Dinuclear ruthenium(II) Schiff base complex: a first in vivo study in Swiss albino mice.

OBJECTIVES: Dinuclear ruthenium(II) Schiff base complex was selected for in vivo study among many other novel metal-based compounds, because of its previously proved in vitro anticancer and antibacterial properties. The aim was to investigate the potential toxicity of this compound in animal model through biochemical and histopathological assessment. METHODS: Adult Swiss albino mice of both sexes were divided into high-dose and low-dose group that received a single intraperitoneal dose of ruthenium complex (175 mg/kg and 25 mg/kg, respectively) and one control group (vehicle only). After a follow-up period of 14 days, animals were sacrificed to obtain blood samples and organs. RESULTS: The test compound was well tolerated in a low-dose group and did not cause any mortality. The histological findings and serum biochemistry suggested a reversible character of alterations found in vital organs of this group. However, in the high-dose group, adverse effects were more severe and indicated dose and gender-related toxicity. CONCLUSION: Mild side effects found in a low-dose group together with excellent in vitro properties, made dinuclear ruthenium(II) Schiff base complex a promising candidate for further investigation and development as anticancer and antimicrobial agent (Tab. 4, Fig. 6, Ref. 32).

Neurologic and histologic outcome after intraneural injections of lidocaine in canine sciatic nerves.

BACKGROUND: Inadvertent intraneural injection of local anesthetics may result in neurologic injury. We hypothesized that an intraneural injection may be associated with higher injection pressures and an increase in the risk of neurologic injury. METHODS: The study was conducted in accordance with the principles of laboratory animal care, and was approved by the Laboratory Animal Care and Use Committee. Fifteen dogs of mixed breed (16-21 kg) were studied. After general endotracheal anesthesia, the sciatic nerves (n= 30) were exposed bilaterally. Under direct vision, a 25-gauge, long-beveled needle (30 degrees) was placed either epineurally (n= 10) or intraneurally (n= 20), and 4 ml of preservative-free lidocaine 20 mg/ml was injected using an automated infusion pump (4 ml/min). Injection pressure data were acquired using an in-line manometer coupled to a computer via an analog-to-digital conversion board. After injection, the animals were awakened and subjected to serial neurologic examinations. One week later, the dogs were killed, the sciatic nerves excised and histologic examination was performed by pathologists blind to the purpose of the study. RESULTS: All perineural injections resulted in low pressures (< or = 5 psi). In contrast, eight of 20 intraneural injections resulted in high pressures (20-38 psi) at the beginning of the injection. Twelve intraneural injections, however, resulted in pressures of less than 12 psi. Neurologic function returned to baseline within 3 h after perineural injections and within 24 h after intraneural injections, when the measured injection pressures were less than 12 psi. Neurologic deficits persisted throughout the study period after all eight intraneural injections that resulted in high injection pressures. Histologic examination of the affected nerves revealed fascicular axonolysis and cellular infiltration. CONCLUSIONS: The data in our canine model of intraneural injection suggest that intraneural injections do not always lead to nerve injury. High injection pressures during intraneural injection may be indicative of intrafascicular injection and may predict the development of neurologic injury.