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H C Pape

Publications and source records attributed to H C Pape.

At least 91 records · Page 5Linked to original sources
PubMed1998

Coagulatory response after femoral instrumentation after severe trauma in sheep.

OBJECTIVE: Pulmonary complications after intramedullary femoral nailing have been attributed to bone marrow fat embolization and a variety of cascade effects. We investigated whether the coagulatory response after intramedullary femoral nailing in merino sheep is altered after severe trauma. METHODS: Adult merino sheep were submitted to hemorrhagic shock (2 hours, 50 mm Hg) and unilateral lung contusion. After recovery (day 3 of the study), reamed femoral intramedullary nailing (RFN), unreamed femoral intramedullary nailing (UFN), or plate osteosynthesis of the femur (P) was performed. Pulmonary artery pressure, central venous levels of factor V, protein C, antithrombin III, and fibrinogen, were determined. At 1 and 3 days before and after femur instrumentation, pulmonary capillary permeability was assessed on the basis of the comparative albumin content in bronchoalveolar lavage fluid. RESULTS: Group RFN, n=8; group UFN, n=7; group P, n=6. A significant (p < 0.05) postoperative increase in the relative albumin content in terms of the BAL/plasma albumin ratio was measured in group RFN (day 3 preoperatively: 0.38+/-0.05 day 3 postoperatively: 0.53+/-0.06, p < 0.05 (RFN vs. P), which contrasted with group UFN (day 3 preoperatively: 0.44+/-0.09, day 3 postoperatively: 0.46+/-0.09, no significant difference). This evidence of increased pulmonary permeability occurred in association with evidence of increased activation of coagulation factors (data presented as percentage of day 3 preoperative baseline values). The data for fibrinogen (15 min postoperatively) is as follows: group RFN, 74+/-9% (p < 0.05 vs. P); group UFN, 83+/-8% (not significant); group P, 98+/-6%. The data for antithrombin III (15 min. postoperatively) is as follows: group RFN, 72+/-6% (p < 0.05 vs. P); group UFN, 79+/-8% (not significant); group P, 92+/-8% (not significant). CONCLUSION: After severe trauma, an increase of pulmonary permeability after reamed femoral nailing was associated with increased consumption of coagulation factors. After unreamed nailing, a similar trend was apparent, but this was not found to be statistically significant. These data provide support for the theory that after severe trauma, unreamed femoral nailing reduces but does not abolish pulmonary sequelae when compared with reamed femoral nailing.

Adolescent↗
PubMed1998

Two types of intrinsic oscillations in neurons of the lateral and basolateral nuclei of the amygdala.

Intracellular recordings in the guinea pig and cat basolateral amygdaloid (BL) complex maintained as slices in vitro revealed that a subpopulation of neurons (79%) in the lateral (AL) and basolateral (ABl) nuclei generated two types of slow oscillations of the membrane potential upon steady depolarization from resting potential. The cells were of a stellate or pyramidal-like shape and possessed spiny dendrites and an axon leaving the local synaptic environment, and thus presumably represented projection neurons. Similar oscillatory activity was observed in projection neurons of the cat AL nucleus recorded in vivo. Oscillatory activity with a low threshold of activation (low-threshold oscillation, LTO) appeared as rhythmic deflections (amplitudes, 2-6 mV) of the membrane potential positive to -60 mV. Fast Fourier transformation (FFT) demonstrated a range of frequencies of LTOs between 0.5 and 9 Hz, with >80% occurring at 1-3.5 Hz and an average at 2.3 +/- 1.1 Hz. LTOs were more regular after pharmacological blockade of synaptic transmission and were blocked by tetrodotoxin (TTX). Blockade of LTOs and Na+ spikes revealed a second type of oscillatory activity (high-threshold oscillation, HTO) at depolarizations beyond -40 mV, which was capable of triggering high-threshold spikes. HTOs ranged between 1 and 7.5 Hz, with >80% occurring at 2-6 Hz and an average at 5.8 +/- 1.1 Hz. HTOs vanished at a steady membrane polarization positive to -20 mV. Current versus voltage relations obtained under voltage-clamp conditions revealed two regions of negative slope conductance at -55 to -40 mV and at around -30 mV, which largely overlapped with the voltage ranges of LTOs and HTOs. TTX abolished the first region of negative slope conductance (-55 to -40 mV) and did not significantly influence the second region of negative slope conductance. Neuronal responses to maintained depolarizing current pulses consisted of an initial high-frequency discharge (up to 100 Hz), the frequency of which depended on the amplitude of the depolarizing current pulse, followed by a progressive decline ("adaptation") toward a slow-rhythmic firing pattern. The decay in firing frequency followed a double-exponential function, with time constants averaging 57 +/- 28 ms and 3.29 +/- 1.85 s, and approached steady-state frequencies at 6.3 +/- 2.9 Hz (n = 17). Slow-rhythmic firing remained at this frequency over a wide range of membrane polarization between approximately -50 and -20 mV, although individual electrogenic events changed from Na+ spikes and underlying LTOs to high-threshold spikes and underlying HTOs. Rhythmic regular firing was only interrupted at an intermediate range of membrane polarization by the occurrence of spike doublets. In conclusion, the integrative behavior of a class of neurons in the BL complex appears to be largely shaped by the slow-oscillatory properties of the membrane. While LTOs are likely to synchronize synaptic signals near firing threshold, HTOs are a major determinant for the slow steady-state firing patterns during maintained depolarizing influence. These intrinsic oscillatory mechanisms, in turn, can be assumed to promote population activity at this particular frequency, which ranges well within that of the limbic theta (Theta) rhythm and the delta (delta) waves in the electroencephalogram during slow-wave sleep.

