared to unburned controls (P less than 0.05). After lactated Ringer's therapy water content increased even in unburned skin and in muscle (P less than 0.05). Tissue albumin mass increased generally slightly more than the increase in water content, from 37% (lactated Ringer's group) to 126% (plasma group) in burned areas. Extravasation rate of radiolabelled albumin increased 5-80 times in burned areas, most following plasma treatment (equivalent to 0.6-1.0 ml plasma/g dry weight/180 min). A major part of the estimated total fluid loss following therapy by lactated Ringer's took place in noninjured tissue. Plasma therapy gave less fluid accumulation in unburned tissues but more edema in the injured areas than lactated Ringer's.

Albumins↗
PubMed1988

Acute postburn edema: role of strongly negative interstitial fluid pressure.

Interstitial fluid hydrostatic pressure (Pif) was measured with micropipettes during the acute edema generation that followed thermal skin injury in rats. Intradermal Pif was reduced from normal level of -1 mmHg to very negative values after thermal injury. The strongly negative Pif reflects a tissue imbibition pressure created by the thermal injury. The magnitude and duration of this pressure was dependent on the extent of the injury and the availability of fluid. After in vivo injury to 10 and 40% of the total body surface area (TBSA), mean intradermal Pif was temporarily reduced to -20 and -31 mmHg, respectively. Intravenous fluid infusion resulted in a rapid return of Pif to slightly positive values. Fluid available for transfer from the circulation was reduced by inducing the injury after killing the animal (postmortem injury) and even more by the subcutaneous insertion of a plastic barrier: this led to more pronounced reductions in Pif to average minimum values of -95 and -135 mmHg, respectively. Our data show that increased tissue imbibition pressure and increased net filtration pressure (tissue mechanisms) are responsible for a major part of the acute fluid shifts into thermally injured skin. Vascular mechanisms (permeability changes and intravascular pressure) are involved in the postburn edema development but are clearly less important than hitherto believed.

Animals↗
PubMed1987

The human chromosomal protein HMG I contains two identical palindrome amino acid sequences.

The sequence of 105 amino acids of the human high mobility group chromosomal protein HMG I has been determined. The most striking feature of this sequence is two identical palindrome sequences: pro-arg-gly-arg-pro, which together with a third related sequence: gly-arg-pro-arg, may represent the binding sites of HMG I to clusters of A-T base pairs in DNA.

Amino Acid Sequence↗
PubMed1987

Fractionation and identification of metaphase-specific phosphorylated forms of high-mobility-group proteins.

In the present work chromatography on phosphocellulose and blue Sepharose have been used to fractionate the different phosphorylated forms of the low-molecular-mass high-mobility-group (HMG) proteins from metaphase arrested HeLa cells. The proteins in the different fractions from the blue Sepharose column were analysed by acetic acid/urea gel electrophoresis. Aliquots from the same fractions were also treated with alkaline phosphatase and the dephosphorylated and phosphorylated proteins were then compared by electrophoresis to identify the phosphorylated proteins. It was found that HMG 14 consisted of a mixture of an unphosphorylated and two phosphorylated forms, while HMG Y existed as one homogeneous superphosphorylated form. These findings remove previous uncertainty about phosphorylation of HMG Y and HMG 14. The presence of HMG M and phosphorylated forms of HMG 17 was confirmed. Peptide mapping of HMG I and HMG M gave further evidence that HMG M is a superphosphorylated form of HMG I, and it is suggested that the term HMG Im be used instead of HMG M. The results suggested that HMG I and Y from HeLa cells contained at least three and two metaphase-specific phosphate groups respectively, while HMG 14 and 17 both consisted of an unphosphorylated form and two phosphorylated forms. A protein corresponding to HMG Im from HeLa cells was also found to be present in metaphase-arrested human lymphocytes, while HMG I and from two different rodent species seemed to be less phosphorylated then their counterparts from HeLa metaphase cells.

Acetates↗
PubMed1987

Transcapillary colloid osmotic pressures in injured and non-injured skin of seriously burned patients.

Thermal skin injury is accompanied by rapid and excessive oedema formation implicating a dramatic increase in the transcapillary fluid transport. In order to clarify the pressure changes occurring across the microvasculature after a thermal skin injury we have measured colloid osmotic pressures (COP) in interstitial fluid (COPi) of injured and non-injured skin as well as in plasma (COPp) from patients suffering major cutaneous burns. Interstitial fluid was collected with a wick-technique and analysed for COP. Measurements were performed as early as 6 h and continued until 56 h after injury. A severe hypoproteinaemia occurred in all patients with a marked reduction in COPp down to about 10 mmHg. Up to 12h post-burn we found a higher COPi in injured skin than in plasma. The first measurement of COPp averaged 9.8 mmHg as compared to an average COPi of 11.1 and 9.3 mmHg in injured and non-injured skin respectively. Measurements performed later than 12h showed a return of the transcapillary COP gradient towards the normal direction (COPp greater than COPi). The gradient was considerably less than in a normal situation. Based on the present observations of transcapillary COP it is suggested that colloids should be withheld until the transcapillary COP gradient returns to the normal direction.

Adult↗
PubMed1986

Synthesis, processing, and secretion of rat immunoglobulin E made in Xenopus oocytes.

