Biomedical subjects

Chaw-Chi Chiu

Publications and source records attributed to Chaw-Chi Chiu.

18 recordsLinked to original sources

PubMed2006

Protective effect of labedipinedilol-A, a novel dihydropyridine-type calcium channel blocker, on myocardial apoptosis in ischemia-reperfusion injury.

The effects of labedipinedilol-A, a novel dihydropyridine-type calcium channel blocker with alpha-/beta-adrenoceptor blocking activities, on myocardial infarct size, apoptosis and necrosis in the rat after myocardial ischemia/reperfusion (45 min/120 min) were investigated. Ten minutes prior to left coronary artery occlusion, rats were treated with vehicle or labedipinedilol-A (0.25 or 0.5 mg/kg, i.v.). In the vehicle group, myocardial ischemia-reperfusion induced creatine kinase (CK) release and caused cardiomyocyte apoptosis, as evidenced by DNA ladder formation and terminal dUTP deoxynucleotidyltransferase nick end-labeling (TUNEL) staining. Treatment with labedipinedilol-A (0.25 or 0.5 mg/kg) reduced infarct size significantly compared to vehicle group (18.75+/-0.65% and 8.27+/-0.29% vs. 41.72+/-0.73%, P<0.01). Labedipinedilol-A also reduced the CK, CK-MB, lactate dehydrogenase (LDH) and troponin T levels in blood. In addition, labedipinedilol-A (0.5 mg/kg) significantly decreased TUNEL positive cells from 19.21+/-0.52% to 9.73+/-0.81% (P<0.01), which is consistent with absence of DNA ladders in the labedipinedilol-A group. Moreover, labedipinedilol-A pretreatment also decreased calcium content in ischemic-reperfused myocardial tissue. In conclusion, these results demonstrate that labedipindielol-A, through reduction of calcium overload and apoptosis, exerts anti-infarct effect during myocardial ischemia-reperfusion and would be useful clinically in the prevention of acute myocardial infarction.

Anesthesia↗

PubMed2006

An avoidable complication of percutaneous coronary intervention-entrapment of stent and disconnected balloon catheter.

During percutaneous coronary intervention, entrapment of catheter materials is a rare but life-threatening complication that sometimes requires emergency surgical treatment. Coronary artery stents have been developed to prevent acute coronary closure and reduce restenosis after coronary angioplasty. The most frequently reported complications of coronary stents are related to stent thrombosis and anticoagulation problems. This case study describes a 60-year-old female who had stable angina pectoris and underwent stent insertion into the left circumflex artery. Unfortunately, the coronary stent with balloon catheter was entrapped while crossing the angulated segment between the left circumflex and left main coronary artery. The stent catheter was surgically removed, and the patient underwent coronary artery bypass grafting successfully. Physicians should keep in mind that extremely angulated segments may reduce the successful rate of coronary stenting and contribute to the stent entrapment complication.

Angioplasty, Balloon, Coronary↗

PubMed2006

Displacement of the beating heart induces an immediate and sustained increase in myocardial reactive oxygen species.

BACKGROUND: Heart manipulation and displacement are common maneuvers during beating heart surgery to expose coronary arteries for revascularization. Effects of heart displacement on free radical generation, reactive oxygen species (ROS) have not been previously described. METHODS AND RESULTS: Seven adult male dogs were anesthetized, a left lateral thoracotomy performed to expose the heart, and the coronary sinus cannulated for ROS sampling during different manipulation protocols: (1) heart in normal position; (2) 90 degree manual heart displacement; (3) Trendelenburg position while the heart displaced 90 degrees and (4) return heart to normal resting anatomical position and plus the operating table returned to horizontal. Heart displacement followed by anatomical re-positioning significantly increased the ROS signal as measured by EPR (50-fold compared with control values; p<0.01). CONCLUSION: Trendelenburg positioning and/or repositioning the heart during cardiac surgery may induce acute reperfusion injury and increase ROS.

