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Biomedical subjects

K van Ackern

Publications and source records attributed to K van Ackern.

At least 37 records · Page 2Linked to original sources
PubMed1998

Lipid mediators in inflammatory disorders.

During the past few decades, intensive collaborative research in the fields of chronic and acute inflammatory disorders has resulted in a better understanding of the pathophysiology and diagnosis of these diseases. Modern therapeutic approaches are still not satisfactory and shock, sepsis and multiple organ failure remain the great challenge in intensive care medicine. However, the treatment of inflammatory diseases like rheumatoid arthritis, ulcerative colitis or psoriasis also represents an unresolved problem. Many factors contribute to the complex course of inflammatory reactions. Microbiological, immunological and toxic agents can initiate the inflammatory response by activating a variety of humoral and cellular mediators. In the early phase of inflammation, excessive amounts of interleukins and lipid-mediators are released and play a crucial role in the pathogenesis of organ dysfunction. Arachidonic acid (AA), the mother substance of the pro-inflammatory eicosanoids, is released from membrane phospholipids in the course of inflammatory activation and is metabolised to prostaglandins and leukotrienes. Various strategies have been evaluated to control the excessive production of lipid mediators on different levels of biochemical pathways, such as inhibition of phospholipase A2, the trigger enzyme for release of AA, blockade of cyclooxygenase and lipoxygenase pathways and the development of receptor antagonists against platelet activating factor and leukotrienes. Some of these agents exert protective effects in different inflammatory disorders such as septic organ failure, rheumatoid arthritis or asthma, whereas others fail to do so. Encouraging results have been obtained by dietary supplementation with long chain omega-3 fatty acids like eicosapentaenoic acid (EPA). In states of inflammation, EPA is released to compete with AA for enzymatic metabolism inducing the production of less inflammatory and chemotactic derivatives.

Animals↗
PubMed1997

Isovolemic hemodilution with a bovine hemoglobin-based oxygen carrier: effects on hemodynamics and oxygen transport in comparison with a nonoxygen-carrying volume substitute.

OBJECTIVE: Stroma-free hemoglobin solutions have been shown to maintain oxygen transport in the absence of red blood cells. This study was designed to investigate the impact of such solutions on hemodynamics and oxygen transport during progressive isovolemic hemodilution within and even beyond a clinically relevant range of hematocrit values. DESIGN: Prospective, randomized experimental study comparing a bovine hemoglobin-based oxygen carrier (bHBOC) with a conventional nonoxygen-carrying volume substitute (hydroxyethyl starch [HES]). SETTING: Animal laboratory of a university cardiovascular research center. PARTICIPANTS: Splenectomized full-grown foxhounds, anesthetized with pentobarbital and piritramid. INTERVENTIONS: Twelve splenectomized foxhounds were anesthetized and mechanically ventilated. Catheters were placed for hemodilution, arterial and venous blood sampling, and hemodynamic measurements. The baseline hematocrit (Hct) value was adjusted to 0.35 by an initial isovolemic exchange of blood for identical volumes of HES (10% HES 200/0.5). Thereafter, the hematocrit was progressively reduced by isovolemic hemodilution using either HES (n = 6) or bHBOC (n = 6). MEASUREMENTS AND MAIN RESULTS: Hemodynamic and laboratory parameters of oxygen transport were measured at Hct values of 0.30, 0.20, and 0.10. Oxygen content was directly estimated using an oxygen-specific fuel cell. Arterial oxygen content at an Hct value of 0.10 nearly doubled in bHBOC-treated dogs as compared with HES-diluted animals (p < 0.001). This gain in oxygen-carrying capacity was completely negated by a decrease in cardiac output (-32% Hct 0.35 v Hct 0.30; p < 0.001) immediately on the first infusion of bovine hemoglobin. Thus, oxygen delivery was significantly lower as compared with HES-treated dogs at Hct 0.30 and 0.20, but remained stable at a level of 60% of baseline until Hct was 0.10. Both the pulmonary and the systemic vascular resistances increased. CONCLUSIONS: Isovolemic hemodilution with bHBOC did not improve systemic oxygen delivery in comparison with a nonoxygen-carrying diluent (HES) in a range of Hct values down to 0.10. Unchanged mixed venous lactate levels and stable oxygen consumption indicate sufficiently maintained oxygen delivery. This might become advantageous in patients who are unable to adequately increase cardiac output during hemodilution.