Rat immunoglobulin E (IgE) synthesized in Xenopus laevis oocytes, injected with rat plasmacytoma mRNA, was analysed by specific immunoprecipitation and SDS-polyacrylamide gel electrophoresis under reducing as well as non-reducing conditions. The results indicate that the oocytes will translate and correctly process the rat IgE heavy and light chains, resulting in secretion of a correctly assembled, normal immunoglobulin molecule. The normal, extensive glycosylation of the IgE heavy chain (e-chain) is faithfully carried out by the oocytes; therefore, this posttranslational modification is apparently of an unspecific nature, and does not depend upon a mechanism specific for plasma cells.

Animals↗
PubMed1986

Method for complete separation of the high mobility group (HMG) proteins HMG I and HMG Y from HMG 14 and HMG 17 and a procedure for purification of HMG I and HMG Y.

A purification procedure which separates the four low-molecular-weight high mobility group (HMG) proteins, HMG 14, 17, I and Y, is described. The procedure includes chromatography on phosphocellulose and Blue Sepharose combined with reversed-phase high-performance liquid chromatography. The blue Sepharose column separates HMG I and Y completely from HMG 14 and 17, and should therefore be an useful tool for the identification of these proteins which in several reports have been confused with HMG 14 and 17. HMG I and Y on the one hand and HMG 14 and 17 on the other exhibited considerable differences in their affinities for Blue Sepharose, probably reflecting fundamental differences in biological function.

Cellulose↗
PubMed1986

The genes for human gastrin and cholecystokinin are located on different chromosomes.

The polypeptide hormones gastrin and cholecystokinin are structurally related, having the identical pentapeptide GWMDF located at their C-terminus. The precursors to these two hormones also show amino acid homology, suggesting that they may have a common ancestral origin. Recombinant DNA clones corresponding to gene fragments encoding human gastrin and cholecystokinin were used to determine their respective chromosomal localization by analyzing human-rodent cell lines. We have assigned the cholecystokinin gene to human chromosome 3q12-3pter and the gastrin gene to chromosome 17q.

Animals↗
PubMed1986

The physiology of stringent factor (ATP:GTP 3'-diphosphotransferase) in Escherichia coli.

The enzyme ATP:GTP 3'-diphosphotransferase catalyzes the transfer of the beta, gamma-pyrophosphate of ATP to the 3' position of GTP or GDP. The amounts of enzyme were measured in cell extracts of a relA+ strain of E. coli grown at different growth rates between 0.4 and 1.9 generations per hour, using precipitation with specific antibodies to purify the enzyme. The amount of enzyme was found to be a constant fraction of total protein at all growth rates corresponding to about 45 molecules of enzyme per genome equivalent of DNA. The purified enzyme has little catalytic activity by itself but has to be activated either by a complex of 70S ribosomes, mRNA and uncharged tRNA or by a solvent like ethanol at a concentration of about 20%. The kinetic constants of the enzyme for the transfer pyrophosphate from ATP to GTP in the ribosome-activated state were determined. The Vmax was estimated to be 140 mumol/min X mg at 37 degrees C and the S0.5 values for GTP and ATP were 0.35 and 0.53 mM, respectively. The reaction was estimated to have an equilibrium constant of about 300. In the pyrophosphate transfer from ATP to GDP the Vmax was estimated to be 90 mumol/min X mg at 37 degrees C and the S0.5 for GDP as 0.3 mM. During amino acid starvation of a relA+ strain of E. coli the amounts of enzyme and the catalytic capacity of the enzyme are sufficient to maintain the observed ppGpp levels in the cells at all growth rates.

Adenosine Triphosphate↗
PubMed1986

A low molecular weight heparin (KABI 2165) for prophylaxis of postoperative deep venous thrombosis.

In a prospective double-blind trial, low molecular weight (LMW) heparin (KABI 2165) 5,000 U (anti-Xa) once daily was compared with conventional heparin 5,000 IU twice daily, both given subcutaneously, as regards prevention of postoperative deep venous thrombosis (DVT) in 52 patients undergoing major abdominal surgery. Radioactive fibrinogen uptake test (FUT) was used for DVT screening. DVT, diagnosed from positive FUT, developed in two patients from each group, but could be phlebographically confirmed in only one (LMW) case. No intergroup differences were found in peroperative blood loss or requirements for blood transfusion. Complications attributable to the prophylactic regimens were few. In the LMW-heparin group, the anti-Xa levels measured during operation showed considerable variation, the higher activities (greater than 0.30 U/ml) being nonsignificantly associated with increased blood loss. Studies with lower doses of LMW-heparin are recommended.

Adult↗
PubMed1986

Acute hemodynamic effects of thermal skin injury in the rat.

Heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), and cardiac index (CI) were measured in anesthetized rats subjected to thermal injury covering 10 and 40% of the body surface area (BSA). These were compared to corresponding sham controls. No fluid substitution was provided. MAP decreased rapidly from 110 mm Hg preburn and leveled off at 75-80 mm Hg after 60 min postburn in the 40% burn group and at 80-95 mm Hg in the 10% burn group. CVP was not influenced by thermal injury. CI fell from about 270 to 208 and to 173 ml X min-1 X kg-1 during the first 15 min after injury in the 10 and 40% burn groups, respectively. Thereafter, CI continued to fall more slowly in both groups, being lower in the 40% than the 10% burn group for the whole postburn course (P less than .001). HR fell slightly in both burn groups (P greater than .05). Stroke volume index followed the same pattern as CI indicating that the fall in CI was caused by reduction in stroke volume. Total peripheral resistance increased slightly after injury. Previous measurement of hematocrit in thermal injury of the same type and extent suggests a 35% increase in viscosity. Consequently, vascular hindrance was unchanged. Compensatory tachycardia or vasoconstriction could not be demonstrated.

Animals↗