Animals↗

PubMed2006

The effects of debanding on the lung expression of ET-1, eNOS, and cGMP in rats with left ventricular pressure overload.

Pulmonary hypertension (PH) usually develops secondary to left ventricular (LV) dysfunction; therefore, it is also called retrograde PH. To investigate our hypothesis that PH is at least partially reversible, as in some congenital heart diseases, in a rat model we investigated whether release of constriction could attenuate pulmonary vascular remodeling and change the expression of endothelin (ET)-1 and endothelial nitric oxide synthase (eNOS). We used rats with LV dysfunction produced by an ascending aortic banding. In this study, there were four groups enrolled: 4-weeks banded (AOB(1-28); n = 7), 7-weeks banded (AOB(1-49); n = 7), debanded groups (AOB(1-28)/DeB(29-49); n = 7), and rats receiving a sham operation (n = 7). Subsequently, there was significant attenuation of medial hypertrophy in pulmonary arterioles and reversal of PH in the AOB(1-28)/DeB(29-49) group (sham, 19 +/- 1.3 mm Hg; AOB(1-28), 31 +/- 2.7 mm Hg; AOB(1-49), 32 +/- 2.7 mm Hg; and AOB(1-28)/DeB(29-49), 20 +/- 1.3 mm Hg). PreproET-1 mRNA and eNOS mRNA were measured by competitive reverse transcriptase (RT) polymerase chain reaction (PCR), and eNOS was measured by Western blotting. Compared with the banded groups, debanding significantly decreased pulmonary preproET-1 mRNA, pulmonary ET-1 (sham, 210 +/- 12 pg/g protein; AOB(1-28), 242 +/- 12 pg/g protein; AOB(1-49), 370 +/- 49 pg/g protein; and AOB(1-28)/DeB(29-49), 206 +/- 1.9 pg/g protein), and plasma ET-1 levels (sham, 10.1 +/- 1.5 pg/ml; AOB(1-28), 13.4 +/- 2.0 pg/ml; AOB(1-49), 15.4 +/- 2.0 pg/ml; and AOB(1-28)/DeB(29-49), 10.3 +/- 0.9 pg/ml protein). Debanding could not, however, alter pulmonary eNOS, eNOS mRNA, or cGMP. These findings suggest that pulmonary vascular remodeling, increased pulmonary arterial pressure, and upregulation of ET-1 gene expression are all reversible. We infer that it is the upregulated gene expression of ET-1, not eNOS, that is closely related to the development of the PH secondary to 4 weeks of aortic banding.

Animals↗

PubMed2005

Tuberculous pericardial abscess: a case report.

We present the case of a 71-year-old diabetic man who came to us complaining of dyspnea for 1 month. Chest X-ray showed cardiomegaly and bilateral pleural effusion. Echocardiography showed a pericardial cystic mass with external compression of the right ventricle. Because of clinically impending cardiac tamponade, we performed urgent sternotomy and removed the pericardial mass without event. Pathologic examination of the excised pericardial specimen showed caseous necrosis compatible with tuberculosis infection. The patient was put on a 1-year treatment regimen of anti-tuberculosis medication. This case is an important reminder that tuberculosis can occur as a pericardial abscess.

Abscess↗

PubMed2005

Ruptured aneurysm of the sinus of valsalva into the right atrium without ventricular septal defect: a case report and literature review.

Aneurysm of the sinus of Valsalva (ASV), frequently associated with ventricular septal defect (VSD), is a rare cardiac disease that may be acquired or congenital. Rupture of an ASV, rare in the noncoronary cusp, usually produces serious hemodynamic change and carries poor prognosis if not treated surgically. We present the case of a 55-year-old female who came to us complaining of exertional dyspnea. Transthoracic echocardiography and aortography showed a noncoronary cusp ASV with rupture into the right atrium but without VSD. Because of high left to right shunt flow, she underwent successful surgical intervention with aneurysm repair approached from both the aorta and right atrium with a knitted Dacron patch. This was a rare case of noncoronary cusp involvement in ASV that ruptured into the right atrium without VSD.

