[Redo-operation for the cusp perforation 5 years after aortic valve replacement with stentless bioprosthesis; report of a case].

A 31-year-old male presented with increase of aortic valve regurgitation 5 years after implantation of Prima Plus Stentless bioprosthesis in a bicuspid aortic valve. He underwent redo aortic valve replacement with a mechanical valve concomitant with replacement of the ascending aorta. Pathological examination of the explanted stentless valve presented no inflammatory cell infiltration. The prosthetic valve regurgitation was considered to be due to small injury at the 1st operation.

[Surgical treatment for ischemic heart disease].

BACKGROUND: Surgical treatment for ischemic heart disease (IHD) has changed after the administration of off-pump coronary artery bypass grafting (CABG) [OPCAB] and left ventricular restoration (LVR). We studied the development of the treatment and the surgical results. PATIENTS AND METHODS: Since May 2000 when the indication for OPCAB and LVR was defined, surgical treatment for IHD has been performed in 1,251 patients. The age ranged from 32 to 91 (mean 66 +/- 10) years and there were 977 men and 274 women. The elective operation was 1,130 and emergency 121. Definite indication for OPCAB was calcified ascending aorta, significant cerebrovascular disease, hemorrhagic tendency, and single vessel lesion. Conventional CABG (C-CAB) was the first choice and morbidity and surgical results were examined. RESULTS: OPCAB was performed in 297 (29.9%) and combined operation with CABG was required in 258 patients (20.6%). In elective operation, hospital mortality was one in OPCAB and one in C-CAB. In OPCAB and C-CAB, stroke was none and one, and mediastinitis was 0 and 0, respectively. CONCLUSION: The technique for OPCAB is necessary for CABG; however, it is not appropriate to persist with only OPCAB for CABG. Combined operation is often required with CABG and it is essential to perform precise C-CAB.

[Effectiveness of high frequency jet ventilation introduced immediately after cardiac surgery].

It is important to establish the lung protective strategy strictly for serious respiratory failure after cardiac surgery, because the hemodynamic state is unstable. High frequency jet ventilation (HFJV) was introduced in 5 patients with respiratory failure after cardiac surgery. Two had been diagnosed with acute aortic dissection and 3 with angina pectorlis. Off pump coronary artery bypass grafting was performed in 2 patients. Hemodynamic variables during HFJV were stable, and the duration of HFJV was 9 to 45 hours. Oxygenations improved immediately by the introduction of HFJV in all patients, and no adverse effect was recognized. Therefore, use of HFJV immediately after cardiac surgery might be an effective respiratory therapy of choice for patients with acute lung injury.

Effect of Propionibacterium acnes on the cellular immune responses to tumor-specific antigens on malignant rat liver cells.

The effect of Propionibacterium acnes on the cellular immune responses to tumor-specific membrane antigens was investigated by microcytotoxicity assays (MA) and 51Cr release assays (CRA) with use of mesenteric lymph node cells (LNC) of syngeneic BD IV and BD VI rats. BD rat liver cell lines transformed in vitro by chemical carcinogens were used as target cells with tumor-specific antigens. By MA, the LNC from rats that were inoculated with malignant liver cells under the adjuvant effect of heat-killed P. acnes showed significant cytotoxic response to the target cells but not to nonmalignant liver cells. By CRA, these LNC did not show specific cytolysis to the malignant liver cells. Assays with various target cells derived from BD rat liver and inhibition tests with syngeneic and xenogeneic antisera against tumor-specific antigens on the malignant liver cells proved that LNC reacted with tumor-specific individual or tumor-specific cross-reacting antigens on the malignant liver cells. Cytotoxic responses against the malignant liver cells were not demonstrated even by MA with use of the LNC from rats inoculated with either the malignant liver cells or P. acnes alone. LNC from the rats inoculated with both nonmalignant liver cells and P. acnes were not cytotoxic to malignant or nonmalignant liver cell lines.

Propionibacterium acnes-mediated humoral immune responses to tumor-specific antigens on rat liver cells transformed in vitro by chemical carcinogens.

Effects of Propionibacterium acnes on production of antibodies against tumor-specific membrane antigens were investigated in syngeneic inbred BD IV and BD VI rats. BD rat liver cell lines transformed in vitro by chemical carcinogens were used as target cells for tumor-specific antigens. By membrane immunofluorescence, antibodies against these rat liver cell lines were detected in syngeneic BD rat sera. Antibodies were produced in syngeneic rats under the adjuvant effect of heat-killed P. acnes only. In assays with various target cells and absorption experiments, the antibodies reacted with a tumor-specific individual antigen or tumor-specific cross-reacting antigen on the surfaces of transformed BD rat liver cells. No antibodies against these antigens were found in the sera obtained from syngeneic rats immunized with either the transformed cell lines or P. acnes but not with both. Freund's complete adjuvant did not induce antibodies against these tumor-specific antigens.

