Preoperative metoprolol improves cardiovascular stability and reduces oxygen consumption after thoracotomy

Background : Increased sympathetic activity perioperatively and associated cardiovascular effects play a central role in cardiovascular complications. High thoracic epidural blockade attenuates the sympathetic response, but even with complete pain relief, haemodynamic and endocrine responses are still present. Beta–adrenoceptor blockade is effective in situations with increased sympathetic activity. This study was designed to evaluate the perioperative haemodynamic effect of preoperative βblockade and its influence on the haemodynamic aspects of the surgical stress response.
Methods : Thirty–six otherwise healthy patients undergoing elective thoracotomy for lung resection were randomised doubleblinded to receive either 100 mg metoprolol or placebo preoperatively. Anaesthesia was combined high thoracic epidural block and general anaesthesia. The epidural analgesia was continued during recovery. Patients were monitored with ECG, pulse oximetry, invasive haemodynamic monitoring, arterial blood gases and electrolytes.
Results : After induction of anaesthesia the mean arterial pressure (MAP) decreased in both groups, and decreased further in the placebo group after initiation of the epidural block. The heart rate (HR) was slightly less throughout the observation period after metoprolol. Peroperatively, the only difference in measured haemodynamics was a marginally higher MAP after metoprolol. Postoperative cardiac index (CI) was lower with a lower variability and cardiac filling pressures were slightly higher in the metoprolol group. The oxygen consumption index was higher after placebo throughout the observation period, with no difference in the oxygen delivery.
Conclusion. We found that preoperative β–blockade during combined general anaesthesia and high thoracic epidural blockade stabilised perioperative HR and CI and decreased total oxygen consumption.     

Application of a 3D volume 19FMR imaging protocol for mapping oxygen tension (pO2) in perfluorocarbons at low field

A limited flip angle gradient-echo 3D volume acquisition imaging protocol for mapping partial pressure of oxygen (pO₂) in perfluorocarbon compounds (PFCs) at low field (0.14 T) is presented. The pO₂ measurement method is based on the paramagnetic effect of dissolved molecular oxygen (O₂) which reduces the PFC ¹⁹F T_1? Specific objectives related to imaging of PFCs through use of the protocol include improved image signal-to-noise characteristics and elimination of ¹⁹F chemical shift artifacts. A parametric Wiener deconvolution filtering algorithm is used for suppression of ¹⁹F chemical shift artifacts. Application of the protocol is illustrated in a series of calculated pO₂ maps of a gas equilibrated, multi-chamber phantom containing perfluorotributylamine (FC-43). The utility of the protocol is demonstrated in vivo through images of a commercially available perfluorocarbon based blood substitute emulsion containing FC-43 sequestered in the liver and spleen of a rat.     

富氧气体防护下暴发性缺氧大鼠大脑超微病理变化

目的 从亚细胞水平观察大鼠在12 000m高度暴发性缺氧及富氧气体防护时大脑顶叶皮质组织超微结构变化，为高空暴发性缺氧的防护和治疗提供理论依据。方法 将24只雄性Wistar大鼠随机分为地面对照组、3000m对照组、12000m暴发性缺氧组、12000m吸90％富氧气体防护组、12000m吸100％氧气防护组、12000m吸50％富氧气体防护组，每组4只。于低压舱内暴露于12000m高度30min，然后将动物即刻处死，取大脑顶叶皮质层组织，制成切片，透射电镜下观察。结果与地面对照组相比，随着吸氧浓度的降低，实验组缺氧程度加重，主要表现为脑组织神经细胞、神经胶质细胞结构模糊不清，核及胞质内线粒体、内质网扩张，突触小泡减少等，以12000m暴发性缺氧组及吸50％氧气防护组明显。结论 吸100％和吸90％富氧气体防护效果是理想的，与地面对照组和3000m对照组的结果无明显差别。     

一种医疗氧舱气路系统设计的改进

本文针对目前医疗氧舱自动化程度不高,各种治疗参数难以定量控制的特点,设计出了以微型计算机为控制核心的医疗氧舱自动供排气系统,并重点介绍了微型计算机的硬件和软件设计。     

