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Abstract

International Journal of Clinical Pharmacology and Therapeutics, Vol. 51 – No. 4/2013 (332-337)

Effects of sevoflurane and propofol on cultured bone-marrow mesenchymal stem cells of rats

Xue Zhou¹, Ying-Qin Li²,³, Wen He⁴, Xiao-Yu Yang¹, Fa-Huan Song², Zhi-Bin Zhou¹, Ying Tang², Xia Feng¹ and Li-Hua Zhou²

¹Department of Anesthesiology, The first affiliated hospital of Sun Yat-Sen University, ²Department of Anatomy, Zhong Shan School of Medicine, Sun Yat-sen University, Guangzhou, ³Department of Radiology, The fifth affiliated hospital of Sun Yat-sen University, Zhuhai, and ⁴Department of Cardiology, The first affiliated hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China
Objective: Bone marrow mesenchymal stem cell (BMSC) is a potentially effective vehicle for the cell and gene therapy in clinical disease treatment. We studied whether the most commonly used anesthetic drugs have negative effects on rat BMSCs in vitro. Materials and methods: The cultured BMSCs were treated with sevoflurane (in 1.7%, 2.3%, and 3%); propofol (5 μg/ml, 10 μg/ml and 20 μg/ml); or 2.3% sevoflurane plus 10 μg/ml propofol. After 4-hour treatment, the cultured BMSCs were prepared for MTT reduction assays and cell morphology observation. Results: Compared to the controls, the 4-hour sevoflurane exposure resulted in decreased cell viability of BMSCs in a concentration-dependent manner; however, 1.7% sevoflurane did not reduce the cell viability. The 4-hour propofol treatment did not affect the cell viability; but combined usage of 2.3% sevoflurane and 10 μg/ml propofol decreased cell viability. In BMSCs treated with higher concentration of sevoflurane (1.7% and 2.3%) and combined usage of the two anesthetics, the cell became raritas with wizened cytoplasm and had fewer connections to each other of BMSCs. More than 2.3%, or 2.3% sevoflurane plus 10 μg/ ml propofol caused cytotoxicity to BMSCs. However, propofol up to 20 μg/ml did not harm the BMSCs. Conclusions: The study indicates that it is necessary to choose the right anesthesia during the BMSCs transplantation therapy.Correspondence to:
Xia Feng, MD
Department of Anesthesiology
The first affiliated hospital of Sun Yat-Sen University
No 58 Zhongshan 2nd, Guangzhou, Guangdong, China
Email: [email protected]

Abstract

International Journal of Clinical Pharmacology and Therapeutics, Vol. 53 – No. 1/2015 (32-40)

Hemodynamic responses during induction: comparison of Marsh and Schnider pharmacokinetic models

Xiao-Yu Yang*, Zhi-Bin Zhou*, Lu Yang, Xue Zhou, Li-Jun Niu, and Xia Feng

Department of Anesthesiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
Background: Hemodynamic stability is one of the most critical concerns during induction of anesthesia. Whether the pharmacokinetic model by Marsh or the one by Schnider will produce better hemodynamic stability remains unclear. This study compared hemodynamic changes during induction between the two models. Methods: 60 patients who underwent elective surgery were randomly assigned to plasma target-controlled infusion by Marsh’s (n = 30) or Schnider’s (n = 30) model with an initial target concentration of 4 μg×mL^–1. The target was then reset and gradually titrated to a sedation level with a narcotrend index (NI) below 64. Stroke volume, cardiac output, systemic vascular resistance, arterial pressure, target, and effect site concentration, and dose of propofol infused were recorded every minute during the first 25 minutes of infusion. Results: Throughout the first 25 minutes, stroke volume index and cardiac index were decreased significantly in both Marsh and Schnider groups, but no statistical difference was detected between the groups (p > 0.05). Central venous pressure (CVP), systemic vascular resistance index (SVRI), and heart rate (HR) did not significantly change during induction (p > 0.05). Time to loss of responsiveness (LOR), and time for NI to decrease to 64 was faster in Marsh than in Schnider (1.51 ± 0.8 minutes vs. 2.8 ± 1.2 min, p < 0.001; 3.3 ± 2.0 minutes vs. 5.2 ± 2.3 minutes, p < 0.01, respectively). Conclusions: When target concentrations are titrated according to NI during induction of anesthesia, Marsh’s model could induce sedation faster than Schnider’s. Meanwhile, hemodynamic changes were not observed to be statistically different between the two models. Hypotension induced by plasma target-controlled infusion of propofol could mainly be attributed to decreased stroke volume instead of vascular dilation.Correspondence to:
Xia Feng MD, PhD
Department of Anesthesiology
First Affiliated Hospital of Sun Yat-Sen University
No.58 Zhongshan 2nd Road, Guangzhou, 510080, PR China
Email: [email protected]