2-Amino-5-phosphonovalerate↗
PubMed1998

Ionic mechanisms of intrinsic oscillations in neurons of the basolateral amygdaloid complex.

Ionic mechanisms underlying low-threshold (LTO) and high-threshold (HTO) oscillations occurring in a class of spiny neurons within the basolateral amygdaloid complex (see companion paper) were investigated in slice preparations of the guinea pig amygdala in vitro. LTOs were abolished through local application of tetrodotoxin (TTX, 10-20 microM) or a decrease in the extracellular sodium concentration ([Na+]o) from 153 to 26 mM, whereas HTOs were more readily elicited under these conditions. The effects of TTX and low [Na+]o were accompanied by a hyperpolarizing shift of the membrane potential by 3 +/- 1 mV and a decrease in apparent input resistance by 14 +/- 11 MOmega. LTOs were not observed during intracellular recording with QX 314 (50 microM) or Cs-acetate (2 M) containing micropipettes. At membrane potentials associated with LTO generation, voltage responses to sinusoidal current input with changing frequency between 0 and 10 Hz were characterized by a peak in the response (resonance) at 2.4 +/- 1 Hz, largely corresponding to the frequency range of the LTOs. Resonance behavior was evident as a peak in the impedance amplitude plot (ZA-plot) and a maximum in the fast Fourier transformation (FFT). Resonance and LTOs were concomitantly reduced by TTX and barium (Ba2+;2-10 mM) and were preserved during action of extracellular cesium (Cs+; 10-30 mM) or tetraethylammonium chloride (TEA; 20-50 mM), although the peak in the frequency domain tended to shift to lower values in TEA. Application of carbachol (50-200 microM) significantly reduced or blocked LTOs, whereas 4-aminopyridine (4-AP; 10 mM), iberiotoxin (Ibtx, 10 microM), and apamin (20 microM) had no effect. Slow depolarizing/repolarizing current ramps (12.5-125 pA/s) evoked HTOs as rhythmic deflections in membrane potential at either phase of the current ramp. Substitution of extracellular calcium (Ca2+) by magnesium and addition of cobalt chloride (2-4 mM) blocked HTOs but had no measurable effect on the propensity of the cells to produce LTOs. HTOs were abolished within approximately 10 min after impalement of the cells with a bis-(2-aminophenoxy)-N,N,N', N'-tetraacetic acid (BAPTA; 200 mM)-containing micropipette. Intracellular Cs+, extracellular Ba2+ (2-10 mM), or extracellular TEA (20-50 mM) induced an increase in amplitude of the rhythmic discharges and an increasingly slowed time course of repolarization at successive oscillatory events, until a steady depolarization was reached at -20 to -10 mV. Application of Ibtx (10 microM) reversibly abolished rhythmic activity during the repolarizing phase of the current ramp, whereas charybdotoxin (2-10 microM) and apamin (20 microM) had no effect. Changes in the chloride (Cl-) equilibrium potential by approximately +30 mV through intracellular recording with a KNO3 (3 M)-containing micropipette or lowering [Cl-]o from 128 to 4 mM, or blockade of Cl- conductances through niflumic acid (100 microM), did not significantly effect LTOs or HTOs. The generation of repetitive spike patterns on membrane depolarization was substantially influenced through removal of extracellular Ca2+ and associated blockade of HTOs, in that the initial high frequent discharge was abolished, frequency adaptation toward slow-rhythmic firing was delayed, and firing occurred at a more irregular pattern during strong depolarizing stimuli. It is concluded that a TTX-sensitive Na+ conductance and the M current contribute to generation of the LTOs, although their exact role in rhythmogenesisremains to be determined. HTOs seem to largely depend on a functional coupling between high-voltage-activated Ca2+ conductances, a Ca2+-activated K+ current presumably carried through BKCa channels, and additional voltage-dependent K+ conductances. In functional terms, the HTOs are important in determining spike frequency adaptation toward a slow-rhythmic firing pattern during maintained depolarizing influence.