Dissimilarities between benzodiazepine-binding sites and adenosine uptake sites in astrocytes and neurons in primary cultures

The question whether the benzodiazepine receptor site in astrocytes or in neurons might be identical to the adenosine uptake site was studied by determining pharmacological profiles, inhibition types, and the effects of benzodiazepine antagonsts in primary cultures of either astrocytes or neurons. Fourteen different benzodiazepines and five different adenosine uptake inhibitors displaced [³H] diazepam and inhibited adenosine uptake in both astrocytes and neurons. However, the rank orders (determined as IC₅₀ values) with which these two parameters were affected were profoundly different, indicating dissimilarities between these two sites. For several of the compounds a difference in inhibition type (competitive vs. noncompetitive) was observed between the benzodiazepine-binding site and the adenosine uptake site in astrocytes and/or neurons, which further corroborated the conclusion of a difference between the benzodiazepine-binding site and the adenosine uptake site. Finally, the neuronal benzodiazepine antagonists RO 15-1788 and CGS-8216 and the astrocytic benzodiazepine antagonist PK 11195, which reverse the action of benzodiazepines, were not able to reverse inhibition of adenosine uptake by diazepam but exerted an inhibitory effect of their own.     

EGF enhances the survival of dopamine neurons in rat embryonic mesencephalon primary cell culture.

Epidermal growth factor (EGF) immunoreactive material has been demonstrated to be present in the basal ganglia. In this study, we investigated the effect of EGF on cells cultured from 16-day embryonic rat mesencephalon, which included dopamine neurons that project to the striatum in vivo. EGF receptors were detected in untreated cultures by [125I]-EGF binding. Treatment of the cultures with EGF resulted in up to 50-fold increases in neuronal high-affinity dopamine uptake. Scatchard analysis of uptake kinetics and counting of tyrosine hydroxylase-immunoreactive cells suggest that the effect of EGF on uptake is due to increased survival and maturation of dopaminergic neurons. By contrast, the high-affinity uptake for serotonin was increased only threefold over its controls. There was no significant effect on high-affinity gamma-aminobutyric acid (GABA) uptake. These results suggest that EGF is acting as a neurotrophic agent preferential for dopaminergic neurons in E16 mesencephalic cultures. Immunocytochemistry for glial fibrillary acidic protein demonstrated an increase in astroglia with EGF treatment. Fluorodeoxyuridine, an agent that is toxic to proliferating cells was able to eliminate the effect of EGF on dopamine uptake, suggesting that EGF may be increasing dopaminergic cell survival largely through a population of dividing cells.     

高压氧结合针灸治疗脑外伤患者的效果观察与分析

目的:观察高压氧结合针灸治疗脑外伤患者的疗效。方法:对96例脑外伤患者采用高压氧、针灸配合药物进行综合治疗。同时,对83例对照组患者根据病情给予降颅压、抗感染、改善脑供血、保护脑细胞等治疗,有手术指征者行清除血肿、减压和清创术。结果:出院时两组患者功能比较,治疗组明显优于对照组,有显著性差异(P<0.O1),疗效治疗组也明显好于对照组。结论:高压氧结合针灸治疗能够明显提高脑损伤患者疗效,对肢体功能有明显提高。     

