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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 21 (1995), S. 832-837 
    ISSN: 1432-1238
    Keywords: Calcium ; Hypocalcemia ; Brain death ; Myocardial function ; Transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background The mechanism of brain death-induced myocardial dysfunction remains debatable. Hypocalcemia is known to induce reversible myocardial dysfunction. However, the incidence of hypocalcemia and its effect on myocardial function during brain death is unknown. Methods In 54 consecutive braindead patients, we measured plasma total and ionized calcium concentrations, QT and corrected QT intervals, and left ventricular ejection fraction area (LVEFa), using transesophageal echocardiography. Results 49 (91%) of brain-dead patients had a decrease in total plasma total calcium concentration but only 19 (35%) had a decrease in plasma ionized calcium. Corrected total plasma calcium failed to predict ionized calcium concentration and QT intervals were not significantly different in normo and hypocalcemic patients. The LVEFa was not significantly different between normo and hypocalcemic patients (53±13 versus 50±20%), and no correlation was found between LVEFa and ionized calcium (R=0.02, NS). Hypocalcemic patients required greater doses of dopamine (8.2±5.2 versus 5.0±3.4 μg·kg−·min−1,p〈0.02) to maintain arterial pressure. Hypocalcemia was associated with a higher volume loading and a lower plasma protide concentration which reflected hemodilution. Conclusion A decrease in plasma ionized calcium is not frequent, rarely severe, and probably not the main mechanism of myocardial dysfunction in brain-dead patients. Hypocalcemic patients required higher doses of dopamine, suggesting a decrease in systemic resistance. Only direct measurement of ionized calcium can assess plasma calcium ion status in brain-dead patients.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 20 (1994), S. 119-123 
    ISSN: 1432-1238
    Keywords: Colchicine poisoning ; Cardiac muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objectives Colchicine poisoning may be lethal and a decrease in cardiac function has been reported in several case reports, but the precise cardiotoxicity of colchicine remains unknown. Design The experimental in vitro study assessed the intrinsic contractility of left ventricular papillary muscle in rats, 24 h after administration of intraperitoneal colchicine or saline. Results The administration of colchicine (2 or 4 mg·kg−1) in adult Wistar rats markedly impaired intrinsic myocardial contractility, as shown by a decrease in maximum shortening velocity (−32 and −61%, respectively), active isometric force (−47 and −65%, respectively), and peak power output (−57 and −69%, respectively) of left ventricular papillary muscle. Colchicine impaired isotonic relaxation and load dependence of relaxation, suggesting a decrease in sarcoplasmic reticulum function. Conversely, colchicine significantly accelerated isometric relaxation, suggesting a decrease in calcium myofilament sensitivity. Myothermal economy was markedly impaired only in some rats (3/10 in each group), in which the negative inotropic effect of colchicine appeared to be more particularly pronounced. Conclusion The results indicate that the administration of high doses of colchicine induced intrinsic cardiotoxic effects. Due to its amplitude, such cardiotoxic action may participate in the fatal outcome of acute colchicine poisoning.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1238
    Keywords: Cobalt ; Cyanide antidote ; Hydroxocobalamin ; Myocardial contractility ; Sodium nitroprusside toxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background Hydroxocobalamin has been shown to be a rapid and powerful antidote in acute cyanide poisoning and to prevent cyanide poisoning during sodium nitroprusside administration. This cobalt-containing compound has been shown to be devoid of significant immediate side effects during acute administration. However, its potential delayed toxicity related to cobalt accumulation in tissue remains unknown. Therefore, we evaluated the toxicity of hydroxocobalamin as compared with that of cobalt salts on rat cardiac and diaphragmatic muscles. Methods For a 21-day period, rats were treated intraperitoneally with either hydroxocobalamin (70 mgkg−1 per day,n=14) cobalt chloride hexahydrate (12 mg kg−1 per day,n=14) or saline (n=10). Hydroxocobalamin and cobalt chloride groups received equimolar doses of cobalt. We studied: (1) the mechanical properties of isolated left ventricular papillary muscles and diaphragmatic strips, (2) the cardiac and diaphragmatic cobalt tissue concentrations, and (3) the myocardial histological aspect. Results During the study period, no significant increase in body weight was noted in the cobalttreated group (−4±1%), which was in contrast to the hydroxocobalamin-treated group (+21±2%) and the saline-treated group (22±2%). Compared with controls, the mechanical properties of cardiac and diaphragmatic muscles were unchanged after either hydroxocobalamin or cobalt salt treatments, and myocardial histological characteristics were similar in all groups. Conversely, large amounts of cobalt deposit were observed in the cobalt-treated group in both the diaphragm (41.90±16.30 vs 0.70±0.40 μmol μg−1 in the control group,P〈0.001). After hydroxocobalamin administration, cobalt concentrations were significantly lower in the diaphragm (25.10±16.50 μmol μg−1,P〈0.001 vs cobalt-treated group) and the myocardium (4.50±1.20 μmol μg,P〈0.001 vs cobalt-treated group). Conclusion These results indicate that repeated administration of hydroxocobalamin was devoid of significant diaphragmatic and cardiac muscle toxicity and therefore remains a safe antidote for acute cyanide poisoning.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 13 (1987), S. 352-354 
