Knowledge on intrapartum care practices among skilled birth attendants in Cambodia-a cross-sectional study.

BACKGROUND: Delivery is a critical moment for pregnant women and babies, and careful monitoring is essential throughout the delivery process. The partograph is a useful tool for monitoring and assessing labour progress as well as maternal and foetal conditions; however, it is often used inaccurately or inappropriately. A gap between practices and evidence-based guidelines has been reported in Cambodia, perhaps due to a lack of evidence-based knowledge in maternity care. This study aims to address to what extent skilled birth attendants in the first-line health services in Cambodia have knowledge on the management of normal delivery, and what factors are associated with their level of knowledge. METHODS: Midwives and nurses were recruited working in maternity in first-line public health facilities in Phnom Penh municipality, Kampong Cham and Svay Rieng provinces. Two self-administered questionnaires were applied. The first consisted of three sections with questions on monitoring aspects of the partograph: progress of labour, foetal, and maternal conditions. The second consisted of questions on diagnostic criteria, normal ranges, and standard intervals of monitoring during labour. A multiple linear regression analysis was performed to identify relationships between characteristics of the participants and the questionnaire scores. RESULTS: Of 542 eligible midwives and nurses, 523 (96%) participated. The overall mean score was 58%. Only 3% got scores of more than 90%. Multivariate analysis revealed that 'Kampong Cham province', 'younger age', and 'higher qualification' were significantly associated with higher scores. Previous training experience was not associated with the score. Substantial proportions of misclassification of monitoring items during labour were found; for example, 61% answered uterine contraction as a foetal condition, and 44% answered foetal head descent and 26% answered foetal heart rate as a maternal condition. CONCLUSION: This study found that knowledge was low on delivery management among skilled birth attendants. Previous training experience did not influence the knowledge level. A lack of understanding of physiology and anatomy was implied. Further experimental approaches should be attempted to improve the knowledge and quality of maternity services in Cambodia.

Pregnancy and childbirth are natural phenomena, but sometimes have risk for mothers and babies. Therefore, childbirth should be carefully and continuously monitored by the health care professional. The 'partograph' is a useful tool that defines three monitoring aspects of the delivery progress, and conditions of the mother and intrauterine baby. However, it is often used inaccurately or inappropriately in low- and middle-income countries. We hypothesised that health professionals who assist childbirth cannot effectively monitor delivery conditions because their knowledge is insufficient. Therefore, we evaluated the knowledge on monitoring the process of childbirth and explored factors which affect the level of knowledge among health care providers in Cambodia.Midwives and nurses were targeted in this study who deal with normal deliveries in the capital city and two provinces. The questionnaire was designed to evaluate if their knowledge on three monitoring aspects is accurate.Of 542 eligible personnel, 523 (96%) participated. The mean score was 58%. Only 3% got scores of more than 90%. According to the statistical analysis, 'working in Kampong Cham province', 'younger age', and 'higher qualification' were significantly associated with higher scores. Previous training experience was not associated with the score.This study found that basic knowledge was low on delivery management among health care providers. We suspect that a deficiency of basic medical knowledge, such as physiology and anatomy, causes the lack of knowledge on the childbirth process. Further intervention should be attempted to improve the knowledge and quality of maternity services in Cambodia.

Nicorandil, a KATP Channel Opener, Attenuates Ischemia-Reperfusion Injury in Isolated Rat Lungs.

PURPOSE: Nicorandil is a hybrid between nitrates and KATP channel opener activators. The aim of this study was to evaluate the nicorandil's effects on ischemia-reperfusion (IR) lung injury and examine the mechanism of its effects. METHODS: Isolated rat lungs were divided into 6 groups. In the sham group, the lungs were perfused and ventilated for 150 min. In the IR group, after perfusion and ventilation for 30 min, they were interrupted (ischemia) for 60 min, and then resumed for 60 min. In the nicorandil (N) + IR group, nicorandil 6 mg was added before ischemia (nicorandil concentration was 75 µg ml-1). In the glibenclamide + N + IR group, the L-NAME (Nω-Nitro-L-arginine methyl ester) + N + IR group and ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one) + N + IR group, glibenclamide 3 µM, L-NAME 100 µM, and ODQ 30 µM were added 5 min before nicorandil administration, respectively. We measured the coefficient of filtration (Kfc) of the lungs, total pulmonary vascular resistance, and the wet-to-dry lung weight ratio (WW/DW ratio). RESULTS: Kfc was significantly increased after 60 min reperfusion compared with baseline in the IR group, but no change in the sham group. An increase in Kfc was inhibited in the N + IR group compared with the IR group (0.92 ± 0.28 vs. 2.82 ± 0.68 ml min-1 mmHg-1 100 g-1; P < 0.01). Also, nicorandil attenuated WW/DW ratio was compared with IR group (8.3 ± 0.41 vs. 10.9 ± 2.5; P < 0.05). Nicorandil's inhibitory effect was blocked by glibenclamide and ODQ (P < 0.01), but not by L-NAME. CONCLUSIONS: Nicorandil attenuated IR injury in isolated rat lungs. This protective effect appears to involve its activation as KATP channel opener as well as that of the sGC-cGMP pathway.

