Effects of IgM-enriched immunoglobulin and fluid replacement on nerve conduction velocity in experimental sepsis.

BACKGROUND: Neuromuscular abnormalities in sepsis, termed critical illness polyneuropathy (CIP), have been suggested to be induced by inflammatory mechanisms and/or relative hypovolemia. CIP is characterized by early electrophysiological findings before the clinical symptoms. This study aimed to investigate the effect of intravenous immunoglobulin (IVIG) and volume replacement therapies on the possible nerve conduction velocity (NCV) alterations in the early phase of experimental sepsis. METHODS: Forty-six Sprague-Dawley rats were randomly assigned to four groups. Cecal ligation/perforation was performed to induce experimental sepsis. NCV was assessed in the tail nerve. RESULTS: There was no statistically significant difference in NCV levels within and among the Sham-operated, colloid- and IVIG-treated groups. In the sepsis without treatment group, there was a statistically significant decrease in NCV levels. CONCLUSION: NCV is decreased in the early stage of experimental sepsis and it may be accepted as an early electrophysiological sign in CIP. Treatment with either IgM-enriched IVIG or early volume replacement appears to prevent the decrease in NCV in the early phase of experimental sepsis. Results were statistically indistinguishable between the IVIG- and colloid-treated groups. No statistical difference between these groups is noteworthy. There is a need to clarify the mechanisms of action with further randomized, clinical and experimental trials.

Neuromuscular deterioration in the early stage of sepsis in rats.

INTRODUCTION: Critical illness polyneuropathy (CIP) is a clinical condition frequently seen in patients being treated in critical care units in the final stage of sepsis. The etiopathology of CIP is still unclear, and the onset time of appearance of the electrophysiological findings has not been elucidated. The very little research that has been carried out on this topic is limited to clinical electrophysiological and histopathological studies. In this study, electrophysiological alterations in the early stage of experimentally induced sepsis were investigated in septic rats. METHODS: We conducted a prospective, randomized, controlled experimental study in an animal basic science laboratory with 30 male Sprague-Dawley rats, weighing 200 to 250 g. All of the rats were randomly assigned to one of two groups. In the sepsis group (n = 20), cecal ligation and puncture (CLP) was performed to induce experimental sepsis. In the sham-operated group (n = 10), laparotomy without CLP was performed. Before and 24 hours after CLP and laparotomy, the right sciatic nerve was stimulated from the sciatic notch and compound muscle action potentials (CMAPs) were recorded from the gastrocnemius muscle. Recordings of latency, amplitude, and duration of the CMAP were evaluated. RESULTS: CMAP durations before and 24 hours after surgery were 0.45 +/- 0.05 ms and 0.48 +/- 0.05 ms, respectively, in the sham-operated group and 0.46 +/- 0.05 ms and 0.55 +/- 0.01 ms, respectively, in the sepsis group. Latency measurements in the sham-operated group were 0.078 +/- 0.010 ms and 0.080 +/- 0.015 ms, respectively, whereas measurements were found to be prolonged in the sepsis group: 0.094 +/- 0.015 ms and 0.149 +/- 0.054 ms before and 24 hours after surgery, respectively (p < 0.05). CMAP amplitudes in the sham-operated group before and 24 hours after surgery were 8.41 +/- 0.79 mV and 8.28 +/- 1.92 mV, respectively, whereas in the sepsis group the amplitude measurements decreased to 7.60 +/- 1.75 mV and 4.87 +/- 3.44 mV, respectively (p < 0.05). CONCLUSION: The results of the study indicate that electrophysiological alterations appear in the first 24 hours after experimental sepsis and are characterized by an increase in latency and a decrease in CMAP amplitude. The results also suggest that electrophysiological findings seen in patients with CIP might appear before clinical signs of CIP.

Old method, new drugs: comparison of the efficacy of sevoflurane, isoflurane, and desflurane in achieving controlled hypotension in spinal surgery.