Aneurysm, Ruptured↗

PubMed2005

Labedipinedilol-C: a third-generation dihydropyridine-type calcium channel antagonist displaying K+ channel opening, NO-dependent and adrenergic antagonist activities.

Intravenous and oral labedipinedilol-C showed a dose-dependent long-lasting hypotension and a decrease of heart rate in normotensive and conscious spontaneously hypertensive rats (SHR). In isolated Wistar rat and guinea pig tissues, labedipinedilol-C competitively antagonized (-)isoproterenol-induced cardiac stimulation, tracheal relaxation, and phenylephrine-, CaCl2-, and high-K-induced aorta contractions in a concentration-dependent manner. The estimated pA2 and pKCa values were 8.22+/-0.04 and 7.11+/-0.52, respectively. [H]CGP-12177 binding to ventricle and lung tissues as well as [H]prazosin and [H]nitrendipine binding to brain membranes were inhibited by labedipinedilol-C with Ki values of 2.86, 9.03, 0.39, and 0.05 muM, respectively. The vasorelaxant effects of labedipinedilol-C on phenylephrine (10 microM)-induced contractions were attenuated by removing endothelium, by pretreatment with soluble guanylyl cyclase (sGC) inhibitors ODQ (10 microM) and methylene blue (10 microM), a NOS inhibitor L-NAME (100 microM), a K channel blocker TEA (10 mM), a KATP channel blocker glibenclamide (1 microM), and Ca-dependent K channel blockers apamin (1 microM) and charybdotoxin (0.1 microM). In human umbilical vein endothelial cells (HUVECs), labedipinedilol-C increased NO release, which was significantly inhibited by L-NAME. The Western blot analysis on HUVECs indicated that labedipinedilol-C increased the expression of eNOS. These results indicate that hypotension effects of labedipinedilol-C result from alpha-adrenoceptor and Ca entry-blocking activities and release of NO or NO-related substance from vascular endothelium. The endothelium-independent relaxation of vascular smooth muscle is probably linked to K channel opening and alpha-adrenoceptor-blocking activities.

Adrenergic Antagonists↗

PubMed2005

Aortic smooth muscle relaxants KMUP-3 and KMUP-4, two nitrophenylpiperazine derivatives of xanthine, display cGMP-enhancing activity: roles of endothelium, phosphodiesterase, and K+ channel.

The cellular mechanisms of vasorelaxant effects of newly synthesized KMUP-3 and KMUP-4 were investigated in rat aortic smooth muscle (RASM). KMUP-3 (7-[2-[4-(4-nitrobenzene)piperazinyl]ethyl]-1,3-dimethylxanthine) and KMUP-4 (7-[2-[4-(2-nitrobenzene)piperazinyl]ethyl]-1,3-dimethylxanthine) elicited concentration-dependent relaxation of endothelium-intact and denuded RASM precontracted with phenylephrine. Relaxant responses were also produced by the PDE inhibitors theophylline, milrinone, rolipram, and zaprinast (1 nM-100 microM). The relaxant responses of KMUP-3 and KMUP-4 were reduced by endothelium removal and by the presence of the NOS inhibitor L-NAME (100 microM), the sGC inhibitor ODQ (1 microM), the adenylyl cyclase (AC) inhibitor SQ 22536 (100 microM), and the prostaglandin inhibitor indomethacin (10 microM). Additionally, the vasorelaxations of both agents were also attenuated by pretreatment with the nonselective K+ channel blocker TEA (10 mM), the KATP channel blocker glibenclamide (1 microM), the voltage-dependent K+ (KV) channel blocker 4-AP (100 microM), and Ca(2+)-dependent K+ (KCa) channel blockers apamin (1 microM) and charybdotoxin (ChTX, 0.1 microM). In addition, elevated extracellular K+ (80 mM) interferes with KMUP-3- and KMUP-4-induced vasorelaxations. Preincubation with both agents (1 microM) significantly enhanced the dilator responses of isoproterenol and SNP. KMUP-3 and KMUP-4 inhibited PDE activities and increased cAMP and cGMP levels in primary culture of RASM that were inhibited by SQ 22536 and ODQ, respectively. In cultured HUVECs, KMUP-3 and KMUP-4 (0.1 microM), more potent than YC-1, significantly increased the expression of eNOS protein. In summary, KMUP-3 and KMUP-4 induce aortic relaxations through both endothelium-dependent and -independent mechanisms. Mechanisms of vasorelaxation induced by both compounds involve multiple processes, such as accumulation of cyclic nucleotides partly as a result of PDE inhibition, K-channel activation, and indomethacin-sensitive endothelium function.

