Effects of warmed carrier fluid on nefopam injection-induced pain.

BACKGROUND: Nefopam is a non-opioid, non-steroidal analgesic drug with fewer adverse effects than narcotic analgesics and nonsteroidal anti-inflammatory drugs, and is widely used for postoperative pain control. Because nefopam sometimes causes side effects such as nausea, vomiting, somnolence, hyperhidrosis and injection-related pain, manufacturers are advised to infuse it slowly, over a duration of 15 minutes. Nevertheless, pain at the injection site is very common. Therefore, we investigated the effect of warmed carrier fluid on nefopam injection-induced pain. METHODS: A total of 48 patients were randomly selected and allocated to either a control or a warming group. Warming was performed by diluting 40 mg of nefopam in 100 ml of normal saline heated to 31-32℃ using two fluid warmers. The control group was administered 40 mg of nefopam dissolved in 100 ml of normal saline stored at room temperature (21-22℃) through the fluid warmers, but the fluid warmers were not activated. RESULTS: The pain intensity was lower in the warming group than in the control group (P < 0.001). The pain severity and tolerance measurements also showed statistically significant differences between groups (P < 0.001). In the analysis of vital signs before and after the injection, the mean blood pressure after the injection differed significantly between the groups (P = 0.005), but the heart rate did not. The incidence of hypertension also showed a significant difference between groups (P = 0.017). CONCLUSIONS: Use of warmed carrier fluid for nefopam injection decreased injection-induced pain compared to mildly cool carrier fluid.

Effects of nefopam on catheter-related bladder discomfort in patients undergoing ureteroscopic litholapaxy.

BACKGROUND: Patients who undergo urinary catheterization may experience postoperative catheter-related bladder discomfort (CRBD). Previous studies have indicated that drugs with antimuscarinic effects could reduce the incidence and severity of CRBD. Accordingly, this study was carried out to investigate whether nefopam, a centrally acting analgesic with concomitant antimuscarinic effect, reduces the incidence and severity of CRBD. METHODS: Sixty patients with American Society of Anesthesiologists physical status I and II and aged 18-70 years who were scheduled to undergo elective ureteroscopic litholapaxy participated in this double-blinded study. Patients were divided into control and nefopam groups, comprising 30 patients each. In the nefopam group, 40 mg nefopam in 100 ml of 0.9% saline was administered intravenously. In the control group, only 100 ml of 0.9% saline was administered. All patients had a urethral catheter and ureter stent inserted during surgery. The incidence and severity of CRBD, numerical rating scale (NRS) score of postoperative pain, rescue pethidine dose, and side effects were recorded in the post-anesthesia care unit after surgery. RESULTS: The incidence (P = 0.020) and severity (P < 0.001) of CRBD were significantly different between the control group and the nefopam group. The NRS score of postoperative pain (P = 0.006) and rescue dose of pethidine (P < 0.001) were significantly higher in the control group than in the nefopam group. CONCLUSIONS: Intravenous administration of nefopam in patients scheduled to undergo ureteroscopic litholapaxy reduced the incidence and severity of CRBD, NRS score of postoperative pain and analgesic requirements.

The correlation between the Trendelenburg position and the stroke volume variation.

BACKGROUND: The stroke volume variation (SVV), based on lung-heart interaction during mechanical ventilation, is a useful dynamic parameter for fluid responsiveness. However, it is affected by many factors. The aim of this study was to evaluate the effects of SVV on Trendelenburg (T) and reverse Trendelenburg (RT) position and to further elaborate on the patterns of the SVV with position. METHODS: Forty-two patients undergoing elective surgery were enrolled in this study. Fifteen minutes after standardized induction of anesthesia with propofol, fentanyl, and rocuronium with volume controlled ventilation (tidal volume of 8 ml/kg of ideal body weight, inspiration : expiration ratio of 1 : 2, and respiratory rate of 10-13 breaths/min), the patients underwent posture changes as follows: supine, T position at slopes of operating table of -5°, -10°, and -15°, and RT position at slopes of operating table of 5°, 10°, and 15°. At each point, SVV, cardiac output (CO), peak airway pressure (PAP), mean blood pressure, and heart rate (HR) were recorded. RESULTS: The SVV was significant decreased with decreased slopes of operating table in T position, and increased with increased slopes of operating table in RT position (P = 0.000). Schematically, it was increased by 1% when the slope of operating table was increased by 5°. But, the CO and PAP were significant increased with decreased slopes of operating table in T position, and decreased with increased slopes of operating table in RT position (P = 0.045, 0.027). CONCLUSIONS: SVV is subjected to the posture, and we should take these findings into account on reading SVV for fluid therapy.