    ISSN: 1432-1238
    Keywords: Pneumococcal pneumonia ; Mixed infection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two cases of co-infection or very early superinfection of pneumococcal pneumonia with Staphylococcus aureus in one case, and Enterobacter cloacae in the other, are reported. The two patients were not fully immunocompetent, had leukopenia and a mild intravascular coagulation, and were bacteremic. Mixed infection probably accounted for the lethal outcome because initial antibiotherapy was only directed against Streptococcus pneumoniae. Accurate bacteriologic methods are required to delineate contaminating and infecting pathogens when another bacteria is found in initial bronchial samples of patients with pneuococcal pneumonia, and the antibiotherapy might be directed against the two pathogens until quantitative bacteriologic results would be available, especially in old and debilitated patients. The incidence of mixed infection in pneumococcal pneumonia seems low.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 14 (1988), S. 610-616 
    ISSN: 1432-1238
    Keywords: Chloroquine poisoning ; Diazepam ; Benzodiazepines ; Suicide attempt
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To assess the effects of diazepam in chloroquine poisoning, we studied pentobarbital anesthetized and mechanically ventilated pigs. All the pigs received 50 mg·kg−1 chloroquine given intravenously for 25 min. Eight pigs acted as control (group C). Another 7 were treated with diazepam given intravenously 5 min after the end of chloroquine infusion: 2 mg·kg−1 of diazepam for 2 min, then 1 mg·kg·h−1 for 25 min (group D). Thereafter, all pigs were sacrified. In both groups the chloroquine infusion induced a large fall in arterial pressure, a decrease in heart rate, and an increase in QRS duration. No difference was observed between the 2 groups for weight, systolic and diastolic arterial pressures, heart rate, QRS and QT durations before diazepam. After diazepam, systolic and diastolic arterial pressures, heart rate, urine volume, urinary excretion of chloroquine, plasma and blood cell chloroquine levels were higher, whereas QRS duration was lower, in group D compared to group C. No difference was observed between the 2 groups for urinary concentration of chloroquine, the ratio between plasma and blood cell chloroquine levels, hepatic, cardiac, and skeletal muscle chloroquine levels, and QT duration. After diazepam, the slope of the regression curve between QRS duration and plasma chloroquine levels was reversed in group D compared to group C. We conclude that diazepam counteracts some haemodynamic and electrocardiographic changes, and increases urinary excretion of chloroquine, in acute experimental chloroquine poisoning.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1238
    Keywords: Chloroquine poisoning ; Diazepam-Benzodiazepines ; Antimalarial drugs ; Cardiac muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Diazepam has been reported to decrease the cardiac toxicity of chloroquine but the precise mechanism involved remains unknown. Left ventricular papillary muscles from adult Wistar rats were exposed to 10-4 M chloroquine and assigned to three groups: group I (n=10) exposed to chloroquine alone; group II (n=8) exposed to chloroquine and 10-5 M diazepam; group III (n=8) exposed to chloroquine and 10-4 M diazepam. The main mechanical parameters measured were: maximum unloaded shortening velocity (Vmax), maximum lengthening velocity (maxVr), active force normalized per cross-sectional area (AF/s), contraction-relaxation coupling under low load (R1), load sensitivity of relaxation (Isot.A/ Isom.A), and peak power output ( $$\mathop {\text{E}}\limits^{\text{o}} $$ max) determined from Hill's equation of the force-velocity curve. Data are expressed as mean percent of control values±SD, for groups I, II, III respectively. No differences between groups I, II, and III were noted for Vmax (87±13, 82±9, 86±7), maxVr (47±6, 48±11, 52±11), AF/s (87±16, 91±10, 83±11), Isot. A/Isom. A (113±9, 108±3, 109±7), or $$\mathop {\text{E}}\limits^{\text{o}} $$ max (75±10, 81±12, 72±16). Chloroquine was shown to be a negative inotropic agent since it decreased Vmax, AF/s and $$\mathop {\text{E}}\limits^{\text{o}} $$ max, but diazepam did not restore the intrinsic mechanical performance of rat cardiac papillary muscle exposed to chloroquine, therefore 1) the protective cardiovascular effects of diazepam in chloroquine poisoning are not related to an improvement in intrinsic cardiac mechanical properties; 2) inotropic agents are therefore necessary in combination with diazepam for the treatment of severe chloroquine poisoning.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 16 (1990), S. 348-348 