Central cardiovascular and oxygen variables during haemorrhage in the pig

Background: We evaluated the ability of the standards issued by the Danish Society of Anaesthesiologists to reflect a blood loss.
Methods: In 9 pigs bled (0–24 ml kg^-1) and retransfused (to 28 ml kg^-1) during halothane anaesthesia, central cardiovascular, thoracic electrical impedance (TI), oxygen, acid-base and temperature variables were recorded.
Results: With the recommendation for minor surgery (mean arterial pressure (MAP) and heart rate (HR)), the correlation to the blood loss was 0.74 ( P < 0.001) and with that for major surgery (MAP, HR, central venous pressure (CVP) and rectal temperature (Temp_r)) it was 0.79 ( P < 0.001). With the recommendation for extensive surgery (MAP, HR, CVP, pulmonary artery catheter variables and the central-peripheral temperature difference (ΔTemp_r-t)), the correlation was 0.84 ( P < 0.001). Non-invasive monitoring (MAP, HR, ΔTemp_r-t TI and near-infrared spectroscopy of the brain (S_invosO₂)) was only slightly better than basal monitoring (r=0.76, P < 0.001). However, adding arterial base excess (BE), TI and peripheral temperature (Temp_t) to the recommendation for major surgery resulted in a correlation of 0.87 ( P < 0.001), while adding BE and TI to the recommendation for extensive surgery raised correlation to only 0.88 ( P < 0.001).
Conclusion: When the recommendations were followed the correlation to the blood loss ranged from 0.74–0.84. However, with the recording of MAP, HR, CVP, ΔTemp_r-t, BE and TI a correlation of 0.87 was achieved, indicating that a pulmonary artery catheter may not be in need for patients undergoing surgical procedures with expected haemorrhage.     

Voltage-Gated calcium channels and nonvoltage-gated calcium uptake pathways in the rat incisor odontoblast plasma membrane

Odontoblasts participate actively in the transport and accumulation of Ca²⁺ ions to the mineralization front during dentinogenesis. These cells are known to carry membrane-bound ATP-driven pumps and Na⁺/Ca²⁺ antiports for Ca²⁺ extrusion, but little is known about Ca²⁺ influx mechanisms into these cells. It has been shown that the administration of Ca²⁺ channel blockers in vivo strongly impairs Ca²⁺ uptake in the mineral phase during dentinogenesis in the rat; the present in vitro study is aimed at further elucidating odontoblast Ca²⁺ uptake mechanisms. Dissected rat incisor odontoblasts exhibited a pronounced fluorescence when incubated with a fluorescently-labeled (STBodipy) dihydropyridine, which is specific for voltage-gated Ca²⁺ channels of the L-type, and this binding was competitively abolished by nifedipine. As assayed by fluorescence spectrometry, odontoblast Ca²⁺ uptake was enhanced by the agonistic dihydropyridine BAYK-8644 (5 μM) as well as by plasma membrane depolarization in a high K⁺ (120 mM) medium. The Ca²⁺ uptake after depolarization was impaired by nifedipine (5 μM). When treated with the Ca²⁺-ATPase inhibitor cyclopiazonic acid (CPA; 10 μM), a nonvoltage-gated uptake of ⁴⁵Ca²⁺ was identified. This uptake was not influenced by nifedipine (20 μM) but was impaired by lanthanum ions (200 μM). A nonvoltage-gated uptake of Mn²⁺ into CPA-treated cells could be traced using the fura-2 quenching technique. This CPA-induced Ca²⁺ flux was not caused by an alteration of the plasma membrane potential, as assayed with di-8-ANEPPS. The results demonstrate that Ca²⁺ flux into dentinogenically active odontoblasts occurs through voltage-gated Ca²⁺ channels of the L-type and by nonvoltage-gated, agonist-sensitive Ca²⁺ uptake pathways. Received: 6 November 1995 / Accepted: 21 February 1996     

Improvement of oxygen metabolic reserve after extracranial-intracranial bypass surgery in patients with severe haemodynamic insufficiency

Summary The effectiveness of extracranial-intracranial arterial bypass (EC-IC bypass) surgery on impaired haemodynamic status was studied in 12 patients with reduced regional cerebral perfusion pressure (rCPP) and elevated regional oxygen extraction fraction (rOEF) in the area distal to the symptomatic arterial lesion. Postoperative positron emission tomography (PET) study demonstrated a statistically significant decrease of rOEF in the operated hemispheres with disappearance of the pre-operative interhemispheric rOEF difference. Regional cerebral blood flow (rCBF) and regional cerebral oxygen metabolism (rCMRO2) were also increased in the operated hemispheres with disappearance of the pre-operative interhemispheric differences. Regional CBF/regional cerebral blood volume (rCBV) ratios of the symptomatic hemispheres were increased after surgery, but were still lower than in the contralateral hemispheres. We conclude that EC-IC bypass surgery improves impaired cerebral oxygen metabolic reserve.