Intraischemic Modest Hypothermia Does Not Prevent Onset of Locomotor Inactivity After Transient Forebrain Ischemia in Rats.

Although modest hypothermia of 35°C has been demonstrated to provide histological neuroprotection in a rodent model of cerebral ischemia, the long-term behavioral outcome is still not clear. This study was designed to investigate whether modest hypothermia of 35°C provides sustained histological and behavioral neuroprotection following transient forebrain ischemia in rats. Male Sprague-Dawley rats were randomly assigned to one of three groups: sham, control, and modest hypothermia group. Each group contained eight rats. Ten-minute transient forebrain ischemia was produced by bilateral carotid artery occlusion plus hemorrhagic hypotension (mean arterial pressure = 40 mmHg). The hypothermic group was cooled to 35°C in preischemic period, and the cooling was continued for 1 hour postischemia. To evaluate behavioral outcome, spontaneous alternation behavior and locomotor activity were assessed using Y-maze test on a weekly basis. The rats were sacrificed after 28 days, and the number of intact neurons per 1 mm in the hippocampal CA1 subfield was counted microscopically. There was significant difference between the control [19(24.5)/mm: median (interquartile range)] and hypothermia groups [116(24)/mm; p < 0.01] in the intact CA1 neuron count. In the control and modest hypothermia groups, the locomotor activities were gradually decreased, and reached significantly lower levels in comparison with the sham group at 14 days postischemia. This study indicates that intraischemic modest hypothermia provided long-term histological neuroprotection, but did not reverse the onset of locomotor inactivity in a rat transient forebrain ischemia model.

Neuroprotective Effects of Fasudil, a Rho-Kinase Inhibitor, After Spinal Cord Ischemia and Reperfusion in Rats.

BACKGROUND: Excessive Rho/Rho-kinase pathway activation occurs subsequent to stroke. We examined the neuroprotective effects of pre- and posttreatment with fasudil (a Rho-kinase inhibitor) in a rat transient spinal cord ischemia-reperfusion model under normothermic conditions. METHODS: After approval by our animal research committee, male Sprague-Dawley rats were assigned to 1 of 6 groups: pre- and postcontrol (C); pre- and postfasudil (F); and pre- and postsham (S). Fasudil (10 mg/kg) or normal saline was administered intravenously over 30 minutes before ischemia in the pre-F or pre-C groups, and over 30 minutes after reperfusion in the post-F or post-C groups. Sham groups were not subjected to ischemia. Ischemia was induced by aortic occlusion using a balloon catheter combined with hypotension for 10 minutes. Neurologic deficit scores (NDS; 0-8 points) were assessed 1, 7, and 14 days after ischemia, and then histopathologic outcomes were assessed. RESULTS: NDS 7 and 14 days after ischemia in the pre-F group (median [range]; 3.5 [2-6] and 2.5 [0-6]) were lower than those in the pre-C group (5.5 [4-7] and 4.5 [4-6]; P = .046 and P = .049), whereas NDS in the post-F group and in the post-C group were not different. The numbers of intact neurons in the gray matter in the pre- and post-F groups (mean ± standard deviation [95% confidence interval]: 25 ± 7 [20-30] and 16 ± 5 [12-19]) were greater than those in the pre- and post-C groups (11 ± 5 [7-14] and 9 ± 3 [7-11]; P < .001 and P = .002). The number of intact neurons in the post-F group (16 ± 5 [12-19]) was lower than the number in the post-S group (26 ± 2 [24-29]; P < .001). The percentages of vacuolation in the white matter in the pre- and post-F groups (21.5 ± 8.4 [15.5-27.5] and 13.6 ± 7.4 [8.3-18.9]) were lower than those in the pre- and post-C groups (43.7 ± 10.4 [36.3-51.1] and 40.6 ± 12.3 [31.8-49.4]; P < .001 and P < .001). CONCLUSIONS: Our results demonstrated that intravenous fasudil administered before ischemia improved both neurologic and histopathologic outcomes even 14 days after ischemia, while fasudil administered postinsult improved histopathologic outcomes only in normothermic rats. Fasudil may be a relevant pretreatment paradigm for planned procedures at risk for spinal cord ischemia.