Animals↗
PubMed1997

Microvascular oxygen delivery and interstitial oxygenation during sodium pentobarbital anesthesia.

BACKGROUND: Anesthesia may represent a considerable bias in experimental medicine, particularly in conditions of stress (such as hemorrhage). Sodium pentobarbital (PB), widely used for cardiovascular investigations, may impair oxygen delivery by hemodynamic and respiratory depression. The critical issue, however, is whether the microcirculation can still maintain tissue oxygenation during anesthesia. To answer this question, the authors studied the effect of PB anesthesia on subcutaneous microvascular oxygen delivery and interstitial oxygenation in Syrian golden hamsters. METHODS: Sodium pentobarbital anesthesia was induced by intravenous injection (30 mg/kg body weight) and maintained by a 15-min infusion (2 mg.kg-1.min-1), with animals breathing spontaneously (PB-S) or ventilated with air (PB-V). Systemic parameters evaluated were mean arterial pressure (MAP), heart rate, cardiac index (CI), arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2), base excess, and pH. Microvascular and interstitial oxygen tension (PO2), vessel diameter, red blood cell velocity (vRBC), and blood flow (Qb) were measured in a dorsal skinfold preparation. Microcirculatory PO2 values were determined by phosphorescence decay. RESULTS: Sodium pentobarbital anesthesia significantly decreased CI, MAP, vRBC, and Qb. During PB infusion, PaO2 values were 56 +/- 12.8 mmHg (PB-S) and 115.9 +/- 14.6 mmHg (PB-V) compared with 69.4 +/- 18.2 mmHg and 61.4 +/- 12.6 mmHg at baseline. However, microvascular PO2 was reduced by 25-55% in both groups, resulting in an interstitial PO2 decrease from 23.9 +/- 5.6 mmHg (control) to 13.1 +/- 9.1 mmHg (PB-S) and 15.2 +/- 7 mmHg (PB-V). Microcirculatory PO2 values were restored 30 min after PB infusion, even though hemodynamic depression and a light anesthetic plane were maintained. CONCLUSIONS: Sodium pentobarbital anesthesia caused impairment of microvascular oxygen delivery and interstitial oxygenation, effects that were not prevented by mechanical ventilation. Although these effects were restricted to deep anesthetic planes, prolonged hemodynamic depression suggests that caution is warranted when using PB as an anesthetic in cardiovascular investigations.

Anesthesia↗
PubMed1997

Impaired bacterial clearance after activation of the complement and coagulation systems.

The aim of this study was to investigate the influence of the activation of the complement and coagulation systems on bacterial clearance and killing capacity of the reticuloendothelial system in rabbits. To enable quantification of the clearance process, defined numbers of exogenous Escherichia coli (1.3 x 10(8) colony-forming units) were injected intravenously, after complement activation with inulin-activated rabbit serum (n = 6), after complete defibrination with the snake toxin ancrod (n = 6), and in sham-operated animals (controls, n = 6). During the following 180 min observation period, parameters monitored were arterial pressure, fibrinogen, blood gases, and bacterial counts in blood and tissue samples of liver, kidney, spleen, and lung. Defibrination produced a significant delay in blood clearance (p < .05) compared with controls, coupled with up to four times higher bacterial counts in organ homogenates. Complement activation did not affect bacterial elimination kinetics, but was associated with accumulation of E. coli in lung and kidney (up to 100-fold of control values, p < .001). The impaired bacterial clearance associated with increased organ colonization after activation of the complement and coagulation systems reflect reticuloendothelial system dysfunction, thus pointing toward a weaker resistance against bacterial infection.

Animals↗
PubMed1997

Perioperative myocardial ischemia is associated with a prolonged cardiac vagal dysfunction after non-cardiac surgery.