A comparative study of emergence agitation between sevoflurane and propofol anesthesia in adults after closed reduction of nasal bone fracture.

BACKGROUND: Emergence agitation is associated with increased morbidity and hospital costs. However, there have been few reports in the medical literature on the occurrence of emergence agitation in adults. The aim of this study was to compare emergence agitation between sevoflurane and propofol anesthesia in adults after closed reduction of nasal bone fracture. METHODS: Forty adults (ASA I-II, 20-60 yr) undergoing closed reduction of nasal bone fracture were randomly assigned to either sevoflurane or propofol group and anesthesia was maintained with sevoflurane or propofol. The bispectral index (BIS) was monitored and maintained within 40-60. At the end of surgery, patients were transported to the post anesthetic care unit (PACU) and agitation state scale was checked by Aono's four-point scale (AFPS). Emergence agitation was defined as and AFPS score of 3 or 4. Pain score were measured by numeric rating scale (NRS) on arrival and peak value at PACU. RESULTS: Nine (45.0%) patients in the sevoflurane group and 2 (10.0%) patients in the propofol group developed emergence agitation in the PACU (P = 0.031). There was no correlation between peak NRS and Aono's four-point scale. CONCLUSIONS: Propofol may decrease incidence of emergence agitation compared to sevoflurane in adults undergoing closed reduction of nasal bone fracture.

Obovatol attenuates LPS-induced memory impairments in mice via inhibition of NF-κB signaling pathway.

Neuroinflammation and accumulation of ß-amyloid are critical pathogenic mechanisms of Alzheimer's disease (AD). In the previous study, we have shown that systemic lipopolysaccharide (LPS) caused neuroinflammation with concomitant increase in ß-amyloid and memory impairments in mice. In an attempt to investigate anti-neuroinflammatory properties of obovatol isolated from Magnolia obovata, we administered obovatol (0.2, 0.5 and 1.0 mg/kg/day, p.o.) to animals for 21 days before injection of LPS (0.25 mg/kg, i.p.). We found that obovatol dose-dependently attenuates LPS-induced memory deficit in the Morris water maze and passive avoidance tasks. Consistent with the results of memory tasks, the compound prevented LPS-induced increases in Aß1₋42 formation, ß- and γ-secretases activities and levels of amyloid precursor protein, neuronal ß-secretase 1 (BACE1), and C99 (a product of BACE1) in the cortex and hippocampus. The LPS-mediated neuroinflammation as determined by Western blots and immunostainings was significantly ameliorated by the compound. Furthermore, LPS-induced nuclear factor (NF)-κB DNA binding activity was drastically abolished by obovatol as shown by the electrophoretic mobility shift assay. The anti-neuroinflammation and anti-amyloidogenesis by obovatol were replicated in in vitro studies. These results show that obovatol mitigates LPS-induced amyloidogenesis and memory impairment via inhibiting NF-κB signal pathway, suggesting that the compound might be plausible therapeutic intervention for neuroinflammation-related diseases such as AD.

The Effects of Postoperative Brachial Plexus Block Using MgSO(4) on the Postoperative Pain after Upper Extremity Surgery.

BACKGROUND: Although a brachial plexus block can be used to provide anesthesia and analgesia for upper extremity surgery, its effects using MgSO(4) on postoperative pain management have not been reported. The aim of this study was to evaluate brachial plexus block using MgSO(4) on postoperative analgesia. METHODS: Thirty-eight patients who were scheduled to undergo upper extremity surgery were randomly allocated into two groups: patients receiving axillary brachial plexus block with 0.2% ropivacaine 20 ml and normal saline 2 ml (group S) or 0.2% ropivacaine 20 ml and MgSO(4) 200 mg (group M). Before extubation, the blocks were done and patient controlled analgesia was started, and then, the patients were transported to a postanesthetic care unit. The postoperative visual analogue scale (VAS), opioid consumption, and side effects were recorded. RESULTS: The two groups were similar regarding the demographic variables and the duration of the surgery. No differences in VAS scores were observed between the two groups. There was no statistically significant difference in opioid consumption between the two groups. Nausea was observed in three patients for each group. CONCLUSIONS: Axillary brachial plexus block using MgSO(4) did not reduce the level of postoperative pain and opioid consumption.