4-Aminopyridine↗
PubMed1998

Internal fixation of multiple fractures in patients with polytrauma.

Within the last decade understanding of the pathogenetic consequences of trauma has been improved significantly. An additional reduction of lethality has been achieved that in part is related to increasing discrimination of complex injury patterns. Accordingly, additional staging in fracture management of these injuries has been developed. An overview of the current status of fracture management in polytrauma is given and certain regimens that are still controversially are discussed. The principles determined are based on the treatment experience of 4003 multiply injured patients within the past 23 years. The most important principles within the first hours after trauma represent adequate hemorrhage control. In fracture treatment the primary goal remains to perform primary stable osteosynthesis. In severe polytrauma with severe injuries to the extremities, the first decision is whether limb salvage can be achieved without risk of deterioration of the patient's condition. If this is the case, open fractures Grades III b and c usually can be stabilized primarily by unreamed intramedullary nailing or percutaneous plating. The priority pattern in multiple closed fractures is as follows: (1) tibia; (2) femur; (3) pelvis; (4) spine; and (5) upper extremity. Exceptions may ensue if severe head or thoracic trauma is present. Delayed treatment is performed for complex joint reconstruction, definitive treatment of maxillofacial injuries, and soft tissue reconstruction.

Algorithms↗
PubMed1997

Lack of regulation by intracellular Ca2+ of the hyperpolarization-activated cation current in rat thalamic neurones.

1. The regulation of the hyperpolarization-activated cation current, Ih, in thalamocortical neurones by intracellular calcium ions has been implemented in a number of mathematical models on the waxing and waning behaviour of synchronized rhythmic activity in thalamocortical circuits. In the present study, the Ca2+ dependence of Ih in thalamocortical neurones was experimentally investigated by combining Ca2+ imaging and patch-clamp techniques in the ventrobasal thalamic complex (VB) in vitro. 2. Properties of Ih were analysed before and during rhythmic stimulation of Ca2+ entry by trains of depolarizing voltage pulses. Despite a significant increase in intracellular Ca2+ concentration ([Ca2+]i) from resting levels of 74 +/- 23 nM to 251 +/- 78 nM upon rhythmic stimulation, significant differences in the voltage dependence of Ih activation did not occur (half-maximal activation at -86.4 +/- 1.3 mV vs. -85.2 +/- 2.9 mV; slope of the activation curve, 11.2 +/- 2.4 mV vs. 12.5 +/- 2.5 mV). Recording of Ih with predefined values of [Ca2+]i (13.2 nM or 10.01 microM in the patch pipette) revealed no significant differences in the activation curve or the fully activated I-V relationship of Ih. 3. In comparison, stimulation of the intracellular cyclic adenosine monophosphate (cAMP) pathway induced a significantly positive shift in Ih voltage dependence of +5.1 +/- 1.9 mV, with no alteration in the fully activated I-V relationship. 4. These data argue against a direct regulation of Ih by intracellular Ca2+, and particularly do not support a primary role of Ca(2+)-dependent modulation of the Ih channels in the waxing and waning of sleep spindle oscillations in thalamocortical neurones.

Animals↗
PubMed1997

Voltage-activated intracellular calcium transients in thalamic relay cells and interneurons.

