Successful Endovascular Therapy in an Elderly Patient with Severe Hemorrhage Caused by Traumatic Injury.

An 85-year-old female suffered pelvic fracture, multiple rib fractures, right hemopneumothorax, and blunt abdominal aortic injury in a traffic accident. After transfer to our hospital, transcatheter arterial embolization (TAE) was performed immediately for hemorrhage from the bilateral internal iliac arteries. Enhanced computed tomography (CT) after TAE showed an increase of hematoma and extravasation at the bifurcation of the abdominal aorta. Therefore, emergency abdominal endovascular aortic repair was performed on the same day. On the 3rd day after transfer, metabolic acidosis worsened suddenly, and enhanced CT revealed intestinal necrosis. Emergency surgery for the intestinal necrosis was performed. The patient was transferred to the previous hospital on the 31st day after transfer. Endovascular treatment is useful for elderly patients with severe trauma. However, the preservation and/or reconstruction of the blood flow to important organs should be monitored.

Anchor Balloon Technique.

Occlusion of an internal iliac artery or its branches is sometimes required prior to abdominal endovascular aneurysm repair. The Amplatzer vascular plug (AVP) is a useful device for this purpose, but it requires a large lumen catheter or guiding sheath to place it in the intended artery. We propose an anchor balloon technique for advancing this guiding sheath/catheter through a tortuous or angulated iliac artery for AVP placement.

Aortocaval fistula associated with ruptured abdominal aortic aneurysm.

Aortocaval fistula (ACF) is a well-known but uncommon complication of ruptured abdominal aortic aneurysm (AAA). Even with attentive care, oversight of ACFs may occur in emergency cases. Because mortality due to ACF is high, a rapid multidirectional analysis of the preoperative state leading to a correct diagnosis is essential. Here, we report the case of an 82-year-old man with a ruptured AAA and ACF. He presented with multiple organ failure that was initially attributed to congestive heart failure. He underwent emergent surgery and was diagnosed intraoperatively as having an AAA with ACF. He left the hospital 1 month after the operation without complications.

Multiple papillary fibroelastomas of the aortic valve detected by real time three-dimensional transesophageal echocardiographic images.

Papillary fibroelastoma (PFE) is a well-known primary cardiac tumor, but multiple PFEs are rare. We report an interesting case with multiple PFEs that were clearly demonstrated and evaluated with real time three-dimensional (RT3D) transesophageal echocardiography (TEE). A 77-year-old woman was referred to our institution with a diagnosis of osteoarthritis of the hip. Transthoracic echocardiography showed an abnormal structure on the aortic valve. Although two-dimensional TEE revealed typical characteristics of multiple PFE, RT3D TEE clearly demonstrated their number and location on the right and non-coronary cusp of the aortic valve. These results were subsequently confirmed by surgery and pathological findings. RT3D TEE is an exceptionally useful tool for pre-surgical evaluation of PFE. .

[Successful surgical case of DeBakey III b dissecting aortic aneurysm associated with right-sided aortic arch].

A 66-year-old man was admitted to our institute for surgical treatment of chronic dissecting aortic arch aneurysm with right-sided aortic arch which occurred 2 months previously. The size of the aortic arch aneurysm was larger than 6 cm. Total arch replacement using open stent grafting was performed through median sternotomy. The postoperative condition was well, and the patient was discharged without any complications.

The suppression of proinflammatory cytokines improves heart function from non-heart-beating donors following transplantation in a canine model.