Animals↗

PubMed2004

Upregulation of endothelial nitric oxide synthase and endothelin-1 in pulmonary hypertension secondary to heart failure in aorta-banded rats.

This study assessed alterations in expression of pulmonary endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) in rats with pulmonary hypertension (PH) after the ascending aorta had been banded. Rats were studied 12 weeks after banding, which resulted in left heart failure with elevated pulmonary arterial pressure (banded: 31.3 +/- 5.9 (mean +/- SD) mmHg; sham: 20.0 +/- 4.7 mmHg, P<0.05). Competitive reverse transcription-polymerase chain reaction demonstrated significant increases in pulmonary expression of preproET-1 mRNA and eNOS mRNA. Western blot analysis indicated increased pulmonary eNOS protein. Radioimmunoassays indicated increased plasma ET-1 concentrations in the pulmonary artery (banded: 12.4 +/- 1.5 pg/ml; sham: 9.0 +/- 1.3 pg/ml, P<0.01) and increased ET-1 content in lungs (banded: 240 +/- 21 ng/g protein; sham: 203 +/- 20 ng/g protein, P<0.05). There was increased immunohistochemical staining of eNOS and ET-1 in the pulmonary vascular endothelium of aorta-banded rats. Even in the presence of increased eNOS expression, it was not clear how nitric oxide (NO) production (decreased, unchanged, or increased) was involved in the compensatory mechanism to offset pulmonary vasoconstriction. Increased ET-1 expression may be important in mediating PH secondary to aortic banding, and may offer insights into the use of ET-1 antagonists in treating patients with PH secondary to heart failure.

Animals↗

PubMed2004

Is pericardium a suitable calibration reference in integrated backscatter analysis?

To evaluate if pericardium is a suitable calibration reference in the integrated backscatter (IBS) analysis, the grossly normal pericardial specimens from 23 patients without a history of pericarditis were mounted on a steel platform and immersed in a 0.9% saline bath. The 2-D IBS images acquired at the uniform time gain compensation settings of 50 and 70 dB were analyzed. For the pericardial IBS, the limits of agreement for intraobserver and interobserver measurements were -1.2 to 1.4 dB and -1.6 to 2.2 dB, respectively. However, the calibrated IBS intensity of the pericardium presented a rather wide range of variation and was -13 +/- 5 (-5 to -29) and -10 +/- 4 (-4 to -22) dB at the overall gain settings of 50 and 70 dB, respectively. Conclusively, pericardium may not be an ideal IBS calibration reference in a population study of cardiac tissue characterization.

Aged↗

PubMed2004

Coronary artery aneurysms in a young patient with acute myocardial infarction: a case report.

Coronary artery aneurysms are not uncommon. They are usually arteriosclerotic in origin, and may be congenital or secondary to injury, dissection, infection, inflammation, or Kawasaki disease (KD). Herein, we report a case involving a 25-year-old male smoker with acute myocardial infarction (AMI). Coronary angiography showed triple-vessel disease, coronary artery aneurysms, and diffuse ectasia. Coronary artery bypass grafting was performed without complications. Based on his history, serologic examinations, and angiographic findings, we suspected that his coronary artery aneurysms and ectasia were the adult sequelae of KD. This case is a good reminder that KD victims may suffer from young-onset AMI.