BACKGROUND: Heart rate variability (HRV), a measure of cardiac autonomic balance seems to be linked to coronary artery disease (CAD). Impaired vagal input facilitates the generation of fatal arrhythmias and has a great impact on morbidity and mortality. The purpose of this study was to determine the relationship between perioperative HRV and the incidence of silent myocardial ischemia (SMI) and ventricular dysrhythmias in CAD-patients undergoing non-cardiac surgery. METHODS: 31 patients were studied by continuous Holter electrocardiography preoperatively and again on the evening before surgery until postoperative day 3. Three frequency and one time domain measures of HRV (TP, 0.01-1.00 Hz: total power of the amplitude spectral plot; LF, 0.04-0.15 Hz: low-frequency power; HF, 0.15-0.40 Hz: high-frequency power; MeanRR: mean of all coupling RR-intervals between normal beats) as well as ischemic events and ventricular couplets and runs were computed. RESULTS: Depending on the presence of ischemic episodes, each patient was assigned to either the no SMI-group (13 pts) or the SMI-group (18 pts). MeanRR, TP and LF significantly declined in both groups over time. The parasympathetically dominated index HF, however, only decreased in the SMI-group. Normalized HF power (HF/TP) even increased in the no SMI-group resulting in a postoperative decrease in LF/HF ratio. TP, LF, and HF inversely correlated with ischemia parameters whereas HF/TP and HF/LF ratio correlated with the number of ventricular couplets. Incidence and severity of SMI significantly increased after surgery. CONCLUSION: Postoperatively, a prolonged vagal withdrawal occurred in CAD-patients exhibiting perioperative SMI. Whether the increased incidence of SMI after surgery in conjunction with the observed parasympathetic derangement contributes to adverse cardiac outcome still has to be determined.

Adult↗
PubMed1996

Regional heterogeneity of cerebral blood flow response to graded volume-controlled hemorrhage.

OBJECTIVE: Of the animal models of human hemorrhagic shock, the volume-controlled hemorrhage model appears to come closer to the clinical situation than the commonly used pressure-controlled model, since the volume-controlled model allows regulatory adjustment of blood pressure. The effects of volume-controlled hemorrhage on local cerebral blood flow (LCBF) of conscious animals are not known. The present study investigates specific reaction patterns of LCBF in comparison to mean cerebral blood flow (CBF) during graded volume-controlled hemorrhagic shock in conscious rats. METHODS: Conscious, spontaneously breathing, and minimally restrained rats were subjected to different degrees of volume-controlled hemorrhage (taking either 25, 30, 35, or 40 ml arterial blood/kg body weight (b.w.). Thirty minutes after the completion of blood taking, LCBF was determined during hemorrhagic hypovolemia using the autoradiographic iodo (14C) antipyrine method. A group of untreated rats (no hemorrhage) served as controls. LCBF was determined in 34 defined brain structures and mean CBF was calculated. RESULTS: During less severe hemorrhage (25 and 30 ml/kg b.w.) mean CBF was significantly higher than in the control group (+19% and +25%). During severe hemorrhage (35 and 40 ml/kg b.w.) mean CBF remained unchanged compared to the control values, although significant increases in LCBF could be detected in many of the brain structures analyzed (maximum +44%). The mean coefficient of variation of CBF was increased, indicating a larger heterogeneity of LCBF values at shed blood volumes of 35 and 40 ml/kg b.w. CONCLUSIONS: A comprehensive and novel description of the local distribution of CBF during graded volume-controlled hemorrhage in conscious rats shows unexpected increases in LCBF and mean CBF. This "hypovolemic cerebral hyperemia" might be caused by endogenous hemodilution, thus maintaining the blood supply to the brain during hypovolemic shock.

Animals↗
PubMed1996

Impairment of bacterial clearance induced by norepinephrine infusion in rabbits.