The dynamics of intracellular calcium concentration ([Ca2+]i) following activation of low voltage-activated (LVA) and high voltage-activated (HVA) Ca2+ currents were studied in identified relay neurons and interneurons of the rat dorsal lateral geniculate nucleus (LGNd) in situ using Ca2+ imaging and patch-clamp techniques. In relay neurons, [Ca2+]i transients associated with the LVA Ca2+ current showed a fairly homogeneous somatodendritic distribution, whereas HVA transients significantly decreased to 65% of the somatic value at 60 microns dendritic distance. In interneurons, LVA transients significantly increased to 239% of the somatic value at 60 microns dendritic distance, whereas HVA transients were not significantly different in the soma and dendrites. These results indicate differences in [Ca2+]i dynamics, which may reflect a heterogeneous distribution of Ca2+ channels contributing to subcellular compartmentation in the two types of thalamic neurons.

Animals↗
PubMed1997

Properties of a Ca2+-activated K+ conductance in acutely isolated pyramidal-like neurons from the rat basolateral amygdaloid complex.

A calcium (Ca2+)-activated potassium (K+) conductance was studied in large pyramidal-like neurons acutely dissociated from the rat basolateral amygdaloid complex. Neurons were immunoreactive to anti-alpha(913-926), a sequence-directed antibody directed against the pore-forming alpha-subunit of the BK(Ca) channel, also termed slo. Whole cell current-voltage (I-V) relationships obtained on application of slow (46.7 mV/s) voltage ramps from -110 to +100 mV were N shaped positive to -30 mV. Maximal current activation occurred at +9.8 +/- 2.7 (SE) mV, with a mean current density of 404.8 +/- 25.0 pA/pF. Substitution of extracellular Ca2+ with manganese (Mn2+), or with magnesium (Mg2+) and addition of 5 mM ethyleneglycol-bis (beta-aminoethylether)-N,N,N',N'-tetraacetic acid, abolished the N-shaped I-V relationship with a reduction in maximal outward current to 15.3 +/- 2.3% of the control value. The Ca2+-sensitive K+ current component, as revealed by voltage step protocols, activated at depolarizations positive to -30 mV with a slow time course (time constant 430.7 +/- 78.6 ms). The current was reduced by 80.4 +/- 4.6% through 1 mM tetraethyammonium chloride and by 66.8 +/- 3.4% through 100 nM iberiotoxin, whereas apamin up to 1 microM had no effect. It is concluded that pyramidal-like neurons of the basolateral amygdaloid complex possess BK(Ca) channels and the corresponding macroscopic Ca2+-sensitive K+ conductance, activation of which will substantially contribute to the Ca2+-dependent regulation of electrogenic behavior in these neurons.

Amygdala↗
PubMed1996

Linear and non-linear components in the centre-surround response of X- and Y-cells in the cat lateral geniculate nucleus.

Thalamocortical projection cells of cat dorsal lateral geniculate nucleus (dLGN) have been described to exhibit different types of non-linear integration of spatial contrast in addition to the linear integration inside their classical receptive field (CRF). We analysed whether a single mechanism might generate the two harmonic distortions of a linear response elicited inside the CRF and the shift effect elicited from regions outside the CRF. Therefore, both non-linear response types were investigated with identical stimulus conditions in the same cell. A quantitative analysis revealed that both response types can be elicited in nearly all Y-cells and in at least 50% of the X-cells. With blockade of GABA(A) inhibition by bicuculline methiodide (BICU) the number of X-cells with shift effect (SE) and second harmonics (2H) increased to more than 80%. Both, SE and 2H exhibited significantly correlated variations in their response-amplitude and -latency and in the frequency of their occurrence with changes in stimulus parameters (contrast, spatial frequency, area) and during BICU application. We assume that both non-linear contrast responses, the SE and the 2H might depend on the same (most probably retinal) mechanisms. We further suggest that the principal organisation of X- and Y-cell receptive fields might be very similar and that the differing spatial contrast responses may result from the different spatial resolution of their CRF subunits.

Animals↗
PubMed1996

Attenuation of multiple organ dysfunction in a chronic sheep model by the 21-aminosteroid U74389G.