Adult↗

PubMed2004

Inhibition of mitogen-mediated proliferation of rat vascular smooth muscle cells by labedipinedilol-A through PKC and ERK 1/2 pathway.

Labedipinedilol-A is a novel 1, 4-dihydropyridine type calcium antagonist with alpha-receptor blocking activity. This study investigates the effects of labedipinedilol-A on mitogen-induced proliferation of rat vascular smooth muscle cells (VSMCs). Labedipinedilol-A's inhibition on cell proliferation was measured by the tetrazolium salt (XTT) test. Labedipinedilol-A dose-dependently inhibited mitogen-induced DNA synthesis, determined by the incorporation of 5-bromo-2'-deoxyuridine (BrdU). Labedipinedilol-A was also found capable of inhibiting the migration of VSMCs induced by PDGF-BB with an IC50 value of 5.6 microM. In accordance with these findings, labedipinedilol-A revealed blocking of the FBS-inducible progression through G0/G1 to S phase of the cell cycle in synchronized cells. Labedipinedilol-A appeared to cause inhibition of mitogens-induced PKC translocation, suggesting the probable involvement of protein kinase C (PKC) in this cellular response. Labedipinedilol-A reduced both intracellular Ca and the phosphorylation of extracellular signal-regulated protein kinase 1/2 in PDGF-BB-stimulated VSMCs. It also suppressed the levels of proliferative cell nuclear antigen (PCNA) in VSMCs both time- and dose-dependently. These results indicate that labedipinedilol-A may inhibit cell proliferation by attenuating activation of the ERK 1/2 pathway, which is regulated by PKC and Ca, suggesting that it may have great potential in the prevention of progressive atherosclerosis.

Animals↗

PubMed2004

Anti-hypertension effect of vanylidilol: a phenylaldehyde alpha/beta-adrenoceptor blocker with endothelium-dependent and K+ channels opening-associated vasorelaxant activities.

The antihypertensive effect of vanylidilol, a new alpha/beta-adrenoceptor antagonist with endothelium-dependent and K(+)-channel-opening activities, was investigated in normotensive and hypertensive Wistar rats. Vanylidilol competitively antagonized (-)isoproterenol-induced positive chronotropic effects, inotropic effects, and tracheal relaxation effects in isolated rat right atria, left atria, and guinea pig tracheal strips in a concentration-dependent manner. Vanylidilol's apparent pA(2) values were 6.36 +/- 0.08 (right atria), 6.41 +/- 0.07 (left atria), and 6.31 +/- 0.06 (trachea). Vanylidilol also produced a competitive antagonism of phenylephrine-induced contraction in the isolated rat aorta with pA(2) values of 6.79 +/- 0.18. In the radioligand binding assay, vanylidilol inhibited [(3)H]CGP-12177 binding to rat ventricle and lung tissues and [(3)H]prazosin binding to brain membranes with Ki values of 535.17, 2,066.69, and 431.11, respectively. In isolated rat thoracic aorta, vanylidilol's vasorelaxant effects on phenylephrine (10 micromol/l)-induced contractions were attenuated by removing endothelium and by the presence of L-N(G)-nitro arginine methyl ester (L-NAME; 100 micromol/l), methylene blue (10 micromol/l), 1H-[1,2,4]oxadiazolol[4,3,-a] quinoxalin-1-one (ODQ; 10 micromol/l), tetraethylammonium (10 mmol/l), glibenclamide (1 micromol/l), apamin (1 micromol/l), and charybdotoxin (0.1 micromol/l). In addition, vanylidilol, in an equally antagonistic activity, inhibited phenylephrine-induced phasic and tonic contractions. Intravenous vanylidilol further reduced mean blood pressure in pentobarbital-anesthetized normotensive Wistar rats in a dose-dependent manner. The oral administration of vanylidilol to conscious spontaneously hypertensive rats had a long-lasting hypotensive effect on the heart rate and decreased it in a dose-dependent manner. Furthermore, vanylidilol's vasodilator effect can be attributed in part to the release of NO or NO-related substance from vascular endothelium, while the endothelium-independent mechanism involved in vanylidilol's relaxation is probably linked to the activation of the K(+) channels and the alpha-adrenoceptor blocking activity in these vessels.

