Dexmedetomidine-propofol vs ketamine-propofol anaesthesia in paediatric and young adult patients undergoing device closure procedures in cardiac catheterisation laboratory: An open label randomised trial.

BACKGROUND AND AIMS: Several drug combinations have been tried in patients with acyanotic congenital heart disease (ACHD) undergoing transcatheter device closure in the cardiac catheterisation laboratory (CCL). Adequate sedation, analgesia, akinesia, cardiorespiratory stability, and prompt recovery are key requirements. Ketamine with propofol is used for this purpose. Dexmedetomidine carries a shorter recovery time. This study compared dexmedetomidine-propofol (DP) with ketamine-propofol (KP) in patients in the CCL. METHODS: This was an open label randomised trial at a CCL over a 2-year period from August 2012 to August 2014. Fifty-six paediatric and 44 young adults with ACHD underwent device closure and were randomised to receive DP or KP. The primary outcome studied was time to regain full consciousness, airway and motor recovery. RESULTS: Baseline characteristics were similar in the study groups. In the DP arm as compared to the KP arm, the time to recovery of consciousness (mean ± SD) was significantly faster in both paediatric patients [30 ± 15 vs. 58 ± 13 min (P < 0.001)] and in young adult patients [22 ± 10 vs. 35 ± 12 min (P < 0.001)]. There was significantly faster motor recovery also (mean ± SD) [paediatric: 25 ± 05 vs. 40 ± 14 (P < 0.001); young adult: 10 ± 05 vs. 22 ± 10 min (P < 0.001)]. CONCLUSION: Procedural anaesthesia with DP in paediatric and young adult patients with ACHD undergoing device closure in the CCL resulted in faster recovery of consciousness and motor recovery compared to KP.

Vanadium suppresses sister-chromatid exchange and DNA-protein crosslink formation and restores antioxidant status and hepatocellular architecture during 2-acetylaminofluorene-induced experimental rat hepatocarcinogenesis.

Vanadium is an important regulator of cellular growth, differentiation, and cell death, and thus has received increasing attention to be an effective cancer chemopreventive agent. In the present study, attempts have been made to investigate the in vivo antineoplastic effect of this micronutrient at the 0.5 ppm dosage in drinking water, by monitoring hepatic nodulogenesis and hepatocellular phenotype followed by antioxidant status and atomic absorption spectrometric estimation of some essential biometals during the multistage of carcinogenesis induced by 2-acetylaminofluorene (2-AAF; 0.05% in basal diet). Finally, sister-chromatid exchange (SCE) and DNA-protein crosslink (DPC) formation, as potential biomarkers were estimated to find out the suppressive effect of vanadium at the molecular level. The results showed that vanadium administration throughout the experiment reduced the relative liver weight, nodular incidence (48.40%), total number, and multiplicity (63.91%), and altered the size of visible persistent nodules (PNs) with concurrent restoration of hepatic glutathione (P < 0.01), glutathione-S-transferase (P < 0.001) and manganese-dependent superoxide dismutase (P < 0.001) activities as well as, hepatic zinc and copper contents (P < 0.001) when compared to the carcinogen control. Moreover, vanadium treatment significantly reduced SCE frequency (50.24%) and DPC coefficient (P < 0.001; 21.30%). Our results, thus, strongly suggest that supplementary vanadium at a dose of 0.5 ppm, when administered continuously throughout the study, than administered either in the initiation or promotion phase alone, is very much effective in suppressing neoplastic transformation during 2-AAF-induced in vivo rat hepatocarcinogenesis.

Vanadium inhibits placental glutathione S-transferase (GST-P) positive foci in 1,2-dimethyl hydrazine induced rat colon carcinogenesis.

Vanadium (V) has recently been found to possess potent anti-neoplastic activity in rat colon carcinogenesis. In the present study attempts have been made to investigate the expression of the number and area of aberrant crypt foci positive for placental glutathione S-transferase (GST-P) during 1,2-dimethyl hydrazine (DMH)-induced rat colon carcinogenesis. Male Sprague Dawley rats were randomly divided into four groups. Rats in group A were designed as normal controls. Group B animals received DMH once a week (20 mg/kg body wt.) intraperitoneally for 16 weeks. Group C rats received the same treatment of DMH as in group B, along with 0.5-ppm vanadium as ammonium monovanadate ad libitum in drinking water throughout the experiment. Vanadium alone was given to Group D rats without any DMH injection. The expression of the number and the area of aberrant crypt foci (ACF) positive for GST-P was maximum in DMH-treated group. Vanadium-treated rats significantly reduced (P < 0.001) the expression of GST-P positive ACF cells (by 71.13%) for the entire period of the study. Moreover the histopathological examination also showed that vanadium action could minimize the aberrant crypt foci (P < 0.001). Furthermore, vanadium supplementation also elevated SOD activities in both liver and colon (P < 0.01, P < 0.02 and P < 0.01, P < 0.02 respectively) when compared to their carcinogen counterparts. Our results confirm that vanadium is particularly effective in limiting the action of the carcinogen, thereby establishing its anticarcinogenicity in chemically induced rat colon carcinogenesis.