Animal studies have shown that 21-aminosteroids have beneficial effects on cell and organ functions in several acute models of traumatic, hemorrhagic, and septic shock. However, it is not known if the 21-aminosteroid U74389G has any beneficial effect on organ functions in a recently developed chronic sheep model of multiple organ dysfunction after trauma. Furthermore, it is not known whether this drug has any effect on in vivo leukocyte function in this animal model. To study this, anesthetized animals were subjected to hemorrhagic shock (2 hr at a mean arterial blood pressure of 50 mmHg) and femoral reaming at Day 0. The following 5 days, endotoxin (ET; 0.75 micrograms/kg BW) and zymosan-activated plasma (ZAP; 20 ml/animal) were given every 12 hr. During the third phase (Days 6-10), the animals were merely observed. This kind of model resulted in progressive organ dysfunction indicated by increased cardiac output, decreased systemic vascular resistance, an increase of plasma-sorbitoldehydrogenase, impaired bilirubin metabolism, and impaired renal and lung function in nontreated animals. Animals receiving U74389G (3 mg/kg BW) during resuscitation from hemorrhagic shock and each time before ET/ZAP administration showed less severe organ dysfunction. Furthermore, U74389G showed beneficial effects on lung function, although it had no effect on accumulation of leukocytes in the lung or on the chemiluminescence response of isolated leukocytes from bronchoalveolar lavage fluid. These results suggest that U74389G may be a useful therapeutic agent in the prevention of multiple organ dysfunction after hemorrhagic and traumatic shock.

Alanine Transaminase↗
PubMed1996

Fatal pulmonary embolization after reaming of the femoral medullary cavity in sclerosing osteomyelitis: a case report.

Reaming of the medullary may be used in cases of sclerosing osteomyelitis (type Garré), refractory to other methods. We report a case of fatal intraoperative complication related to this procedure. An otherwise healthy young patient died during reaming using a machine-driven reamer of the femoral medullary canal due to pulmonary bone embolism. The technique and the indication for this procedure as well as the intraoperative monitoring options are discussed.

Adult↗
PubMed1996

Interaction between low voltage-activated currents in reticular thalamic neurons in a rat model of absence epilepsy.

A transient potassium (K+) outward current (IA) contributes to the distinctive patterns of low-threshold spike firing observed in various classes of thalamic neurons through a functional interaction with a calcium (Ca2+)-mediated inward current (IT). The present study was undertaken to investigate the properties of transient K+ currents and their interaction with IT in neurons of the reticular thalamic nucleus, and to compare these properties in reticular thalamic nucleus neurons from a rat model of absence epilepsy, designated the Genetic Absence Epilepsy Rat from Strasbourg (GAERS), with those from a Non-epileptic Control strain (NEC). This comparative approach appeared to be particularly important in view of the recent finding of a selective increase in IT in reticular thalamic nucleus neurons from GAERS. Neurons were acutely isolated from the reticular thalamic nucleus through enzymatic procedures, and identified by morphological and immunocytochemical criteria. Ionic currents were analysed using whole-cell patch-clamp techniques. Transient K+ currents in reticular thalamic nucleus neurons with properties indicative of IA activated at approximately -55 mV (with half-activation at -27 and -33 mV in NEC and GAERS respectively), declined rapidly with a voltage-dependent time constant (tau = 4 ms at +45 mV), were 50% steady-state-inactivated at -81 and -86 mV in the two strains of rats respectively, and rapidly recovered from inactivation with a monoexponential time course (tau = 31 and 37 ms respectively). No significant differences in IA properties or densities were found between reticular thalamic nucleus neurons from GAERS and NEC rats. Analysis of the interaction between IA and IT indicated a shift in the balance between the two opposing membrane conductances towards the generation of a low-voltage-activated inward current in reticular thalamic nucleus neurons from GAERS compared with NEC, and a lack of IA to functionally compensate for this shift, which in turn may contribute to pathological forms of low-threshold spike firing characterizing spike-and-wave discharges.

Animals↗
PubMed1996

Queer current and pacemaker: the hyperpolarization-activated cation current in neurons.

The cation conductance activated upon hyperpolarization of the membrane beyond the resting value appears to represent an ubiquitous type of membrane channel. Our understanding of the respective membrane current, termed Ih, in neurons has matured from that of a "queer" current toward that of a highly regulated mechanism that is particularly important in determining integrative behavior near rest and providing the pacemaker depolarization during rhythmic-oscillatory activity.

Animals↗
PubMed1996

Aprotinin prevents the development of the trauma-induced multiple organ failure in a chronic sheep model.