Administration, Oral↗

PubMed2004

Hypotensive effects of eugenosedin-A with serotonin, alpha- and beta-adrenoceptor antagonistic activities in spontaneously hypertensive and normotensive rats.

Eugenosedin-A is a newly synthesized compound with special serotonergic, alpha- and beta1-adrenergic blocking actions. Intravenous injection of eugenosedin-A significantly caused dose-dependent decreases in the mean arterial blood pressure and heart rate in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). The effects of eugenosedin-A-decreased blood pressure and heart rate in SHR were more potent than in WKY. In in vitro experiments, eugenosedin-A competitively antagonized the serotonin-, norepinephrine- and clonidine-induced vasocontraction in a concentration-dependent manner in isolated thoracic aorta of WKY and SHR. We also observed that eugenosedin-A competitively antagonized the isoproterenol-induced positive inotropic effects in a concentration-dependent manner in the isolated left atrium of WKY and SHR. These findings clearly suggested that eugenosedin-A possesses alpha1/alpha2, beta1 and 5-HT2A receptor-blocking activities. The order of pA2 values in isolated tissues of WKY was 5-HT2A > alpha1/alpha2 > beta1. However, the order of pA2 values in isolated tissues of SHR was alpha1/alpha2 > 5-HT2A > beta1. Similarly, we found that the in vitro functional activity of eugenosedin-A is quite different between WKY and SHR. On the other hand, in the isolated rabbit ear artery sensitized with 16 mmol/l K+, eugenosedin-A antagonized 5-nonyloxytryptamine- and serotonin-induced vasocontractions, indicating that it also blocked 5-HT1B and 5-HT2A receptors. In radioligand binding experiments, eugenosedin-A had significant binding affinities on alpha1/alpha2, beta1, 5-HT1B and 5-HT2A receptors. Finally, we suggest that the hypotensive effects of eugenosedin-A can be attributed to its multiple actions on the blockade of 5-HT1B, 5-HT2A, alpha and beta1 receptors in both WKY and SHR strains.

Adrenergic alpha-Antagonists↗

PubMed2003

Exogenous lipoid pneumonia: serial chest plain roentgenography and high-resolution computerized tomography findings.

Between May 1988 and July 2002, six patients with pneumonia due to diesel, animal, or vegetable oil aspiration were admitted to Kaohsiung Medical University Hospital. The purpose of this study was to demonstrate distinctive radiographic findings of oil-induced lipoid pneumonitis on initial serial chest roentgenograms and high-resolution computerized tomography (CT) scans. Initial chest roentgenograms (n = 6), CT scans (n = 6), and roentgenography and CT follow-up studies were analyzed retrospectively by two chest radiologists and two surgeons, focusing on the pattern and distribution of parenchymal abnormalities. The most common location was the right middle lobe, followed by the right lower lobe, the left lower lobe, and the lingular lobe. Follow-up chest roentgenograms (n = 6) showed complete disappearance of the parenchymal lesions in only one patient and partial decrease in the extent of lesions in five patients. Lipoid pneumonia presents non-specific findings on chest roentgenography. It is commonly located in both lower and the right middle lobes. On high-resolution CT, the lesions appear most commonly as areas of consolidation, ground-glass attenuation mixed with paving pattern, and poorly defined nodules.

Adult↗

PubMed2002

Vanillylamide-based propanolamine derivative displays alpha/beta-adrenoceptor blocking and vasodilating properties.