OBJECTIVE: Purpose of the study was to investigate the potential influence of norepinephrine (NE) on immune functions in terms of systemic and organ-specific bacterial clearance in rabbits. DESIGN: To enable quantification of the clearance process, defined numbers of exogenous Escherichia coli (1.3 x 10(8) CFU) were injected intravenously 60 min after starting the NE infusion at a low dose (1 microgram/kg per min, n = 6), causing an increase (30 mmHg) in mean arterial pressure without affecting the oxygen uptake, and at a higher dose (7.5 micrograms/kg per min, n = 6), resulting in a marked decrease (20%) in oxygen uptake, after infusion of NaCl solution (control, n = 6). In additional experiments (n = 6) NE (1 microgram/kg per min) was tested in endotoxemia induced by simultaneous infusion of endotoxin (40 micrograms/kg per h). Parameters monitored were arterial pressure, oxygen uptake, and rates of bacterial elimination from the blood. At 180 min after E. coli injection, the animals were sacrificed, and tissue samples of liver, kidney, spleen, and lung were collected for bacterial counts. RESULTS: NE infusion resulted in a dose-dependent prolonged elimination of the injected E. coli from the blood and in significantly higher (p < 0.05) numbers of CFU in liver and lung compared to the controls. Significant impairment of bacterial clearance was found after shock-producing endotoxemia, whereas simultaneous infusion of NE and endotoxin caused only a slightly delayed blood clearance of the injected bacteria. CONCLUSION: NE dose dependently affected bacterial clearance, which might be due to ischemia-derived hypoxic impairment of the phagocytosis and lysis function of the reticuloendothelial system, whereas NE improved elimination of bacteria in a state of endotoxic shock.

Animals↗
PubMed1996

[New airbag-associated injuries in traffic accidents].

Experimental studies have shown that in traffic accidents with frontal impact the new airbag system can significantly reduce the incidence of severe injuries and fatal outcome. The question of whether the airbag itself induces specific patterns of injury needs further investigation. Two cases of traffic accidents with airbag protection are presented here. The first case report clearly shows the life-saving and injury-reducing effect of the airbag system in a traffic accident with frontal impact at 100 km/h. In the second case only minor injuries of the face were diagnosed initially. Hemodynamic instability occurred after 3 h of hospitalization due to rupture of the azygos vein. Analysis of the presented cases shows that, besides the well-known benefits, there are certain injury patterns that seem to be related to the use of airbags. These have not been described before. It is concluded that patients who were involved in traffic accidents with airbag deployment have to be hospitalized and followed up carefully over time, even though they are initially stable, as potentially fatal sequelae of deceleration trauma can occur later. In our opinion it is not possible to estimate the severity of airbag-associated injuries with conventional methods.

Accidents, Traffic↗
PubMed1996

Coupling between local cerebral blood flow and metabolism after hypertonic/hyperoncotic fluid resuscitation from hemorrhage in conscious rats.

The effects of small volume hypertonic/hyperoncotic fluid resuscitation from hemorrhage on brain metabolism and blood flow were evaluated by autoradiographic techniques with high spatial resolution. The data were compared to fluid resuscitation with a volume equal to shed blood of isotonic 6% hydroxyethyl starch solution (HES) and a control group without hemorrhage and fluid resuscitation (n = 6 in each group). In conscious rats, volume-controlled hemorrhage for 30 min (30 mL/kg body weight, resulting in a blood loss of approximately 50% of the circulating blood volume) was followed by intravenous infusion of a hypertonic/hyperoncotic saline hydroxyethyl starch solution (HTHO; 7.5% saline/10% hydroxyethyl starch, 4.0 mL/kg body weight). Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures 2 h after fluid resuscitation by means of the quantitative autoradiographic iodo [14C]antipyrine and 2-[14C]-deoxy-D-glucose methods. Compared to the untreated control group, LCBF increased significantly in all brain regions analyzed after fluid resuscitation with HTHO (mean, +63%) or HES (mean, +56%). The increases in LCBF after fluid resuscitation were sufficient to restore cerebral oxygen delivery to the level calculated for the untreated control group. LCGU was unchanged after fluid resuscitation. The close relationship between LCGU and LCBF observed in the control group (r = 0.95) was preserved after hemorrhage and fluid resuscitation with HTHO (r = 0.97) and HES (r = 0.96), although the LCBF-to-LCGU ratio was reset to a higher level (1.5 mL/mumol in the control group and 2.7 mL/mumol after fluid resuscitation with HTHO and HES, P < 0.05). We conclude that the increase in LCBF compensates for the reduction of arterial oxygen content to maintain cerebral oxygen delivery. Therefore, "small volume resuscitation" appears to be as effective as resuscitation with large volumes of isotonic HES in meeting the circulatory and metabolic demands of the brain tissue within the first 2 h after fluid resuscitation from hemorrhage.

