PubMed Health⌕ Search

Biomedical subjects

K Holzer

Publications and source records attributed to K Holzer.

26 records · Page 2Linked to original sources

Partial improvement of crystal quality for microgravity-grown apocrustacyanin C1.

The protein apocrustacyanin C1 has been crystallized by vapour diffusion in both microgravity (the NASA space shuttle USML-2 mission) and on the ground. Rocking width measurements were made on the crystals at the ESRF Swiss-Norwegian beamline using a high-resolution psi-circle diffractometer from the University of Karlsruhe. Crystal perfection was then evaluated, from comparison of the reflection rocking curves from a total of five crystals (three grown in microgravity and two earth controls), and by plotting mosaicity versus reflection signal/noise. Comparison was then made with previous measurements of almost 'perfect' lysozyme crystals grown aboard IML-2 and Spacehab-1 and reported by Snell et al. [Snell, Weisgerber, Helliwell, Weckert, Holzer & Schroer (1995). Acta Cryst. D51, 1099-1102]. Overall, the best diffraction-quality apocrustacyanin C1 crystal was microgravity grown, but one earth-grown crystal was as good as one of the other microgravity-grown crystals. The remaining two crystals (one from microgravity and one from earth) were poorer than the other three and of fairly equal quality. Crystal movement during growth in microgravity, resulting from the use of vapour-diffusion geometry, may be the cause of not realising the 'theoretical' limit of perfect protein crystal quality.

Carrier Proteins↗

Effects of adenosine on the functions of circulating polymorphonuclear leukocytes during hyperdynamic endotoxemia.

Endotoxin-activated polymorphonuclear leukocytes (PMNL) adhere to the vascular endothelium and cause damage by the release of toxic superoxide anions (O2-). Because adenosine is a potent inhibitor of PMNL in vitro, the present study investigates the effects of this nucleoside on the functions of circulating PMNL in a standardized porcine model of hyperdynamic endotoxemia. Ten anesthesized pigs received an intravenous (i.v.) 330-min infusion of endotoxin (5 microg/kg of body weight per h). Another 10 pigs were also infused with endotoxin plus adenosine (150 microg/kg/min [i.v.]); this treatment was begun 30 min prior to the beginning of endotoxin treatment. Control groups (five animals per group) received either adenosine or physiological saline. Infusion of endotoxin caused severe neutropenia, shedding of L-selectin, upregulation of beta2-integrins, increased binding of C3-coated zymosan particles, and subsequent phagocytosis by PMNL. While phagocytosis-induced production of oxygen radicals appeared to decrease, extracellular release of superoxide anions was strongly enhanced. Infusion of adenosine during endotoxemia had no effect on neutropenia, expression of adhesion molecules, C3-induced adhesion, phagocytosis, or intracellular production of oxygen radicals, whereas extracellular release of O2- was strongly inhibited. Thus, i.v. infusion of adenosine during endotoxemia could be useful in protecting from O2(-)-mediated tissue injury without compromising the bactericidal mechanisms of PMNL.

2-Chloroadenosine↗

Hypovolemic shock and cardiac contractility: assessment by end-systolic pressure-volume relations.

The end-systolic pressure-volume relation (ESPVR) is accepted as a load-independent measure of cardiac contractility. Potential curvilinearity of the ESPVR, dependency on coronary perfusion pressure (CPP) and sensitivity to the type of loading intervention might limit its use in hemorrhagic shock. This study compared ESPVRs obtained by caval and aortic occlusion under physiological loading conditions at baseline with those obtained during hemorrhagic shock (mean arterial pressure 45 mmHg). The left ventricular (LV) pressure (tip manometer) and volume (conductance catheter) were measured in ten anesthetized pigs. ESPVRs were fitted to linear and quadratic models. Within end-systolic pressure (Pes) ranges obtained under baseline conditions, ESPVR displayed only minimal curvilinearity (second-order coefficient a < 0.007) and could be accurately described by a linear model. However, nonlinearity of ESPVRs obtained over wider load ranges is suggested by negative volume axis intercepts of the linear model. Steeper ESPVR with aortic than with caval occlusion (2.28 +/- 0.22 vs 3.41 +/- 0.51 mmHg/ml, ns) could not be proven owing to the large interindividual variance of ESPVR slopes with both loading interventions. During shock the Pes range obtained by caval occlusion decreased to very low levels (from 49 +/- 2 to 34 +/- 1 mmHg), ESPVR did not adequately fit either of the two models (mean R < 0.66), and critical reduction of CPP induced negative ESPVR slope in four of ten experiments. In contrast, aortic occlusion at shock resulted in linear ESPVR (R = 0.927 +/- 0.029), Pes ranges (92 +/- 3 to 58 +/- 4 mmHg) comparable to the ones obtained by caval occlusion at control (113 +/- 5 to 73 +/- 6 mmHg), and steeper ESPVR than at control (3.41 +/- 0.51 to 7.38 +/- 1.0 mmHg/ml, P < 0.05). Interpretation of the increased ESPVR slope obtained with aortic occlusion as due to increased contractility in shock is, however, complicated by different Pes ranges. It is concluded that within Pes ranges obtained with caval or aortic occlusion in situ the ESPVR can be adequately fitted to a linear model. For assessment of the inotropic response to shock the ESPVR is of limited value because (1) caval occlusion is not suitable to generate ESPVR during shock, and (2) Pes ranges obtained with identical loading interventions differ greatly between baseline and shock and, therefore, apparent ESPVR changes are influenced by the potential nonlinearity of the ESPVR. Combining caval occlusion at baseline with aortic occlusion at shock would result in comparable Pes ranges. Interpretation of results is, however, complicated by diverging effects of the different loading interventions on the shape and slope of the ESPVR.