A propanolamine derivative with vanillylamide base, KMUP 880602, was first investigated under in vivo and in vitro conditions. IV KMUP 880602 (0.1, 0.5, 1.0, and 2.0 mg/kg) produced dose-dependent hypotensive and bradycardia responses in pentobarbital-anesthetized Wistar rats. KMUP 880602 also markedly inhibited both the tachycardia effects induced by (-)isoproterenol and arterial pressor responses induced by phenylephrine. In isolated guinea pig tissues, KMUP 880602 competitively antagonized (-)isoproterenol-induced positive inotropic and chronotropic effects of the atria and tracheal relaxation responses. The apparent pA2 values KMUP 880602 were 7.24 +/- 0.08 (right atria), 7.42 +/- 0.07 (left atria), and 6.24 +/- 0.06 (trachea). KMUP 880602 also produced a competitive antagonism of norepinephrine-induced contraction in the isolated rat aorta with pA2 values of 7.64 +/- 0.18. In the radioligand-binding assay, [3H]CGP-12177 binding to rat ventricle and lung tissues and [3H]prazosin binding to brain membranes were inhibited by KMUP 880602 with pKi values of 7.27, 6.08, and 8.25, respectively. In isolated rat thoracic aorta, the vasorelaxant effects of KMUP 880602 on phenylephrine-induced contractions were attenuated by pretreatment with tetraethylammonium (10-3 M) and charybdotoxin (10-7 M) but not by glibenclamide, 4-aminopyridine, and apamin. In conclusion, KMUP 880602 is an alpha/beta-adrenoceptor blocker, with selective beta1-adrenoceptor blocking and vascular smooth muscle relaxation activities. Particularly, the vasorelaxant effect of KMUP 880602 is partially mediated by the opening of charybdotoxin-sensitive K+ channel.

Adrenergic alpha-Antagonists↗

PubMed2002

Impact of management of abdominal aortic dissection following the successful operation of annulo-aortic ectasia in Marfan's syndrome--a case report.

A 21-year-old female patient with Marfan's syndrome suffering from chronic ascending aortic dissection and aortic insufficiency was treated with total aortic root replacement by Cabrol technique (or procedure). The post-operative course was smooth and the patient recovered satisfactorily with very stable hemodynamic condition and good appetite. Unfortunately she complained of sudden severe abdominal pain followed by complete anuria on the fifth post-operative day. The MRI demonstrated abdominal aortic dissection with malperfusion of all the abdominal organs. Rapid increase of aminotransferases (SGOT and SGPT), severe acidosis and rapid deterioration of vital signs within 10 hours discouraged us from trying surgical intervention. The puzzle of management in those cases will be discussed.

Adult↗

PubMedDate not supplied

Management of intractable sternal wound infections with topical negative pressure dressing.

BACKGROUND: Sternal osteomyelitis after cardiac surgery is a life-threatening complication. The potential spread of infection into the mediastinum, involving the prosthetic valve, grafts, and suture lines, makes this an extremely serious complication confronting both cardiac and plastic surgeons. AIM: Topical negative pressure (TNP) dressing has been proven to be effective for wound healing. We want to take advantages of this equipment to improve the results of intractable sternal wound infection. The results are discussed. METHODS: From December 1996 to July 2002, 25 patients with sternal wound infections were treated at Kaohsiung Medical University Hospital. Nine patients suffering intractable sternal osteomyelitis were managed with debridement and TNP dressings. These patients received 1-3 debridements (an average of 2.2 debridements), and the average TNP dressing treatment period was 20.2 days (ranging from 3 to 43 days). After management, the infections were controlled and healthy vascularized wounds were achieved. Then, flap reconstruction could be performed for complete wound closure. Seven of the nine patients survived, and there was no recurrence of sternal osteomyelitis during follow-up period (ranging from 5 to 70 months). CONCLUSION: The advantages of applying TNP dressings in cases of intractable sternal wound infections include (1) protecting the underlying mediasternal structure from infection, (2) permitting delayed sternal closure to avoid cardiac compression induced compromised cardiopulmonary function, (3) possibility of repeated wound inspection and bedside debridement, (4) cost-effectiveness of wound care, and (5) providing an option to promote sternal wound secondary healing for patients in poor physical condition.

Aged↗