Neuroprotective effects of selective ß-1 adrenoceptor antagonists, landiolol and esmolol, on transient forebrain ischemia in rats; a dose-response study.

Although selective beta-1 adrenoceptor antagonists are known to provide neuroprotective effects after brain ischemia, dose-response relationships of their neuroprotective effects have not been examined. The present study was conducted to evaluate whether the degree of brain protection against transient forebrain ischemia would be influenced by different doses of selective beta-1 adrenoceptor antagonists, esmolol and landiolol, in rats. Adult male S.D. rats received intravenous infusion of saline 0.5 ml/h, esmolol 20, 200, 2,000 µg/kg/min, or landiolol 5, 50, 500 µg/kg/min. Infusion was initiated 30 min prior to ischemia and continued for 24h. Ten-minute forebrain ischemia was induced by hemorrhagic hypotension and occlusion of the bilateral carotid arteries. Neurological and histological examinations were performed. Neurological deficit scores at 1, 4 and 7 days were lower, and the number of intact neurons in CA1 hippocampal region was larger in the rats treated with esmolol and landiolol after ischemia, compared with saline-treated rats (P<0.05), whereas no difference was found among different doses of esmolol and landiolol. These results suggested that selective beta-1 adrenoceptor antagonists improved neurological and histological outcomes following forebrain ischemia in rats, irrespective of their doses.

Esmolol and landiolol, selective beta1-adrenoreceptor antagonists, provide neuroprotection against spinal cord ischemia and reperfusion in rats.

BACKGROUND: Paraplegia is a devastating and unpredictable complication occasionally resulting from surgery of the thoracic and thoracoabdominal aorta. Because ultrashort-acting selective beta(1)-adrenoreceptor antagonists provide neuroprotective effects after brain ischemia, we hypothesized that they would also ameliorate spinal cord injury after transient ischemia and reperfusion in rats. METHODS: Male Sprague-Dawley rats were randomly assigned to one of the following 4 groups: saline (received IV infusion of 0.9% saline at a rate of 0.5 mL/h, n = 8), esmolol (esmolol 200 microg/kg/min, n = 8), landiolol (landiolol 50 microg/kg/min), or sham surgical (n = 6). Infusion of saline or drugs was initiated 30 minutes before spinal cord ischemia and continued for the subsequent 24-hour reperfusion. Spinal cord ischemia was induced by intraaortic balloon occlusion combined with proximal arterial hypotension for 10 minutes. The spinal cord was then reperfused for 24 hours. Ischemic injury was assessed in terms of the motor deficit index score of the hindlimb and the number of viable motor nerve cells in the anterior spinal cord at 24 hours after reperfusion. RESULTS: The motor deficit index scores were significantly lower in the esmolol and landiolol groups compared with the saline group (P < 0.05). Histopathologic evaluation of the spinal cord showed less damage in the esmolol and landiolol groups than in the saline group (P < 0.05). CONCLUSIONS: These data show that ultrashort-acting selective beta(1)-adrenoreceptor antagonists can reduce neurological injury in a rat model of spinal cord ischemia-reperfusion.

Intravenous dexmedetomidine decreases lung permeability induced by intracranial hypertension in rats.

BACKGROUND: Intracisternal dexmedetomidine (Dex) attenuates cardiac dysfunction in rats with intracranial hypertension (ICH). However, the effects of IV Dex on cardiac function and lung permeability during ICH have not been evaluated. We tested the hypothesis that IV Dex attenuates hemodynamic changes and decreases lung permeability induced by ICH in rats. METHODS: Halothane-anesthetized and mechanically ventilated rats were divided into four groups. In two groups, a subdural balloon catheter was inflated for 60 s to produce ICH. Arterial blood gas analysis was performed before and 30 min after ICH. Mean arterial blood pressure, heart rate (HR) and intracranial pressure were monitored for 30 min. The Dex group (n = 8) received IV Dex 80 microg/kg, followed by 6 microg.kg(-1).min(-1) (40 microg/mL) for 10 min and the control group (n = 8) received IV saline 2 mL/kg, followed by at 0.15 mL.kg(-1).min(-1) for 10 min. Surgery was performed without ICH with Dex (Sham-Dex group, n = 5) and without Dex (Sham-control, n = 5). In all groups, pulmonary permeability was measured using a modification of the Evans blue dye extravasation technique. IV Evans blue dye 20 mg/kg was administered 2 h before being killed and Evans blue dye in plasma and lung tissue was quantified by dual-wavelength spectrophotometric analysis. RESULTS: There were no significant differences in basal arterial blood pressure, HR, and Pao(2) among groups. In the control group, ICH resulted in transient increases in mean arterial blood pressure and HR, followed by a rapid decline and a plateau. In the Dex group, mean arterial blood pressure showed a transient increase and subsequent, rapid decrease to baseline, whereas HR did not change during ICH. Pao2 was higher in the Dex group than in the control group after ICH [138 (127-169) vs 78 (59-124) mm Hg, median (range), P < 0.01]. The pulmonary permeability index was lower in the Dex group than the control group [430 (182-450) vs 570 (427-1170), P < 0.01]. It was however, higher in the Sham-Dex group than the Sham-Control group [25 (24-35) vs 6 (4-7), P < 0.01]. CONCLUSIONS: Prophylactic IV Dex decreases lung permeability as well as hemodynamic changes induced by ICH in rats.

