Pharmacological and mechanical management of calcium channel blocker toxicity.

Cardiovascular instability associated with calcium channel blocker toxicity comprises a small percentage of overdose presentations, yet they are associated with a high mortality rate. We detail the management of a 64-year-old man who took an intentional overdose of 840 mg nimodipine. We include the treatment he received and highlight the scarcity of evidence behind the use of gastric decontamination, calcium, glucagon, intravenous lipid emulsion, high-dose insulin therapy, sodium bicarbonate, vasopressors and methylene blue in calcium channel blocker toxicity. Additionally, the article explores the use of electrical pacing and venoarterial extracorporeal membrane oxygenation (VA-ECMO). Following successful weaning of VA-ECMO, the patient was successfully extubated but remained neurologically impaired due to hypoxic-ischaemic brain injury, critical care polyneuropathy and renal failure requiring dialysis. He has cerebral performance category 3; he has mild cognitive impairment but able to perform some activities of daily living independently and communicate his thoughts and needs. He requires no respiratory or cardiovascular support.

Effect of hypoxic-ischemic insults on the composition of fatty acids in the brain of neonatal rats.

BACKGROUND: Long-chain polyunsaturated fatty acids, especially docosahexaenoic acid (DHA; 22:6 n-3), comprise a major component of brain membrane phospholipids. The effect of neonatal hypoxic-ischemic insults on brain fatty acid composition is not completely understood. The aim of this study was to investigate alterations in brain fatty acid composition during development and in response to hypoxic-ischemic insults in neonatal rats. METHODS: Postnatal day 7 pups were randomly assigned to two experimental groups: a control group or a hypoxic-ischemic group in which hypoxia-ischemia was produced by left common carotid artery occlusion and exposure to 8% oxygen for 1.5 h. Various brain fatty acids were measured on postnatal days 8, 10 and 14. RESULTS: On postnatal day 14, the ratio of DHA to total fatty acids increased in the control group, but not in the hypoxic-ischemic group (p < 0.05). We observed no significant differences in arachidonic acid content in the brain between the two groups. CONCLUSIONS: These results suggest that hypoxic-ischemic insults interfere with accumulation of brain DHA in developing rats. DHA supplementation may be beneficial for treating neonatal hypoxic-ischemic encephalopathy.

[Effects of radix morindae from different processed products on anti-hypoxia and reproductive system of mice].

OBJECTIVE: To investigate the effects of Radix Morindae from different processed products on anti-hypoxia and reproductive system of mice. METHODS: The experimental study on anti-hypoxia was through the anti-anoxia action under normal-pressure, sodium nitrite poisoning and acute cerebral ischemia anoxia test; the experimental study on reproductive system was through observing the testis weight of immature male mice and the development of accessory sex organs in castrated mice. RESULTS: Both Radix Morindae of drying product and salt product could markedly increase the mice breathing time under acute cerebral ischemia anoxia, the salt product also could markedly increase the breathing frequency, prolong the mice survival time under atmospheric hypoxia and increase the testis weight of immature male mice. CONCLUSION: Both Radix Morindae of drying product and salt product can enhance anti-hypoxia and reproductive system of mice, and the effect of the salt product was superior to the drying product.

Electro-acupuncture preconditioning abrogates the elevation of c-Fos and c-Jun expression in neonatal hypoxic-ischemic rat brains induced by glibenclamide, an ATP-sensitive potassium channel blocker.

This study aimed to clarify the neuroprotective mechanism of electro-acupuncture (EA) preconditioning on hypoxic-ischemic brain injury (HIBI). Using Western blot, the expression of c-fos protein (c-Fos) and c-jun protein (c-Jun) induced by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker was examined from cerebral cortical and hippocampal samples in neonatal hypoxic-ischemic rats, with or without EA preconditioning. EA was performed on Hegu (LI4), a well-known acupoint commonly used in Oriental medicine for the treatment of neuronal injury resulting from hypoxia-ischemia (HI). Preconditioned rats were treated with either diazoxide, a K(ATP) channel opener, glibenclamide, or sterile saline injected into the left lateral ventricle (i.c.v.), with or without EA administration before HI insult. Interestingly, low c-Fos and c-Jun expressions were found both in diazoxide and EA groups, 24 h after HI. Furthermore, significant differences in relative optical density (ROD) were found between glibenclamide and HI control groups (P< or =0.05), as well as between the group administered glibenclamide after EA and the HI control group (P< or =0.05). However, the level of c-Fos and c-Jun expression in the group administered glibenclamide after EA was significantly lower than in the glibenclamide group (P< or =0.05). The present findings indicate that the effectiveness of EA preconditioning against HIBI may be mediated via the opening of K(ATP) channels.