Background:General anaesthesia is currently the conventional technique used for surgical treatment of breast lump. Paravertebral block (PVB) has been used for unilateral procedures such as thoracotomy, breast surgery, chest wall trauma, hernia repair or renal surgery.Methods:We compared unilateral thoracic PVB with general anaesthesia (GA) in 60 consenting ASA physical status I and II female patients of 18–65 years age, scheduled for unilateral breast surgery. Patients were randomly assigned into two groups, P (n=30) or G (n=30), to receive either PVB or GA, respectively.Results:The average time to first post-operative analgesic requirement at visual analogue scale score≥4 (primary endpoint) was significantly longer in group P (303.97±76.08 min) than in group G (131.33±21.36 min), P<0.001. Total rescue analgesic (Inj. Tramadol) requirements in the first 24 h were 105.17±20.46 mg in group P as compared with 176.67±52.08 mg in group G (P<0.001). Significant post-operative nausea and vomiting requiring treatment occurred in three (10.34%) patients of the PVB group and eight (26.67%) patients in the GA group.Conclusion:The present study concludes that unilateral PVB is more efficacious in terms of prolonging post-operative analgesia and reducing morbidities in patients undergoing elective unilateral breast surgery.

It can be concluded that unilateral PVB is more efficacious than conventional SA in terms of prolonging post-operative analgesia and reducing morbidities in patients undergoing elective unilateral inguinal hernia repair.

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We may suggest that planned pregnancy during therapy may be encouraged but imatinib therapy in unplanned pregnancy can cause spontaneous abortion or congenital anomaly.

Cyanide inhibits aerobic metabolism by binding to the binuclear heme center of cytochrome c oxidase (CcOX). Amyl nitrite and sodium nitrite (NaNO(2)) antagonize cyanide toxicity in part by oxidizing hemoglobin to methemoglobin (mHb), which then scavenges cyanide. mHb generation is thought to be a primary mechanism by which the NO(2)(-) ion antagonizes cyanide. On the other hand, NO(2)(-) can undergo biotransformation to generate nitric oxide (NO), which may then directly antagonize cyanide inhibition of CcOX. In this study, nitrite-mediated antagonism of cyanide inhibition of oxidative phosphorylation was examined in rat dopaminergic N27 cells. NaNO(2) produced a time- and concentration-dependent increase in whole-cell and mitochondrial levels of NO. The NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxy 3-oxide (PTIO) reversed this increase in cellular and mitochondrial NO. NO generated from NaNO(2) decreased cellular oxygen consumption and inhibited CcOX activity. PTIO reversed the NO-mediated inhibition, thus providing strong evidence that NO mediates the action of NaNO(2). Under similar conditions, KCN (20muM) inhibited cellular state-3 oxygen consumption and CcOX activity. Pretreatment with NaNO(2) reversed KCN-mediated inhibition of both oxygen consumption and CcOX activity. The NaNO(2) antagonism of cyanide was blocked by pretreatment with the NO scavenger PTIO. It was concluded that NaNO(2) antagonizes cyanide inhibition of CcOX by generating of NO, which then interacts directly with the binding of KCN x CcOX to reverse the toxicity. In vivo antagonism of cyanide by NO(2)(-) appears to be due to both generation of mHb and direct displacement of cyanide from CcOX by NO.