4-O-methylhonokiol attenuated memory impairment through modulation of oxidative damage of enzymes involving amyloid-ß generation and accumulation in a mouse model of Alzheimer's disease.

Accumulations of amyloid-ß (Aß) and oxidative damage are critical pathological mechanisms in the development of Alzheimer's disease (AD). We previously found that 4-O-methylhonokiol, a compound extracted from Magnolia officinalis, improved memory dysfunction in Aß-injected and presenilin 2 mutant mice through the reduction of accumulated Aß. To investigate mechanisms of the reduced Aß accumulation, we examined generation, degradation, efflux and aggregation of Aß in Swedish AßPP AD model (AßPPsw) mice pre-treated with 4-O-methylhonokiol (1.0 mg/kg) for 3 months. 4-O-methylhonokiol treatment recovered memory impairment and prevented neuronal cell death. This memory improving activity was associated with 4-O-methylhonokiol-induced reduction of Aß1-42 accumulation in the brains of AßPPsw mice. According to the reduction of Aß1-42 accumulation, 4-O-methylhonkiol modulated oxidative damage sensitive enzymes. 4-O-methylhonkiol decreased expression and activity of brain beta-site AßPP cleaving enzyme (BACE1), but increased clearance of Aß in the brain through an increase of expressions and activities of Aß degradation enzymes; insulin degrading enzyme and neprilysin. 4-O-methylhonkiol also increased expression of Aß transport molecule, low density lipoprotein receptor-related protein-1 in the brain and liver. 4-O-methylhonkiol decreased carbonyl protein and lipid peroxidation, but increased glutathione levels in the brains of AßPPsw mice suggesting that oxidative damage of protein and lipid is critical in the impairment of those enzyme activities. 4-O-methylhonokiol treatment also prevented neuronal cell death in the AßPPsw mousee brain through inactivation of caspase-3 and BAX. These results suggest that 4-O-methylhonokiol might prevent the development and progression of AD by reducing Aß accumulation through an increase of clearance and decrease of Aß generation via antioxidant mechanisms.

4-O-methylhonokiol attenuated ß-amyloid-induced memory impairment through reduction of oxidative damages via inactivation of p38 MAP kinase.

Oxidative stress induced neuronal cell death by accumulation of ß-amyloid (Aß) is a critical pathological mechanism of Alzheimer's disease (AD). Intracerebroventrical infusion of Aß(1-42) (300 pmol/day per mouse) for 14 days induced neuronal cell death and memory impairment, but pre-treatment of 4-O-methylhonokiol (4-O-MH), a novel compound extracted from Magnolia officinalis for 3 weeks (0.2, 0.5 and 1.0 mg/kg) prior to the infusion of Aß(1-42) and during the infusion dose dependently improved Aß(1-42)-induced memory impairment and prevented neuronal cell death. Additionally, 4-O-MH reduced Aß(1-42) infusion-induced oxidative damages of protein and lipid but reduced glutathione levels in the cortex and hippocampus. Aß(1-42) infusion-induced activation of astrocytes and p38 mitogenic activated protein (MAP) kinase was also prevented by 4-O-MH in mice brains. In further study using culture cortical neurons, p38 MAP kinase inhibitor abolished the inhibitory effect of 4-O-MH (10 µM) on the Aß(1-42) (5 µM)-induced reactive oxidative species generation and neuronal cell death. These results suggest that 4-O-MH might prevent the development and progression of AD through the reduction of oxidative stress and neuronal cell death via inactivation of p38 MAP kinase pathway.

The effect of milrinone infusion on right ventricular function during coronary anastomosis and early outcomes in patients undergoing off-pump coronary artery bypass surgery.