Trauma-induced multiple organ failure in sheep was prevented by aprotinin therapy. Multiple organ failure was induced in 16 female merino sheep by initial haemorrhagic shock and intramedullary femoral nailing (day 0), and 12 hourly injections of 0.75 micrograms/kg Escherichia coli endotoxin +0.7 ml/kg zymosan-activated plasma (days 1-5). In addition, the aprotinin group (n = 6) received simultaneous injections of 5 mg/kg (35 695 KIU/kg) aprotinin, whereas ten animals did not receive aprotinin and served as the control group (n = 10). Organ functions were monitored for a total of 11 days by measuring haemodynamic, cardio-respiratory and biochemical quantities of blood, urine and epithelial lining fluid. During the subsequent eleven day period, aprotinin induced a significant (p < 0.05) reduction of the pathological changes (development of multiple organ failure) seen in the control group. Thus, aprotinin prevented an alteration of cardiac function (cardiac index for control/aprotinin groups at day 1: 6.5/6.2, and at day 10: 10.47/7.0 1/min x m2), an impairment of lung function (mean pulmonary arterial pressure at day 1: 2.26/1.86, and at day 10: 3.83/2.13 kPa; epithelial lining fluid/plasma ratio of albumin concentrations as a direct marker of lung capillary permeability damage at day 0: 0.18/0.16, and at day 10: 0.45/0.15), a deterioration of liver function (plasma sorbitol dehydrogenase at day 0: 7.9/7.6, and at day 10: 29.6/7.4 U/1), but not of renal function (creatinine clearance at day 1: 91.4/66.1, and at day 10: 53.1/59.2 ml/min). Urinary aprotinin excretion increased up to day 3, then decreased rapidly despite further aprotinin administration. As a non-specific marker of cell damage, plasma lactate dehydrogenase indicated an aprotinin-induced organ protection (day 0: 501/409, and at day 10: 719/329 U/1). The neutrophil count and the measured chemiluminescence of neutrophils from the blood and epithelial lining fluid showed that aprotinin reduced the in vivo neutrophil activation, the alveolar neutrophil invasion, the production of inflammatory mediators, and the production of reactive oxygen metabolites during the passage of the capillary-interstitial-alveolar space by neutrophils.

Animals↗
PubMed1996

[Intestinal cytokine liberation after intestinal ischemia in the rat--studies in the Ussing chamber system].

UNLABELLED: Intestinal ischemia, frequently found in clinical states such as aortic bypass operations or hemorrhagic shock, is associated with loss of gut barrier function. Subsequent translocation of indigenous bacteria and endotoxin have been implicated as a major contributor to a systemic immuno-inflammatory response, which finally leads to multiple organ failure. There is increasing evidence that intestinal injury can result in the gut becoming a cytokine generating organ. This study was designed to show direct evidence of the gut as a major source of proinflammatory cytokines after intestinal ischemia and to further relate this cytokine response to the extent of intestinal ischemia/reperfusion. Additionally the potential role of the altered intestinal barrier function after intestinal ischemia for this cytokine response was investigated. METHODS: Rats were subjected to occlusion of the superior mesenteric artery for 45 min. (SMAO45), 75 min. (SMAO75), SMAO for 45 min. and 30 min. reperfusion (SMAO45/30), or sham SMAO, and then killed. Mucosal membranes from the terminal ileum were mounted in a Ussing chamber. E. coli C25 was added to the mucosal side of the stripped gut epithelium in half of the chambers. TNF and IL-6 levels on mucosal and serosal side of the stripped gut epithelium were assessed serially over 3 hrs. Gut barrier function was assessed by in vitro bacterial translocation (BT) and the transepithelial resistance (TER) of the mucosal membrane. RESULTS: The TNF response was greatest in the SMAO75 group, the IL-6 response in the SMAO75 and SMAO45/30 groups. In the absence of E. coli C25. IL-6 was produced to a greater extent on the serosal side, while addition of bacteria led to a significantly increased TNF/IL-6 response at the mucosal side of the stripped gut epithelium. BT was increased in SMAO75 and SMAO45/30 rats. Baseline TER was decreased in all experimental compared to sham SMAO groups. Although gut barrier function was impaired after intestinal ischemia/reperfusion there was no correlation between intestinal cytokine response and gut permeability. CONCLUSIONS: The gut becomes a cytokine liberating organ alter intestinal ischemia/reperfusion. This cytokine response is affected by certain conditions, but is not directly related to an impaired intestinal barrier function.