Beta-adrenoreceptor antagonists attenuate brain injury after transient focal ischemia in rats.

Beta-adrenoreceptor antagonists experimentally reduce cardiac and renal injury after ischemia and are also clinically useful for myocardial infarction and severe burns. In addition, beta-adrenoreceptor antagonists provide neuroprotective effects after focal cerebral ischemia in experimental settings. We conducted the present study to compare the neuroprotective effects of several beta-adrenoreceptor antagonists in rat transient focal cerebral ischemia. Halothane-anesthetized normothermic adult male Sprague-Dawley rats were subjected to 2 h of middle cerebral artery occlusion using the intraluminal suture technique confirmed by laser Doppler flowmetry. Rats received an IV infusion of saline 0.5 mL/h, propranolol 100 microg x kg(-1) x min(-1), carvedilol 4 microg x kg(-1) x min(-1), esmolol 200 microg x kg(-1) x min(-1), or landiolol 50 microg x kg(-1) x min(-1) (n = 6 in each group). Infusion was initiated 30 min before middle cerebral artery occlusion and continued for 24 h. Additional rats received esmolol 50 microg x kg(-1) x min(-1) or landiolol 10 microg x kg(-1) x min(-1) intrathecally (IT) via the cisterna magna (n = 5 in each group), according to the same experimental protocol. The neurological deficit score was evaluated at 22 h after reperfusion, and the brains were removed and stained with triphenyltetrazolium chloride for evaluation of infarct volume. Additional rats that received saline, esmolol, and landiolol IV (n = 6 in each group) were allowed to survive for 7 days followed by measurement of infarct size. Neurological deficit scores were smaller in rats treated with propranolol-IV, carvedilol-IV, esmolol-IV, landiolol-IV, esmolol-IT, and landiolol-IT compared with saline-treated rats (P < 0.05). Cortical and striatum infarct volumes were less in the rats receiving beta-adrenoreceptor antagonists via either IV or IT than in saline-treated rats (P < 0.05). We conclude that beta-adrenoreceptor antagonists improve neurological and histological outcomes after transient focal cerebral ischemia in rats independent of administration route.

Physicochemical compatibility of propofol-lidocaine mixture.

UNLABELLED: To examine the physicochemical stability of combinations of propofol-lidocaine mixtures frequently used in clinical practice, we added lidocaine 5, 10, 20, or 40 mg to commercially available 1% propofol 20 mL. To assess chemical stability, propofol concentrations were determined by gas chromatography assay for 24 h after preparation of the mixture. In addition, scanning electron microscopy was used to determine the maximum detectable droplet size in randomly selected fields. Macroscopically, separate, colorless layers were first seen at 3 and 24 h after the addition of 40 and 20 mg of lidocaine to propofol, respectively, whereas the mixture with 5 or 10 mg of lidocaine was macroscopically stable. Propofol concentrations in the mixture with 40 mg of lidocaine decreased linearly and significantly from 4 to 24 h after preparation, whereas those combined with other lidocaine doses were unchanged compared with baseline concentrations. Scanning electron microscopy showed that droplets with diameters >or=5 microm first appeared 30 min after the addition of 40 mg of lidocaine to propofol, and the emulsion droplets were enlarged in a time- and dose-dependent fashion. Our results indicate that the addition of lidocaine to propofol results in a coalescence of oil droplets, which finally proceeds to a visible separate layer. Depending on the dose of lidocaine and the duration between its preparation and administration, this combination may pose the risk of pulmonary embolism. IMPLICATIONS: The addition of lidocaine to propofol results in time- and dose-dependent increases in oil droplet diameters in emulsion. This mixture is physicochemically unstable over time and may cause pulmonary embolism, depending on the dose of lidocaine.