Localization of IL-1 beta mRNA and cell adhesion molecules in the maxillary sinus mucosa of patients with chronic sinusitis.

Interleukin-1 beta (IL-1 beta) is a predominant cytokine in retained paranasal sinus fluid of chronic sinusitis where infiltration by polymorphonuclear neutrophils (PMNs) of nasal and paranasal mucosa is characteristic. The authors investigated the localization of IL-1 beta messenger RNA (mRNA) in the maxillary sinus mucosa of patients with chronic sinusitis, using digoxigenin-labeled oligonucleotide probes. IL-1 beta mRNA was detected in some extravascular PMNs and small numbers of mononuclear leukocytes but was not detected in other tissue cells or intravascular leukocytes. The expression and distribution of the cell adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and endothelial-leukocyte adhesion molecule-1 (ELAM-1), were also studied in cultured human mucosal microvascular endothelial cells and in the maxillary sinus mucosa in chronic sinusitis by immunohistochemistry using monoclonal antibodies against these cell adhesion molecules. Only ICAM-1 was expressed on cultured human mucosal microvascular endothelial cells without IL-1 beta stimulation. With IL-1 beta activation of these cells, ELAM-1 was expressed strongly and the expression of ICAM-1 was enhanced. In the maxillary sinus mucosa, ICAM-1 was strongly and universally expressed on endothelial cells of all small vessels, whereas ELAM-1 was expressed only in the subepithelial region. These findings suggest that IL-1 beta, one of mediators in chronic sinusitis, is produced by PMNs, induces the expression of ICAM-1 and ELAM-1 on endothelial cells, and, thereby, stimulates PMN infiltration in chronic sinusitis.

Effects of clarithromycin on cultured human nasal epithelial cells and fibroblasts.

OBJECTIVE/METHODS: Long-term administration of clarithromycin has been reported to be effective in the treatment of chronic sinusitis. To investigate the mechanism underlying the anti-inflammatory activity of clarithromycin, the authors evaluated the effect of clarithromycin on the gene expression of proinflammatory cytokine and the DNA-binding activity of nuclear factor (NF)-kappa B in cultured human nasal epithelial cells and fibroblasts. Cells were incubated with endotoxin purified from nontypable Haemophilus influenzae or interleukin (IL)-1 beta in the presence of clarithromycin. RESULTS: Northern blot analysis revealed that clarithromycin suppressed IL-1 beta gene expression in human nasal epithelial cells stimulated by H. influenzae endotoxin (HIE). Intercellular adhesion molecule-1 gene expression in nasal fibroblasts stimulated by IL-1 beta was also suppressed by clarithromycin. Furthermore, electrophoretic mobility shift assay demonstrated that clarithromycin reduced DNA-binding activity of NF-kappa B in both human nasal epithelial cells and fibroblasts stimulated by HIE or IL-1 beta, respectively. CONCLUSION: The present results suggest that clarithromycin may reduce gene expression of proinflammatory cytokines and adhesion molecules from nasal mucosa at the transcriptional factor level and exert an anti-inflammatory effect on nasal mucosa in chronic sinusitis.

Retention fluids of chronic sinusitis induce neutrophil adherence to microvascular endothelial cells.

The adherence of circulating leukocytes to the vascular endothelium is a critical step in the emigration of leukocytes through blood vessel walls to inflammatory lesions. The influence of nasal secretions on the adherence of neutrophils to the vascular endothelium was investigated using monolayers of human mucosal microvascular endothelial cells derived from the inferior turbinate. Preincubation of vascular endothelial cells with retention fluids from the maxillary sinus of the patients with chronic sinusitis showed increased neutrophil adherence. Recombinant IL-1 beta was also tested and found to induce adherence of neutrophils to human mucosal microvascular endothelial cells. However, no adhesive effect was observed with the nasal secretions of nasal allergy. An enzyme-linked immunosorbent assay detected considerable amounts of IL-1 beta in the chronic sinusitis retention fluids, while the amounts of IL-1 alpha and TNF-alpha were very low. The increased adhesion of the neutrophils by the retention fluids of chronic sinusitis was also neutralized by the incubation with anti-IL-1 beta antibody in a dose dependent manner. These findings suggest that IL-1 beta in the paranasal secretion of chronic sinusitis induces the adherence of neutrophils to vascular endothelium and subsequent infiltration of neutrophils in the paranasal sinuses, thus contributing to the persistence of chronic sinusitis.