Animals↗
PubMed1996

Alteration of n-3 fatty acid composition in lung tissue after short-term infusion of fish oil emulsion attenuates inflammatory vascular reaction.

OBJECTIVES: To investigate whether modulation of the fatty acid profile can be achieved by the short-term infusion of a fish oil emulsion which may attenuate the pulmonary response to inflammatory stimulation. Changes of fatty acid pattern in-lung tissue and perfusate were analyzed and correlated with physiologic data after a 3-hr infusion of fish oil in comparison with a soybean oil preparation. DESIGN: Prospective, randomized, controlled trial. SETTING: Experimental laboratory in a university teaching hospital. SUBJECTS: Forty standard breed rabbits of either gender. INTERVENTIONS: Isolated lungs from anesthetized rabbits were ventilated and recirculation-perfused (200 mL/min) with 200 mL of cell-free buffer solution to which either 2 mL of saline (control, n = 6), 2 mL of a 10% soybean oil preparation (n = 6), or 2 mL of a 10% fish oil emulsion (n = 6) were added. Samples of perfusate and lung tissue were collected for analysis of fatty acid composition. Tissue and perfusate fatty acid composition were analyzed by capillary gas chromatography. To study metabolic alterations in states of inflammatory stimulation, lungs of each group were stimulated with small doses of the calcium ionophore, A23187 (10(-8) M), during the 180-min lipid perfusion period and again after washing out the lipids by exchanging the perfusion fluid. Pulmonary arterial pressure and lung weight gain were monitored, and eicosanoids were analyzed in the perfusate. MEASUREMENTS AND MAIN RESULTS: Free eicosapentaenoic acids increased several-fold in lung tissue and perfusate during a 3-hr infusion with fish oil. The intravenously administered n-3 fatty acids were rapidly hydrolyzed, as indicated by the appearance of substantial quantities of eicosapentaenoic acid in the perfusate free fatty acid fraction. This increase of perfusion levels of eicosapentaenoic acid was paralleled by an attenuated pressure increase and edema formation due to calcium ionophore challenge and an altered eicosanoid spectrum determined in the perfusate compared with soybean oil-treated lungs. CONCLUSION: Short-term n-3 lipid application (fish oil emulsion) exerts anti-inflammatory effects on lung vasculature, which may be due to the metabolism of eicosapentaenoic acid resulting in the generation of less potent inflammatory eicosanoids.

Animals↗
PubMed1996

Effects of N-acetylcysteine on bacterial clearance.

The aim of this study was to investigate whether the oxygen radical scavenger N-acetylcysteine (N-AC) impairs bacterial clearance, thus predisposing the host to increased risk of disease. Blood clearance of Escherichia coli and organ colonization were investigated in anaesthetized rabbits after pretreatment with N-AC (250 mg kg-1 body weight, n = 16) and in sham-operated animals (n = 12). To enable quantification of the clearance process, defined numbers of exogenous E. coli [1.3 x 108 colony-forming units (CFUs)] were injected intravenously. Parameters monitored were kinetics of bacterial elimination from the blood, and polymorphonuclear leucocyte (PMN) oxidative burst activity. Samples of liver, kidney, spleen and lung were collected for bacterial counts. Compared with controls, pretreatment with N-AC resulted in delayed bacterial elimination from blood and higher organ colonization with increased numbers of E. coli in liver, lung and kidney (P < 0.05). N-AC treatment was associated with a suppressed PMN oxidative burst activity. Impaired bacterial clearance and enhanced organ colonization in N-AC-treated animals correlated with reduced oxidative burst activity, suggesting impaired granulocyte-dependent bacterial killing due to N-AC application.

Acetylcysteine↗
PubMed1995

Effect of cyclooxygenase inhibition in a canine model of unilateral pulmonary occlusion and reperfusion.