BACKGROUND: During coronary anastomosis in off-pump coronary artery bypass surgery (OPCAB), hemodynamic alternations can be induced by impaired diastolic function of the right ventricle. This study was designed to examine the effect of milrinone on right ventricular function and early outcomes in patients undergoing OPCAB. METHODS: Forty patients undergoing OPCAB were randomly assigned in a double-blind manner to receive either milrinone (milrinone group, n = 20) or normal saline (control group, n = 20). Hemodynamic variables were measured after pericardiotomy (T1), 5 min after stabilizer application for anastomosis of the left anterior descending coronary artery (LAD, T2), the obtuse marginalis branch (OM, T3), the right coronary artery (RCA, T4), 5 min after sternal closure (T5), and after ICU arrival. The right ventricular ejection fraction (RVEF) and right ventricular volumetric parameters were also measured using the thermodilution technique. For evaluation of early outcomes, the 30-day operative mortality and morbidity risk models were used. RESULTS: There was no significant difference in hemodynamic variables, including mean arterial pressure, between the 2 groups, except for the cardiac index and RVEF. The cardiac index and RVEF were significantly greater at T3 in the milrinone group than in the control group. CONCLUSIONS: Continuous infusion of milrinone demonstrated a beneficial effect on cardiac output and right ventricular function in patients undergoing OPCAB, especially during anastomosis of the graft to the OM artery, and it had no adverse effect on early outcomes.

Inhibitory effect of ethanol extract of Magnolia officinalis and 4-O-methylhonokiol on memory impairment and neuronal toxicity induced by beta-amyloid.

The components of the herb Magnolia officinalis have exhibited antioxidant and neuroprotective activities. In this study, we investigated effects of ethanol extract of M.officinalis and its major component 4-O-methylhonokiol on memory dysfunction and neuronal cell damages caused by A beta. Oral pretreatment of ethanol extract of M. officinalis (2.5, 5 and 10mg/kg) and 4-O-methylhonokiol (1mg/kg) into drinking water for 5 weeks suppressed the intraventricular treatment of A beta(1-42) (0.5 microg/mouse, i.c.v.)-induced memory impairments. In addition, 4-O-methylhonokiol prevented the A beta(1-42)-induced apoptotic cell death as well as beta-secretase expression. 4-O-methylhonokiol also inhibited H(2)O(2) and A beta(1-42)-induced neurotoxicity in cultured neurons as well as PC12 cells by prevention of the reactive oxygen species generation. 4-O-methylhonokiol also directly inhibited beta-secretase activity and A beta fibrilization in vitro. Thus, ethanol extract of M. officinalis may be useful for prevention of the development or progression of AD, and 4-O-methylhonokiol may be a major active component.

l-Theanine, an amino acid in green tea, attenuates beta-amyloid-induced cognitive dysfunction and neurotoxicity: reduction in oxidative damage and inactivation of ERK/p38 kinase and NF-kappaB pathways.

Amyloid beta (Abeta)-induced neurotoxicity is a major pathological mechanism of Alzheimer disease (AD). In this study, we investigated the inhibitory effect of l-theanine, a component of green tea (Camellia sinensis), on Abeta(1-42)-induced neuronal cell death and memory impairment. Oral treatment of l-theanine (2 and 4 mg/kg) for 5 weeks in the drinking water of mice, followed by injection of Abeta(1-42) (2 microg/mouse, icv), significantly attenuated Abeta(1-42)-induced memory impairment. Furthermore, l-theanine reduced Abeta(1-42) levels and the accompanying Abeta(1-42)-induced neuronal cell death in the cortex and hippocampus of the brain. Moreover, l-theanine inhibited Abeta(1-42)-induced extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase as well as the activity of nuclear factor kappaB (NF-kappaB). l-Theanine also significantly reduced oxidative protein and lipid damage and the elevation of glutathione levels in the brain. These data suggest that the positive effects of l-theanine on memory may be mediated by suppression of ERK/p38 and NF-kappaB as well as the reduction of macromolecular oxidative damage. Thus, l-theanine may be useful in the prevention and treatment of AD.

Chemokines released from astrocytes promote chemokine receptor 5-mediated neuronal cell differentiation.

Astrocytes are one of major glial cell types in the central nervous system (CNS), and can support many functions of neuronal cells. In the present study, we demonstrated that the differentiation of rat embryonic neuronal cells was promoted by treatment with astrocyte and microglia-conditioned medium. Cytokine assays identified that the IL-4, MIP-1, KC, and RANTES as were released from astrocyte, and these chemokines promote differentiation of rat embryonic neuronal cells. However, chemokine-promoted neuronal cell differentiation was suppressed by antibodies of these chemokines and their receptor (CCR5). CCR5 and neuronal cell differentiation marker proteins were found to be colocalized, and their expressions were enhanced by chemokines. Furthermore, the differentiation of neuronal cells from CCR5 knock-out mice and of neuronal cells from mice knocked down with the CCR5 siRNA were significantly reduced and delayed. Bradykinin elevated calcium influx in the embryonic neuronal cells. These data suggest that specific chemokines derived from astrocytes may significantly have influence on the CCR5-mediated differentiation of embryonic neuronal cells.