This study compared the efficacy of isoflurane, sevoflurane, and desflurane in achieving hemodynamic stability in spinal procedures using moderate levels of controlled hypotension. After obtaining ethics committee approval and written informed consent, 32 American Surgical Association I-II patients were randomly allocated to receive isoflurane (n=12), sevoflurane (n=10), or desflurane (n=10) in O2-N2O (1:1) for maintenance of anesthesia. The induction of anesthesia, fentanyl dosage, and initial and maintenance volume replacements were standardized. Blood pressure was invasively monitored and maintained within a target systolic blood pressure (SBP) range of 80 to 90 mm Hg during the study. SBP outside this range was recorded. Volatile anesthetic concentration was adjusted according to the same protocol for all 3 agents. SPB control was maintained better with sevoflurane and isoflurane than desflurane; median SBP was outside the target range during 32% (range, 15%-55%) of study time with isoflurane, 26% (12%-42%) with sevoflurane, and 44% (20%-80%) with desflurane. Total blood loss did not differ among the groups. Sevoflurane and isoflurane administered in 2 L/min fresh gas flow were more effective than desflurane in achieving controlled hypotension in spinal surgery.

The comparison of therapeutic effects of atropine and pralidoxime on cardiac signs in rats with experimental organophosphate poisoning.

Organophosphate poisoning causes disturbances in cardiac conduction and potentially fatal severe cardiac rhythm abnormalities. This study investigated the cardiac effects of atropine and pralidoxime in the treatment of organophosphate poisoning in rats. Three groups of 10 adult male Wistar rats were anesthetized with an intraperitoneal injection of ketamine 100 mg/kg and xylazine 10 mg/kg and connected to a computerized electrocardiographic monitor. Each rat was then injected intraperitoneally with the pesticide dichlorvos 70 mg/kg. Sixty seconds after the injection, 10 rats were injected with saline, 10 with pralidoxime mesylate 20 mg/kg, and 10 with atropine 10 mg/kg. During the computerized electrocardiographic monitoring, each rat's heart rate and QT(c) intervals were recorded and analyzed as the injections were administered. The heart rates in all 3 groups did not differ before the dichlorvos was administered, nor at 60 seconds afterward, but in the atropine group, the time elapsed before the first decline in heart rate was significantly longer than that in the control group (P<.05). In addition, the interval before death was significantly longer in the atropine group than in either the control group or the pralidoxime group (P<.05 for both). The QT(c) was almost identical in each of the groups. Atropine has beneficial effects on the heart rate, prolongs the time before the heart rate declines, and delays death but has no effect on the QT(c) interval. Further research about the toxic effects of organophosphate compounds on myocardial cells is warranted.

The effects of N-acetylcysteine on oxidative stress in organophosphate poisoning model.

Organophosphate compounds act by irreversible inhibition of cholinesterase. In addition to their muscarinic, nicotinic, and central nervous system effects, some organophosphate insecticides cause oxidative stress by increasing lipid peroxidation in erythrocytes and by increasing levels of the enzymes superoxide dismutase and catalase. In this study, the effects of an antioxidant, N-acetylcysteine (NAC), in organophosphate poisoning were investigated. After obtaining Animal Ethics Committee approval, 16 male Wistar rats were divided into 2 groups. Following anesthesia, rats were tracheostomized and mechanically ventilated. Invasive hemodynamic monitoring was begun and all rats were injected with 70 mg/kg of dichlorvos (DDVP) intraperitoneally. The rats in group 1 received placebo intravenous 0.9% NaCl and the rats in group 2 received 150 mg/kg intravenous NAC. Blood samples were obtained before injection of DDVP and 60 minutes after injection to determine levels of malondialdehyde, superoxide dismutase, and catalase. Hemodynamic data and biochemistry test results were compared by analysis of variance and Wilcoxon test. P<.05 was regarded as statistically significant. Superoxide dismutase and malondialdehyde levels were significantly increased in group 1 while no difference was observed in group 2. It was concluded that organophosphate compounds might cause oxidative stress by interfering with antioxidant defense mechanisms in erythrocytes and that NAC might prevent increased lipid peroxidation. In addition to classic treatments, drugs with antioxidant effects might therefore be promising in the treatment of organophosphate poisoning.