OBJECTIVE: To assess the effects of the cyclooxygenase inhibitor diclofenac in a canine model of pulmonary occlusion and reperfusion of the left lower lobe (LLL). DESIGN: Twelve adult beagle dogs (13-17 kg) were randomly assigned to a control group (n = 6) and a diclofenac-treated group (n = 6). Animals in the treatment group received 20 mg diclofenac sodium/kg as a single dose both before the experiment and at the end of surgical preparation; six animals served as controls. INTERVENTIONS: In the anesthetized animals, the left upper and middle lobes were resected. Circulation and ventilation of the LLL were selectively blocked by clamping. Complete occlusion of the LLL (30 min) was followed by periods of selective reperfusion (10 min, RP) and combined reperfusion and reventilation (120 min, RP/RV). MEASUREMENTS AND RESULTS: Reperfusion of the LLL resulted in a significant increase in pulmonary arterial pressure (Ppa) in the early RP/RV period as compared to baseline values (25.3 +/- 4.7 vs 15.8 +/- 1.9 mmHg, p < 0.05, paired t-test). This increase was significantly inhibited in the diclofenac-treated animals (17.0 +/- 2.0 mmHg, p < 0.01 vs controls, ANOVA). Gravimetrically determined extravascular lung water (EVLW) showed no significant difference in the continuously ventilated lobes of the right lung between diclofenac-treated animals (3.8 ml/g dry weight) and controls (3.9 +/- 0.9 ml/g dry weight) at the end of the experiment. EVLW, however, increased significantly in the LLL of control animals after 2 h of combined reperfusion and reventilation, whereas this increase was significantly inhibited in the diclofenac-treated animals (4.5 +/- 0.7 ml/g dry weight in the diclofenac group vs 6.5 +/- 1.3 ml/g dry weight in the control group, p < 0.05). CONCLUSIONS: Diclofenac inhibits the increase in both pulmonary arterial pressure and EVLW during reperfusion and reventilation of LLL. Thus, these changes appear to be mediated by cyclooxygenase metabolites.

Analysis of Variance↗
PubMed1995

Influence of B2 receptor antagonists on bradykinin-induced vasodilation and edema formation in isolated rabbit hindlimbs.

In search of new possibilities to prevent acute inflammatory vascular reaction, we examined the effect of two selective B2 receptor antagonists, CP 0127 ([Bissuccimidohexane (L-Cys6)-1] and HOE 140 (D-Arg[Hyp3, Thi5, D-Tic7, Oic8]BK), on changes in perfusion pressure and on edema formation caused by bradykinin (BK) in the isolated perfused rabbit hindlimbs. CP 0127 and HOE 140 were added to the perfusion fluid 2 min prior to the first BK-administration (5 x 10(-9) mol/l). A second BK-stimulation was performed after 30 minutes. The antagonists were tested in groups of 6 experiments each at concentrations of 10(-6) mol/l, 5 x 10(-9) mol/l and 10(-10) mol/l. CP 0127 was also tested in a concentration of 10(-8) mol/l. The application of BK resulted in an acute decrease of the mean arterial pressure and in a continual edema formation, reflected by an increase of organ weight (controls, n = 6). Pretreatment with CP 0127 as well as with HOE 140 attenuated dose-dependently the BK-induced vasodilation (p < 0.005) and edema formation. The current results indicate that CP 0127 and HOE 140 are able to reduce BK-induced effects on vascular tone and edema formation.

Amino Acid Sequence↗
PubMed1994

[Randomized use of an active compression-decompression technique within the scope of preclinical resuscitation].

