CLINICAL PRESENTATION AND INTERVENTION: A 41-year-old man with previous bilateral pheochromocytoma presented with chest pain. He was suffering from cardiac failure and persistent hypotension requiring an inotrope. Cardiac markers, an electrocardiogram and an echocardiogram confirmed acute myocardial infarct with poor ejection fraction and global hypokinesia. An (18)F-fluorodeoxyglucose PET/CT scan showed progressive left suprarenal and organ of Zuckerkandl pheochromocytomas. Blood pressure stabilisation proved challenging but was achieved by titrating an incremental dose of α-blocker against a tapering inotropic dose.
CONCLUSION: This case showed the efficacy of an α-blocker despite persistent hypotension in a patient with pheochromocytoma-induced cardiomyopathy.
MATERIALS AND METHODS: Tincture of the roots was concentrated to dryness by evaporating the ethanol in vacuo. This ethanolic extract was partitioned into 5 fractions sequentially with hexane, dichloromethane (DCM), ethyl acetate, butanol, and water. The corpus cavernosum relaxant activity of each fraction was investigated. The DCM fraction which showed the highest potency in relaxing phenylephrine-precontracted corpora cavernosa was purified by column chromatography. The effects of the most potent DCM subfraction in relaxing phenylephrine-precontracted corpora cavernosa, DCM-I, on angiotensin I- or angiotensin II-induced contractions in corpora cavernosa were investigated. The effects of DCM-I pretreatment on the responses of phenylephrine-precontracted corpora cavernosa to angiotensin II or bradykinin were also studied. An in vitro assay was conducted to evaluate the effect of DCM-I on angiotensin-converting enzyme activity.
RESULTS: Fraction DCM-I decreased the maximal contractions (100%) evoked by angiotensin I and angiotensin II to 30 ± 14% and 26 ± 16% (p < 0.001), respectively. In phenylephrine-precontracted corpora cavernosa, DCM-I pretreatment caused angiotensin II to induce 82 ± 27% relaxation of maximal contraction (p < 0.01) and enhanced (p < 0.001) bradykinin-induced relaxations from 47 ± 8% to 100 ± 5%. In vitro, DCM-I was able to reduce (p < 0.001) the maximal angiotensin-converting enzyme activity to 78 ± 0.24%.
CONCLUSION: Fraction DCM-I was able to antagonize angiotensin II-induced contraction to cause corpus cavernosum relaxation via inhibition of angiotensin II type 1 receptor and enhance bradykinin-induced relaxation through inhibition of angiotensin-converting enzyme.
MATERIALS AND METHODS: A total of 180 root slices from 60 single-canal anterior teeth were prepared and assigned to 5 experimental groups (n = 36 in each group), designated as G1 (AH Plus®/gutta-percha), G2 (TotalFill BC™ sealer/BC-coated gutta-percha), G3 (TotalFill BC™ sealer/gutta-percha), G4 (EndoREZ® sealer/EndoREZ®-coated gutta-percha), and G5 (EndoREZ® sealer/gutta-percha). Push-out bond strengths of 18 root slices in each group were assessed at 2 weeks and the other 18 at 3 months after obturation using a universal testing machine. Data were analyzed using repeated measures ANOVA. An independent t test was used to compare the mean push-out bond strength for each group at 2 weeks and 3 months after obturation.
RESULTS: The mean push-out bond strengths of G4 and G5 were significantly lower than those of G1, G2, and G3 (p < 0.05) at both 2 weeks (G1: 1.46 ± 0.29 MPa, G2: 1.74 ± 0.43 MPa, G3: 1.74 ± 0.43 MPa, G4: 0.66 ± 0.31 MPa, G5: 0.74 ± 0.47 MPa) and 3 months after obturation (G1: 1.70 ± 1.05 MPa, G2: 3.69 ± 1.20 MPa, G3: 2.84 ± 0.83 MPa, G4: 0.14 ± 0.05 MPa, G5: 0.24 ± 0.10 MPa). The mean push-out bond strengths of G2 (3.69 ± 1.20 MPa) and G3 (2.84 ± 0.83 MPa) were higher at 3 months compared to 2 weeks after obturation (G2: 1.74 ± 0.43 MPa, G3: 1.33 ± 0.29 MPa).
CONCLUSION: The TotalFill BC™ obturation system (G2) and the TotalFill BC™ sealer/gutta-percha (G3) showed comparable bond strength to AH Plus®. Their bond strength increased over time, whereas the EndoREZ® obturation system (G4) and EndoREZ sealer (G5) had low push-out bond strength which decreased over time.