Protective effect of the ethanol extract of Magnolia officinalis and 4-O-methylhonokiol on scopolamine-induced memory impairment and the inhibition of acetylcholinesterase activity.

Magnolol, honokiol, and obovatol are well-known bioactive constituents of the bark of Magnolia officinalis and have been used as traditional Chinese medicines for the treatment of neurosis, anxiety, and stroke. We recently isolated novel active compound (named 4-O-methylhonokiol) from the ethanol extract of Magnolia officinalis. The present study aimed to test two different doses of ethanol extracts of Magnolia officinalis (5 and 10 mg/kg/mouse, p.o., 1 week) and 4-O-methylhonokiol (0.75 and 1.5 mg/kg/mouse, p.o., 1 week) administered for 7 days on memory impairment induced by scopolamine (1 mg/kg body weight i.p.) in mice. Memory and learning were evaluated using the Morris water maze and the step-down avoidance test. Both the ethanol extract of Magnolia officinalis and 4-O-methylhonokiol prevented memory impairment induced by scopolamine in a dose-dependent manner. The ethanol extract of Magnolia officinalis and 4-O-methylhonokiol also dose-dependently attenuated the scopolamine-induced increase of acetylcholinesterase (AChE) activity in the cortex and hippocampus of mice, and inhibited AChE activity in vitro with IC(50) (12 nM). This study, therefore, suggests that the ethanol extract of Magnolia officinalis and its major ingredient, 4-O-methylhonokiol, may be useful for the prevention of the development or progression of AD.

Reduced anxiety in the mice expressing mutant (N141I) presenilin 2.

Alzheimer's disease (AD) is characterized by progressive cognitive impairment. The effect of presenilin 1 (PS1) and PS2 mutation on cognition has been well characterized in a variety of transgenic mice. However, noncognitive behaviors have not been considered in these mice. In the present study, we found that transgenic mice expressing mutant PS2 (N141I) displayed decreased anxiety behavior determined by the elevated plus maze test and the light dark box test. However, these mice showed biphasic ambulatory activity (hyperactivity followed by hypoactivity) in an open field test. Correlated well with the reduced anxiety, expression of GABA(A)alpha(1) receptor was higher whereas c-Fos was lower in the cortex, hippocampus, and amygdala of the mice expressing PS2 mutation than those of the wild-type PS2 or nontransgenic control mice. These data indicate that PS2 mutation causes reduction of anxiety, and this effect may be related to the change of the expression of GABA(A)alpha(1) receptor and c-Fos. These findings could be useful in the understanding and the treatment of AD patients.

The effects of lidocaine and fentanyl on airway irritability during inhalation induction with desflurane.

BACKGROUND: Inhalation induction with desflurane can cause airway irritability and sympathetic stimulation. The aim of this study was to investigate whether lidocaine and fentanyl could reduce these unwanted reactions. METHODS: Seventy-five patients who had premedication with midazolam were randomly allocated to one of three groups to receive intravenous saline (S group), lidocaine 1.5 mg/kg (L group), fentanyl 1 microgram/kg (F group), respectively, before tidal volume induction with desflurane in oxygen and nitrous oxide. We recorded airway irritability such as cough, apnea, laryngospasm and excitatory movement and hemodynamic changes. RESULTS: Airway irritability was not significantly different between the groups. In F group, mean blood pressure at LOC ver and LOC BIS and heart rate at LOC ver, LOC BIS and just before intubation were lower than those of S group (P < 0.05). Other results were not significantly different. CONCLUSIONS: The results of the study showed that intravenous fentanyl and lidocaine had no beneficial effects to reduce airway irritability, but intravenous fentanyl could significantly reduce hemodynamic stimulation during inhalation induction with desflurane in the patients who were premedicated with midazolam.

Neuro-inflammation induced by lipopolysaccharide causes cognitive impairment through enhancement of beta-amyloid generation.