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 17 (1991), S. 175-177 
    ISSN: 1432-1238
    Keywords: Hydroxocobalamin ; Cyanide antidote ; Myocardial contractility ; In vitro experiments
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hydroxocobalamin is a rapid and powerful antidote in acute cyanide poisoning. The effects of hydroxocobalamin (0.1, 0.3, and 1 mM) on intrinsic myocardial contractility were studied on isolated rat cardiac papillary muscles (n=10). Whatever the concentration, hydroxocobalamin did not modify the active isometric force and a slight increase in maximum unloaded shortening velocity was noted at 1 mM. Only 0.3 mM significantly impaired contraction-relaxation coupling under low load, suggesting a slight decrease in sarcoplasmic reticulum function. No changes in contraction relaxation coupling under heavy load were noted, suggesting the lack of modification of myofilament calcium sensitivity. These results suggest that hydroxocobalamin does not induce noticeable changes in intrinsic myocardial contractility. An indirect mechanism might be involved in the previously reported decrease in cardiac function at supratherapeutic concentrations of hydroxocobalamin.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1238
    Keywords: Cyanide ; Hydroxocobalamin ; Cobalt edetate ; Catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objectives The hemodynamic effects of two cyanide antidotes, hydroxocobalamin and cobalt edetate were compared. Design This experimental study was performed in chronically instrumented conscious dogs and at equipotent cyanide antidotal doses (hydroxocobalamin 70 mg·kg−1; cobalt edetate 10.5 mg·kg−1). Results Peak plasma cobalt concentrations did not differ in the two groups (412±183 vs 400±160 μmol·1−1). Hydroxocobalamin induced a slight increase in mean arterial pressure (+17±9%,p〈0.05) and systemic resistance (+19±15%,p〈0.05). In contrast, cobalt edetate induced an increase in heart rate (+78±33%,p〈0.05), in cardiac output (+63±39%,p〈0.05), and in maximum rise of left ventricular pressure (+33±15%,p〈0.05), did not modify mean arterial pressure, and decreased systemic resistance (−36±15%,p〈0.05). These hemodynamic effects were associated with an increase in plasma catecholamine concentrations (epinephrine: 2524±3025 vs. 58±37 pg·ml−1,p〈0.05; norepinephrine: 1106±609 vs. 343±146 pg·ml−1,p〈0.05), which in contrast remained unchanged after hydroxocobalamin administration. Cobalt edetate also induced an increase in blood glucose concentrations (9.9±1.9 vs. 6.1±1.2 mmol·l−1,p〈0.05) and a moderate metabolic acidosis, whereas hydroxocobalamin did not. After adrenergic (α1,β) and cholinergic receptor blockade, cobalt edetate did not modify heart rate and various indices of cardiac function, suggesting that it has no direct cardiac effects. Conclusion Considering its lack of hemodynamically relevant effects, these results indicate that hydroxocobalamin is potentially a safer cyanide antidote than cobalt edetate.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1238
    Keywords: Pneumonia ; Mechanical ventilation ; Lower respiratory tract secretion sample ; Protected specimen brush
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this prospective study was to compare the results obtained with the non-protected lower respiratory tract secretions samples (LRS) with the protected specimen brushes (PSB) performed through a fiberoptic bronchoscope in mechanically ventilated patients, when pneumonia was suspected. The diagnosis of pneumonia was ultimately made at the end of the hospitalisation, in a double-blind manner by 2 members of the medical staff not aware of the bacteriologic results of LRS and PSB. LRS and PSB were performed in 24 patients. PSB culture was considered as positive at a level of 103 colony-forming units per milliliter (cfu/ml) microorganisms. Twentyfive samples from 24 patients were divided as follows: (1) LRS (-) and PSB (-) 5 samples: the clinical diagnosis of pneumonia was never established. (2) LRS (+) and PSB (+) 10 samples: the clinical diagnosis of pneumonia was always established, 2 microorganisms were involved 4 times and 1 microorganism 6 times. (3) LRS (+) and PSB (-) 10 samples: the clinical diagnosis of pneumonia was retained in 3 with the possibility of false negative PSB. We conclude that (1) a negative LRS eliminated the diagnosis of pneumonia without PSB; (2) a positive LRS was not sufficient to diagnose pneumonia since PSB was negative in 50% of all LRS (+) cases; (3) the possibility of a false negative PSB must be kept in mind particularly in patients previously treated with antibiotics; (4) 2 microorganisms may be responsible for the pneumonia if the previously determined, as significant, bacteriological count (〉-103 cfu/ml) appears to be accurate.
    Type of Medium: Electronic Resource
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