Cyclic-vomiting syndrome (CVS) is a chronic functional gastrointestinal disorder characterized by recurrent episodes of nausea and vomiting. Although once thought to be a pediatric disorder, there has been a considerable increase in recognition of CVS in adults. The exact pathogenesis is unknown and several theories have been proposed. Migraine and CVS share a similar pathophysiology as suggested by several studies. Since there are no specific biomarkers available for this disorder, physicians should rely on Rome criteria for the diagnosis. Due to the lack of randomized control trials, the treatment of CVS is primarily empirical.

Objective Lidocaine is one of the most widely used local anesthetics with well-known pharmacological properties. The purpose of this systematic review is to investigate the effects of lidocaine on postoperative pain scores and recovery after cardiac surgery. Methods A comprehensive database search was conducted by a reference librarian for randomized clinical trials (RCT) from January 1, 1980 to September 1, 2019. Eligible study designs included randomized controlled trials of lidocaine for postoperative pain management in adults undergoing cardiac surgery. After removal of duplicates, 947 records were screened for eligibility and 3 RCTs met inclusion criteria. Results Sources of bias were identified in 2 of 3 RCTs. Lidocaine was administered intravenously, topically, and intrapleurally. Key findings included [1] 2% lidocaine placed topically on chest tube prior to intraoperative insertion was associated with significantly lower pain scores and lower cumulative doses of fentanyl; and [2] 2% lidocaine administered intrapleurally was associated with significantly lower pain scores and significant improvements in pulmonary mechanics. Lidocaine infusions were not associated with significant changes in pain scores or measures of recovery. No significant associations were observed between lidocaine and overall mortality, hospital length of stay or ICU length of stay. No data were reported for postoperative nausea and vomiting or arrhythmias. Conclusions Due to the favorable risk profile of topical lidocaine and the need for further advancements in the postoperative care of adults after cardiac surgery, topically administered lidocaine could be considered for incorporation into established postoperative recovery protocols.

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The presence of an endogenous nitric oxide synthase (NOS) isoform in cardiac mitochondria remains controversial. NOS catalyzes production of the gaseous signaling molecule nitric oxide (NO•) from arginine. During cardiac ischemia/reperfusion (IR) injury, NO• can react with superoxide (O2•−), derived from a free electron and O2, to form the strong oxidant peroxynitrite (ONOO−), which initiates deleterious post‐translational modifications of cellular proteins and can cause tissue damage. We hypothesized that isolated mitochondria contain endogenous NOS. Our aim was to assess production of ONOO− in isolated cardiac mitochondria under conditions of oxidative/nitrosative stress, and to determine if ONOO− production is dependent on the presence of endogenous mitochondrial NOS. To investigate first if isolated guinea pig cardiac mitochondria contain NOS, Western blot analyses were performed using whole‐heart tissue and percoll‐purified cardiac mitochondria samples with anti‐eNOS and anti‐nNOS antibodies. The bands showed that the reacted eNOS antibody (140 kDa), but not the nNOS, antibody, was detected in both the whole‐heart and isolated mitochondria samples, where band density was much higher. Additionally, mitochondria were suspended in respiratory buffer (pH 7.15), and treated with succinate, a complex II substrate, and CaCl2 followed by menadione, a redox cycler that generates large amounts of O2•−. In physiological buffer, added L‐tyrosine is oxidized by ONOO− to form the fluorescent dimer dityrosine (diTyr). We found that exposing isolated mitochondria energized with succinate to CaCl2 and menadione resulted in an increase in the diTyr fluorescence signal, indicating that the simulated IR injury conditions enhanced mitochondrial ONOO− production. To verify that mitochondrial ONOO− production was dependent on NOS, mitochondria were incubated with the NOS inhibitors L‐NAME/L‐NNA, PTIO, a potent global NO• scavenger, and TEMPOL, a superoxide dismutase (SOD) mimetic. L‐NAME, L‐NNA and PTIO significantly decreased succinate, Ca2+ and menadione‐mediated ONOO− production. TEMPOL also decreased ONOO− levels by converting O2•− to H2O2, as assessed by the HRP/amplex red assay. Some reports furnish evidence that NOS migrates from the cytosol to locate in mitochondrial outer membrane. These results suggest that mitochondrial NOS is responsible for the production of ONOO− during simulated oxidative/ nitrosative stress.Support or Funding InformationNational Heart, Lung, and Blood Institute Training Grant T35 HL072483