BACKGROUND: Alzheimer's disease (AD) is characterized by extensive loss of neurons in the brain of AD patients. Intracellular accumulation of beta-amyloid peptide (Abeta) has also shown to occur in AD. Neuro-inflammation has been known to play a role in the pathogenesis of AD. METHODS: In this study, we investigated neuro-inflammation and amyloidogenesis and memory impairment following the systemic inflammation generated by lipopolysaccharide (LPS) using immunohistochemistry, ELISA, behavioral tests and Western blotting. RESULTS: Intraperitoneal injection of LPS, (250 microg/kg) induced memory impairment determined by passive avoidance and water maze tests in mice. Repeated injection of LPS (250 microg/kg, 3 or 7 times) resulted in an accumulation of Abeta1-42 in the hippocampus and cerebralcortex of mice brains through increased beta- and gamma-secretase activities accompanied with the increased expression of amyloid precursor protein (APP), 99-residue carboxy-terminal fragment of APP (C99) and generation of Abeta1-42 as well as activation of astrocytes in vivo. 3 weeks of pretreatment of sulindac sulfide (3.75 and 7.5 mg/kg, orally), an anti-inflammatory agent, suppressed the LPS-induced amyloidogenesis, memory dysfunction as well as neuronal cell death in vivo. Sulindac sulfide (12.5-50 microM) also suppressed LPS (1 microg/ml)-induced amyloidogenesis in cultured neurons and astrocytes in vitro. CONCLUSION: This study suggests that neuro-inflammatory reaction could contribute to AD pathology, and anti-inflammatory agent could be useful for the prevention of AD.

Traumatic tricuspid regurgitation following cardiac massage.

We report a 66-yr-old male patient who developed tricuspid regurgitation secondary to internal cardiac massage. After uneventful off-pump coronary artery bypass surgery, the subject experienced cardiac arrest in the intensive care unit. External cardiac massage was initiated and internal cardiac massage was performed eventually. A transesophageal echocardiography revealed avulsion of the anterior papillary muscle and chordae to the anterior leaflet after successful cardiopulmonary resuscitation. Emergency repair of the papillary muscle was performed under cardiopulmonary bypass.

Estrogen receptor independent neurotoxic mechanism of bisphenol A, an environmental estrogen.

Bisphenol A (BPA), a ubiquitous environmental contaminant, has been shown to cause developmental toxicity and carcinogenic effects. BPA may have physiological activity through estrogen receptor (ER) -alpha and -beta, which are expressed in the central nervous system. We previously found that exposure of BPA to immature mice resulted in behavioral alternation, suggesting that overexposure of BPA could be neurotoxic. In this study, we further investigated the molecular neurotoxic mechanisms of BPA. BPA increased vulnerability (decrease of cell viability and differentiation, and increase of apoptotic cell death) of undifferentiated PC12 cells and cortical neuronal cells isolated from gestation 18 day rat embryos in a concentration-dependent manner (more than 50 microM). The ER antagonists, ICI 182,780, and tamoxifen, did not block these effects. The cell vulnerability against BPA was not significantly different in the PC12 cells overexpressing ER-alpha and ER-beta compared with PC12 cells expressing vector alone. In addition, there was no difference observed between BPA and 17-beta estradiol, a well-known agonist of ER receptor in the induction of neurotoxic responses. Further study of the mechanism showed that BPA significantly activated extracellular signal-regulated kinase (ERK) but inhibited anti-apoptotic nuclear factor kappa B (NF-kappaB) activation. In addition, ERK-specific inhibitor, PD 98,059, reversed BPA-induced cell death and restored NF-kappaB activity. This study demonstrated that exposure to BPA can cause neuronal cell death which may eventually be related with behavioral alternation in vivo. However, this neurotoxic effect may not be directly mediated through an ER receptor, as an ERK/NF-kappaB pathway may be more closely involved in BPA-induced neuronal toxicity.

Tearing of the mitral valve during vent removal after a successful mitral valve repair: a beneficial role of transesophageal echocardiography.

In this case, a successful mitral valve repair was confirmed by transesophageal echocardiography (TEE) at the end of a cardiopulmonary bypass. The left ventricular vent was placed through the mitral valve to remove the air after the TEE examination, and on its way out, the left ventricular vent damaged the anterior mitral leaflet (AML). Re-examination of the valve with TEE detected the new mitral valve insufficiency. The CPB was reinstituted, and tearing of the lateral third part of the anterior mitral leaflet was found. This case emphasizes the importance of TEE in the operating room as a continuous monitor, not only to evaluate the result of the cardiac surgery, but also to detect any unpredictable events during the surgery.