Animals↗

Expression of adhesion molecules on circulating PMN during hyperdynamic endotoxemia.

In a porcine model of hyperdynamic endotoxemia, we studied the numerical expression of L-selectin and beta 2-integrins on circulating polymorphonuclear leukocytes (PMN). Functional changes of beta 2-integrins were determined by the adhesion of PMN to C3-coated zymosan particles. Anesthesized pigs received a continuous infusion of Salmonella abortus-equi endotoxin (5 micrograms.kg body wt-1.h-1) for 270 min (endotoxin group; n = 7). A control group received 0.9% NaCl (n = 6). L-selectin had decreased 30 min after the induction of endotoxemia [59.1 +/- 11.9 vs. 91.6 +/- 15.5 relative fluorescence units (RFU) at baseline; P < 0.05], reaching minimal values after 150 min (23.9 +/- 3.9 RFU in endotoxin group vs. 95.2 +/- 30.4 RFU in control group; P < 0.05). PMN adhesion to C3-coated zymosan increased at 30 min (41.3 +/- 9.9% in endotoxin group vs. 2.4 +/- 1.1% in control group; P < 0.05) and remained significantly elevated thereafter. In contrast to the rapid shedding of L-selectin and functional upregulation of beta 2-integrins, the numerical expression of beta 2-integrins remained unchanged until 60 min (44.8 +/- 2.8 vs. 32.2 +/- 1.7 RFU at baseline; P < 0.05); compared with the control group, significantly elevated values were observed 150 min after the start of endotoxin (48.9 +/- 2.4 RFU in endotoxin group vs. 36.5 +/- 2.7 RFU in control group; P < 0.05). We conclude that numerical and functional expressions of beta 2-integrins are dissociated during endotoxemia. Although upregulation of beta 2-integrins might render PMN more adhesive to the vascular endothelium, the presence of activated PMN in the circulation suggests that low expression of L-selectin might impede adhesion.

Animals↗

Hypertonic saline dextran does not increase cardiac contractile function during small volume resuscitation from hemorrhagic shock in anesthetized pigs.

Small volumes of hypertonic saline dextran (10% of shed blood volume [SBV] restore cardiac output (CO) and increase arterial pressure in hemorrhagic shock. Besides rapid expansion of plasma volume, a positive inotropic effect has been proposed as an additional mechanism for the immediate onset of the cardiovascular response. This study compares the effects of 7.2% saline/10% dextran 60 (HSDex, n = 8) and normal saline (NS; n = 6) on central hemodynamics and cardiac contractility assessed by end-systolic elastance (Ees; conductance technique) and segmental preload recruitable stroke work (sPRSW; sonomicrometry). In anesthetized open chest pigs (28 +/- 1 kg, mean +/- SEM) shock was induced by blood withdrawal (40% of blood volume) to maintain mean arterial pressure (MAP) at 45 mm Hg for 75 min. Resuscitation was started by bolus infusion (2 min) of either HSDex (10% of SBV) or the identical sodium load of NS (80% of SBV); 30 min later both groups received 6% dextran (10% of SBV). Hemorrhagic shock reduced CO (-45%) and left ventricular end-diastolic volume (Ved; -70%) while Ees increased (NS:2.2 +/- 0.4 to 7.5 +/- 1.8 mm Hg/mL, P < 0.05; HSDex: 1.9 +/- 0.2 to 9.1 +/- 2.6 mm Hg/mL, P = 0.085). Within 5 min after infusion of either solution CO returned to baseline values and MAP (NS +55%, HSDex +64%) and Ved (+100%) increased. Neither HSDex nor NS increased Ees above shock levels (NS, 8.7 +/- 4.9 mm Hg/mL; HSDex, 7.3 +/- 2.6 mm Hg/mL) and no group differences occurred in other measurements of contractility (dP/dt40,sPRSW). Plasma osmolality increased to 328 +/- 3 mOsmol/kg with HSDex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Short bowl syndrome and quality of life in childhood].

From 1985 to 1988, six patients suffered from short gut syndrome due to congenital malformations. The children were aged 4-24 months at the time of the operation in which the gut was doubled in length by a Bianchi procedure. It is necessary to interview the parents about their own and the child's psychological and physical stress during the pre- and postoperative periods. Collective reactions were found which must be considered for indication and time of operation.

Adaptation, Psychological↗

Blunt and penetrating liver trauma: surgical strategies.

From our own experience with 104 patients with liver trauma treated by laparotomy we confirmed the present trends in treating blunt liver trauma, i.e. conservative therapy of minor lesions under closed observation with imaging procedures (US and CT-scan); minor local measures in superficial liver injuries when laparotomy is performed for other reasons; generous use of the Pringle maneuver in primary hemostasis; temporary or final treatment by perihepatic packing in all parenchymal fractures with predominant venous bleeding; direct suture or ligation of arterial bleeding; liver resection only for the debridement of destroyed tissue. With primary packing the patient can be transferred to an experienced center. The overall mortality is more dependent on combined lesions from polytrauma. The early and efficient hemostasis of liver trauma may, however, stabilize the border-line patient and give him a better chance. This is underlined by the experience, that isolated liver injuries have a much better prognosis except central lesions of the retrohepatic vena cava and large central hepatic veins.

Adult↗