Animals↗
PubMed1995

Electrophysiological and pharmacological properties of interneurons in the cat dorsal lateral geniculate nucleus.

We investigated the electrophysiological and pharmacological properties of morphologically identified and putative interneurons within laminae A and A1 of the cat dorsal lateral geniculate nucleus maintained in vitro. These intralaminar interneurons possess unique electrophysiological characteristics, including (1) action potentials of a short duration (average width at half amplitude of 0.34 ms). (2) the ability to generate high-frequency trains of action potentials exceeding 500 Hz, without strong spike frequency adaptation, and (3) a low-threshold regenerative response with variable magnitude of expression, ranging from a subthreshold depolarization towards the generation of one to several action potentials in different cells. The low-threshold regenerative depolarization following a hyperpolarizing current pulse was increased in size by application of 4-aminopyridine, was reduced by nickel, and was not influenced by extracellular cesium. These findings indicate that this event is mediated by an underlying Ca(2+)-dependent mechanism, such as a low-threshold Ca(2+) current, that is regulated by the activation of opposing transient K+ currents. Every interneuron tested responded to glutamate, kainate, quisqualate, or N-methyl-D-aspartate with depolarization and action potential discharge. In contrast, we did not observe a postsynaptic response to activation of the metabotropic receptors with 1S,3R-(+/-)-1-amino-cyclopentane-1,3-dicarboxylate. Application of gamma-amino-butyric acid (GABA) strongly inhibited spike firing through a biphasic hyperpolarization and increase in membrane conductance, a response that reversed close to the presumed chloride equilibrium potential and was imitated by the GABAA receptor agonist muscimol. The GABAB receptor agonist baclofen evoked only a weak membrane hyperpolarization from rest and suppression of spontaneous spike activity. Application of acetylcholine, or the muscarinic agonist acetyl-beta-methylcholine, inhibited spontaneous action potential activity through hyperpolarization of the membrane potential, presumably resulting from an increase in membrane potassium conductance. In contrast, application of serotonin only slightly facilitated tonic activity in a subpopulation of interneurons, histamine induced a small slow depolarization apparently through activation of presynaptic excitatory pathways, and noradrenaline and adenosine had no detectable effect on the spontaneous firing or resting potential of interneurons. We suggest that intralaminar interneurons may function in a relatively linear manner to transform retinal and cortical inputs into a local field of inhibition in the dorsal lateral geniculate and that the excitability of these neurons is largely controlled by retinal, cortical, GABAergic, and cholinergic (brainstem) afferents.

Action Potentials↗
PubMed1995

Treatment results of patients with multiple trauma: an analysis of 3406 cases treated between 1972 and 1991 at a German Level I Trauma Center.

The quality and progress of treatment for 3406 multiple trauma patients was reviewed retrospectively. Two periods (1972 to 1981, the first decade, and 1982 to 1991, the second decade) were compared. Sixty-nine percent of patients with multiple trauma had cerebral injuries, 62% thoracic trauma, and 86% fractures (40% open fractures). Concerning injury combinations, there was an increase of head/extremity injuries and thoracic/extremity injuries, whereas all combinations with abdominal injuries decreased. The relation between severity of injury as well as number of injured body regions and the mortality rate was significant. In the second decade prehospital care became more aggressive with an increase in use of intravenous fluid resuscitation (from 80% to 98%), intubation (from 84% to 91%), and chest tube insertion (from 37% to 76%). Rescue times were progressively shortened. For initial clinical diagnosis of massive abdominal hemorrhage, ultrasound (89%) nearly replaced peritoneal lavage (10%) and led to earlier surgical approach. For diagnosis of head injury, CT scan was used more frequently. Primary stabilization of long bone fractures, especially of the lower limb, is recommended. Concerning complications, the change in volume therapy helped to nearly eliminate acute renal failure (from 8.4% to 3.7%), the modification of respirator treatment led to a decrease of pulmonary insufficiency (ARDS; from 18.2% to 12.0%), whereas the rate of multiple organ failure increased. The mortality rate declined from 37% in the first decade to 22% in the second decade. The incidence of lethal multiple organ failure increased from 13.8% in the first decade to 18.6% in the second decade, whereas the mortality rate of ARDS decreased from 32.4% to 15.9%. Further reduction of incidents of death is only possible with causal therapy of posttraumatic organ failure immediately after injury.

Accidents, Traffic↗