Experimental infection of immunocompromised mice with Achromobacter xylosoxidans.

The natural resistance of mice to Achromobacter (A.) xylosoxidans was decreased to 1/80 by a single dose of 250 mg of cylophosphamide (CY) per kg intraperitoneally. When mice were infected with 1 X 10(9) A. xylosoxidans, the numbers of organisms in the liver, spleen, kidneys, lungs and heart blood reached to more than 10(6) per g at 6 hr after infection, and then decreased to less than 10(4) at 96 hr after infection. However, in the CY-treated mice, the numbers of organisms in these organs began to increase rapidly at 6 hr after infection and exceeded 10(9) per g at 48 hr when the mice died. Seventeen of 18 immunocompromised mice and 23 of 24 normal mice which were infected with 1 to 2 X 10(9) organisms of A. xylosoxidans, respectively, were still living until 4 weeks after infection when they were killed and examined. Thirteen of the 33 surviving mice which were examined for bacteriological assay were chronically infected with A. xylosoxidans, some in the spleen, others in the kidney, lung, brain and/or heart blood but none were infected in the liver. Most of the infected and surviving mice had produced an antibody against A. xylosoxidans and its titer was higher in the bacteriologically "cured" group than in the chronically infected one. All surviving mice were resistant to the 2nd challenge with a lethal dose of A. xylosoxidans even when they received an effective dose of CY. The surviving mice showed activated cellular immunity and rather depressed humoral immunity as compared with normal mice or the mice which were infected with killed A. xylosoxidans.

[Effect of therapy using the "receptor-destroying enzyme" of T and B cells on antibody production]. / Influence du traitement par le "receptor destroying enzyme" des cellules T et B sur la production des anticorps

Being interested in knowing if there is any relation between the sialic acid present on the surface of the immunocyte and the antibody formation by the latter, an attempt was made to treat immunocytes, T and B, by RDE before their inoculation into irradiated mice. C57Bl mice of more than 8 weeks of age were used throughout. Cells derived from thymus and those from bone marrow were used as T- and B-cells, respectively. On intravenous injection into irradiated mice of syngeneic T and B cells associated with SRBC, if the T cells were treated by RDE beforehand, the antibody production, as expressed in number of PFC/spleen, was remarkably suppressed when compared with that of mice inoculated with normal cells. It was not the case with the B cells. These facts would permit us to suppose that the sialic acid present on the surface of T cell has an intimate relation with the recognition of antigen by this cell, or else, with the mechanism of transmission of antigenic informations from T cell to B cell.

Effects of magnesium sulfate on the canine cardiovascular system complicating astemizole overdose.

Polymorphic ventricular arrhythmias induced by astemizole overdose have been reported to be successfully managed with intravenous magnesium sulfate. This study was designed to assess the effects of magnesium sulfate on the cardiovascular system, complicating astemizole overdose, the better to understand the therapeutic utility and undesirable effects of magnesium sulfate. Beagle dogs were anesthetized with halothane inhalation (n = 6). Monophasic action potential of the right ventricle, electrocardiogram, and systemic and left ventricular pressure were continuously monitored. Cardiac output was measured by a thermodilution method. Effective refractory period of the right ventricle was assessed by programmed electrical stimulation. An intentionally high dose of astemizole (3 mg/kg, i.v.) prolonged the repolarization and refractory period, while it decreased the sinus automaticity, ventricular contraction, and conduction. A canine antiarrhythmic dose of magnesium sulfate (100 mg/kg, i.v.) was additionally injected 1 h after i.v. astemizole. Magnesium sulfate increased the atrioventricular conduction time, electrical vulnerability, and preload of the left ventricle, while it decreased the blood pressure and cardiac output, besides the effects similar to those observed after i.v. astemizole. The plasma concentration of astemizole was at least 10 times higher than its therapeutic concentration during the experimental period. Magnesium sulfate could be expected to act as a calcium channel blocker during astemizole overdose; however, it may not antagonize the proarrhythmic effects of astemizole.

Rupture of an isolated internal iliac artery aneurysm into the rectum: report of a case.

Aneurysmal rupture into the intestinal tract is a rare but disastrous complication of an internal iliac artery aneurysm. We report herein the successful surgical repair of a fistula between a huge aneurysm of the right internal iliac artery and the rectum in an 81-year-old man. After a femoro-femoral cross-over bypass had been performed, the aneurysm was opened and its patent arterial branches were ligated with sutures. The fistula was then intra-aneurysmally sutured and covered with an omental flap. The diagnostic and therapeutic approaches to this severe complication are discussed with a review of the literature following the presentation of this case.