INTRODUCTION: Despite its worldwide propagation, external chest compression is of limited efficacy. Recently a new method of cardiac resuscitation, active compression-decompression (ACD), was presented. In animals and a small series of patients resuscitated within the hospital ACD proved to augment blood flow during cardiac resuscitation as a result of greater intrathoracic pressure gradients. AIM OF THE STUDY: We investigated whether ACD does provide superior survival in patients suffering from out-of-hospital cardiac arrest. METHODS: Doctors and paramedics of the mobile intensive care unit at Mannheim University Hospital were trained in the new method. 56 patients were randomly assigned to either standard chest compression according to recommendations of the American Heart Association, AHA (Group I, 30 patients) or to ACD (Group II, 26 patients). ACD was performed by use of a hand-held suction device (CardioPump, Ambu Int.). Compression (30-50 kp) and decompression (10-15 kp) were alternately applied to the patients' chest with a frequency of 80/min. Duration of compression was 50% of the cycle. In both groups advanced life support was performed according to AHA standards. RESULTS: In Group I, 40% of the patients could be resuscitated; and 13.3% were discharged from hospital. In Group II, 38.5% of the patients regained spontaneous circulation, and 11.5% of the patients were discharged. (Group I vs. Group II: n.s.). One patient in each group survived with a severe neurological deficit. ACD caused greater physical efforts than standard chest compression. Furthermore ACD was difficult to perform in patients with ventricular fibrillation once electrode gel had been used. ACD was not feasible in five patients because of large breast (four women) and kyphoscoliosis (one patient). The rate of serious complications was lower in Group II. CONCLUSIONS: Methods to verify the efficacy of ACD in dummy training should be developed. Paramedics performing ACD should relieve each other every 5 minutes. In patients resuscitated by ACD self-adhesive defibrillation paddles instead of electrode gel should be used. Modifications in the design of the CardioPump are desirable to enhance the efficacy of ACD. With regard to future multicentre trials all paramedics should be skilled in the new technique to reach more patients in a shorter period of time.

Adult↗
PubMed1994

Autoradiographic determination of regional cerebral blood flow and metabolism in conscious rats after fluid resuscitation from haemorrhage with a haemoglobin-based oxygen carrier.

The effects of resuscitation fluids on the brain have been investigated in previous studies by global measurements of cerebral blood flow and metabolism. In this study we have examined the effects of a novel haemoglobin-based oxygen carrier on local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) after resuscitation from a volume-controlled haemorrhage of 30 min (3.0 ml/100 g body weight) with ultrapurified, polymerized, bovine haemoglobin (UPBHB). LCBF and LCGU were measured in 34 brain structures of conscious rats 2 h after resuscitation using quantitative iodo(14C)antipyrine and 2-(14C)-deoxy-D-glucose methods. The data were compared with a control group without haemorrhage and fluid resuscitation. In the haemorrhage group, LCBF increased after resuscitation by 12-56% in the different brain structures (mean 36%). LCGU changed less (0 to +18%, mean +9%). In the control group there was a close relationship between LCGU and LCBF (r = 0.95). After fluid resuscitation the relationship was preserved (r = 0.95), although it was reset at a higher ratio of LCBF to LCGU (P < 0.05). We conclude that fluid resuscitation of a 30 min volume-controlled haemorrhage using the haemoglobin-based oxygen carrier, UPBHB, induced a moderate degree of heterogeneity in the resulting changes of LCGU and LCBF. Local disturbances of cerebral blood flow or metabolism were not observed.

Animals↗
PubMed1994

Effects of stroma-free hemoglobin solutions on pulmonary vascular resistance and mediator release in the isolated perfused rabbit lung.

The aim of this study was to evaluate the effect of an ultrapure bovine stroma-free hemoglobin (SFH) on pulmonary vascular resistance and mediator release and to analyze potential mechanisms of action in the isolated perfused rabbit lung model. Repetitive bolus applications of small amounts of bovine SFH were examined which resulted in a reproducible acute increase of pulmonary vascular resistance of approx. 9 mmHg (controls, n = 6). It was tested whether the platelet-activating factor (PAF) antagonist WEB 2086 (50 microM; n = 6), the cyclooxygenase blocker diclofenac (10 micrograms/ml; n = 6), the iron-chelating agent deferoxamine (500 micrograms/ml, n = 6) and the radical scavenger catalase (5000 U/ml; n = 6) exert a protective effect on vasoconstrictor response to SFH. The pressure increase was completely suppressed in the lungs pretreated with WEB 2086, whereas diclofenac, deferoxamine and catalase failed to inhibit the vasoconstriction due to SFH. No significant differences in either TXB2 generation or in histamine release were found in the WEB 2086 group compared with untreated lungs. The results point towards the crucial role of PAF in mediation of vasoconstrictor side effects due to SFH.

Animals↗