Abstract

International Journal of Clinical Pharmacology and Therapeutics, Vol. 53 – No. 10/2015 (890-894)

Propofol-induced rhabdomyolysis: a case report

Zhi-Bin Zhou, Xiao-Yu Yang, Xue Zhou, Li-Jun Niu, Liang-Can Xiao, Wen-Qi Huang, and Xia Feng

Department of Anesthesiology, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
Objective: To report a case of propofol-induced rhabdomyolysis. In this case, widespread myolysis was detected after induction of anesthesia. Case summary: A 54-year-old female patient was scheduled for a hysterectomy. Beginning shortly after the induction of anesthesia with propofol, several episodes of ventricular fibrillation occurred. Despite intensive care, the patient failed to recover. During most episodes of ventricular fibrillation, marked hyperthermia or hyperkalemia were not observed. Unexplained, widespread myolysis affecting both skeletal and cardiac muscle was observed at autopsy. Discussion: In this patient, the evidence for rhabdomyolysis is robust. Clinical characteristics are similar to those observed in propofol infusion syndrome. The absence of a body temperature over 40 °C precludes the possibility of malignant hyperthermia. Widespread rhabdomyolysis locations cannot be explained by precordial electric shocks. Propofol is the only drug used in this case that has been reported to induce rhabodomyolysis. Conclusions: Signs of propofol-induced rhabdomyolysis may be different from those of malignant hyperthermia. Even a regular induction dose of propofol for adults could possibly trigger rhabdomyolysis similar to what is observed in children diagnosed with propofol infusion syndrome. Though rare, care should still be taken when administering propofol.Correspondence to:
Xia Feng, MD, PhD
Department of Anesthesiology
First Affiliated Hospital of Sun Yat-Sen University
No.58 Zhongshan 2nd Road, Guangzhou, 510080, China
Email: [email protected]

Abstract

Jian Zhang¹,², Junyue Huang¹, Bin Zhou³, Limin Tian⁴,⁵, Zhigang Ma⁶, Wenhui Huang¹, and Hui Zhao¹,⁴

¹Department of Nephrology, Gansu Provincial Hospital, ²The Second Hospital & Clinical Medical School, Lanzhou University, ³The Blood Purification Center of Gansu Provincial Hospital, ⁴College of Integrated Traditional Chinese and Western Medicine, Gansu University of Traditional Chinese Medicine, Lanzhou, ⁵Department of Endocrinology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, and ⁶Department of Nephrology, The Second Affiliated Hospital of The Chinese University of Hong Kong, Shenzhen (Longgang District People’s Hospital), Shenzhen, China
Renal clear cell carcinoma (RCC), the predominant subtype of kidney cancer, is characterized by paraneoplastic syndromes, of which membranous nephropathy (MN) represents the most common paraneoplastic glomerulonephritis. While phospholipase A2 receptor (PLA2R) antibodies indicate primary MN, the concurrent presence of light-chain amyloidosis may further complicate the clinical manifestations in malignancy-associated cases. A rare case of RCC concurrent with phospholipase A2 receptor PLA2R-positive MN and light chain amyloidosis is reported in this paper. An elderly male patient presented with nephrotic syndrome and a right renal mass. The patient underwent a nephrectomy after admission. Pathological examination confirmed the diagnosis of right kidney renal clear cell carcinoma. Renal biopsy revealed PLA2R-positive MN and AL amyloidosis. Interestingly, in this case, glomerular light chain staining showed no monoclonal restriction, but λ light chain deposition was found in the vessels. However, the nephrotic syndrome showed no improvement after tumor resection. The patient achieved remission following sequential treatment with bortezomib, dexamethasone, daratumumab, and rituximab. This case illustrates the complex interplay among RCC, PLA2R-positive MN, and AL amyloidosis, complicating patient management. Future research should focus on the immunological mechanisms of PLA2R antibody production in malignancy and the pathophysiological links among these conditions. Clinicians should remain vigilant for secondary causes of nephrotic syndrome in renal malignancy patients and adopt comprehensive, multidisciplinary approaches to improve outcomes. Correspondence to:
Hui Zhao, MD, 204 Donggang West Road, Chengguan District, Lanzhou 730000, Gansu, China
Email: [email protected]

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