Delayed manifestation of aortic stenosis after blunt abdominal trauma: report of a case.

Delayed manifestation of aortic stenosis caused by abdominal blunt trauma is rare. We report herein the case of a 67-year-old man who was taken to a nearby hospital after being crushed between a heavy truck and a wall. An emergency laparotomy was performed, revealing only a mesenteric tear which was repaired. He was discharged after an uneventful postoperative course; however, 1 month later he began to experience intermittent claudication, and presented to our hospital in December 1994, 1 year after the first operation. Angiography and enhanced computed tomography (CT) demonstrated infrarenal abdominal aortic dilatation with distal stenosis. Both the dilated and stenotic lesions were resected and bypass surgery ws performed. Pathologic examination demonstrated that the intima had been lacerated circumferentially and everted distally, causing the aortic stenosis. To our knowledge, this is the first case of the delayed manifestation of traumatic aortic stenosis to be documented in Japan. The etiology of this rare complication of blunt trauma is described in this report.

[Modification of the surgical strategy based on intraoperative echographic findings of atherosclerotic ascending aorta].

To prevent the atheroembolic complications such as brain infarction due to the manipulation of atherosclerotic ascending aorta during cardiac surgery, the ascending aorta of 55 patients including 6 emergencies (mean age: 67.7 +/- 6.9 years, valvular disease: n = 12, ischemic heart disease only or combined with valvular disease: n = 43) were evaluated with intraoperative echography as a routine, to enable a proper placement of the cannulae, clamp etc. Irregular elevated lesions into the aortic lumen from the intima were identified in 7 patients (13%, mean age: 71.0 +/- 6.9 years) of ischemic heart disease, which included 2 emergent cases. Arch cannulation was employed in 3 patients with wide-spread lesions on the posterior wall and femoral cannulation was done in 1 patient with wide-spread lesions on the anterior wall. Two of these patients received CABG with in situ arterial conduits under ventricular fibrillation, and the other 2 patients received CABG with aortic cross clamping at the lesion-free site during proximal anastomosis of vein grafts (single clamp technique). Two patients with localized lesion were done CABG with partial aortic clamping and one of them had cerebral infarction during the operation. We recognized that manipulation of the ascending aorta has to be done with a meticulous care and well away from the diseased site. In another patient with localized lesion, the arch cannulation and the single clamp technique were used 2 cm away from that lesion. The brain infarcted patient completely recovered without any sequelae and the others also had no atheroembolic complications. Although calcified lesions on CT were correlated with atheromatous lesions on echogram (p = 0.004), these atheromatous plaques were not detected by enhanced CT, except in only one patient. For screening of the atherosclerosis of ascending aorta, the CT examination was not so effective and the intraoperative echography was the most sensitive and could be easily accomplished. In conclusion, in order to prevent the atheroembolism that might occur due to the improper manipulation of the diseased ascending aorta during usual procedures, surgical strategies have to be modified according to the position, extent and quality of the atherosclerotic lesions, diagnosed by intraoperative echoscanning of the aorta.

Effects of nonsedating antihistamine, astemizole, on the in situ canine heart assessed by cardiohemodynamic and monophasic action potential monitoring.

The possible mechanisms of cardiac adverse effects of astemizole were studied using a halothane-anesthetized in vivo canine model under the cardiohemodynamic and monophasic action potential monitoring. A dose of 0.3 mg/kg of iv astemizole (n = 7), which is close to the recommended dose for clinical use, showed a bradycardic effect and a reversed use-dependent lengthening of repolarization. The increase in the repolarization was greater than in the effective refractory period. These effects persisted even when the plasma drug concentration became undetectable. Additional administration of 3.0 mg/kg of iv astemizole (n = 7) decreased the mean blood pressure, suppressed the cardiac contraction and conduction, and induced early after depolarization-like potential in addition to the qualitatively similar effects compared to those observed by the lower dose. The decrease of the plasma concentration of astemizole followed the pattern predicted by the two-compartment theory of pharmacokinetics, but the drug concentration in the cardiac muscle was estimated to be more than 100 times greater than that in plasma. Our study emphasizes that each cardiac consequence of astemizole overdose may be related to proarrhythmic effects and the monitoring of plasma drug concentration will be less helpful in predicting the cardiac adverse effects of astemizole. The results provide some insights into the clinical cardiotoxicity of astemizole. Drugs or interventions inducing positive chronotropic, inotropic, and dromotropic effects can become good candidates for the treatment of astemizole intoxication, which may attenuate the cardiac effects of astemizole including the lengthening of repolarization.