We evaluated the effectiveness of a suppressant of the production of proinflammatory cytokines such as interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha on a canine heart transplantation model with non-heart-beating donors (NHBDs).Adult mongrel dogs were divided into 3 groups of 5: a control group; FR-1 in which donors were given FR167653, a potent suppressant of IL-1beta and TNF-alpha production; and FR-2 in which both donors and recipients were given FR167653. After measuring the baseline hemodynamic parameters, including cardiac output (CO), left ventricular pressure (LVP), and maximum and minimum rates of increase in LVP (+/- LVdp/dt), FR167653 was administered continuously for 30 minutes before ischemia in the FR-1 and FR-2 groups. Cardiac arrest was obtained by rapid exsanguination from the abdominal aorta and inferior vena cava. The organ was left in the cadaver for 30 minutes. The coronary vascular beds were washed out with 4 degrees C Celsior solution, and then the donor heart was preserved in 4 degrees C Celsior solution for 4 hours. The donor heart was transplanted orthotopically with cardiopulmonary bypass (CPB). FR167653 was administered intravenously from 15 minutes before aortic-cross clamping until the end of the experiment in the FR-2 group. The recipient was weaned from CPB 1 hour after reperfusion. We compared the hemodynamic parameters at 3 hours after reperfusion with the preoperative values in donor animals with the right atrial pressure at 10 mmHg and a 5 microg/kg/min dopamine infusion. Histopathological analysis was also performed.There were no significant differences in the recovery rates of the hemodynamic parameters between the control and FR-1 groups and between the FR-1 and FR-2 groups. However, the recovery rates of CO and -LVdp/dt in the FR-2 group were significantly (P < 0.05) higher than those in the control group. Histopathological analysis showed that myofilaments were better preserved in the FR-2 group compared with the control group.The administration of a suppressant of proinflammatory cytokines before both ischemia and reperfusion effectively preserves donor heart function after transplantation with NHBDs.

The comparison of mitogen-activated protein kinases that become activated within the left ventricular and right atrial tissues following heart transplantation in canine model.

The activation of p38 mitogen-activated protein kinase (MAPK) plays an important role in ischemia/reperfusion injury. Some reports have documented MAPKs activation of the myocardium in human models, using right atrial (RA) tissue for samples. This study compared the activation of MAPKs in left ventricle (LV) and RA tissues in canine heart transplantation. Four dogs were used as baseline data at two points, before and 20 min after warm ischemia (baseline model), and eight dogs (four pairs of donor and recipient) were used at other points: 4 h after cold ischemia, and at 10, 60, and 180 min after reperfusion (transplantation model). In the transplantation model, donor hearts were left in situ for 20 min after cardiac arrest, and were immersed in Celsior solution for 4 h after coronary flushing. Orthotopic heart transplantation was then performed. Two groups were created: the LV and RA groups (n = 4 in each group). Heart tissue was harvested from the left ventricular wall in the LV group and from the right atrial appendage in the RA group. The activation of MAPKs, including p38 MAPK, c-Jun N-terminal protein kinase (JNK), and extracellular signal-regulated protein kinase (ERK), was evaluated at each point. The activation patterns of p38 MAPK and ERK were similar in the RA and LV groups, but JNK activation was different in the two groups, after ischemia and reperfusion. Thus, RA tissue may be deliberately used as a substitute for LV tissue when investigating the activation of MAPKs in a human model.

Inhibition of cyclooxygenase-2 improves cardiac function following long-term preservation.

BACKGROUND: Cyclooxygenase (COX) is an intracellular enzyme that converts arachidonic acid to prostaglandin endoperoxide (PGG(2)). There are two isoforms of COX, namely constitutive COX-1 and inducible COX-2. It has been reported that COX-2 plays an important role in ischemia-reperfusion injury and that COX-2 mRNA and protein expression were up-regulated during cardiac allograft rejection. FK3311 is a suppressor of COX-2 activation. The purpose of this study was to evaluate the effectiveness of inhibiting COX-2 with FK3311 for the minimization of ischemia-reperfusion injury and for the improvement of donor heart function following transplantation in a canine model. MATERIALS AND METHODS: Adult mongrel dogs were used. After the measurement of hemodynamic parameters [cardiac output (CO), left ventricular pressure (LVP), and the maximum rates of increase and decrease in LVP (+/-LVdp/dt)], coronary vascular beds were washed out with a hypothermic (4 degrees C) University of Wisconsin (UW) solution following cardiac arrest in response to cold (4 degrees C) glucose-insulin-potassium solution. The heart was then excised and preserved in hypothermic (4 degrees C) UW solution for 12 h. FK3311 (3 mg/kg) was administered intravenously to five dogs prior to reperfusion, while vehicle was administered intravenously to a control group (n = 5). After 3 h of orthotopic transplantation using cardiopulmonary bypass, the hemodynamic parameters were compared with preoperative values of the donor animals under the condition of 10 mm Hg right atrial pressure and 5 mug/kg/min dopamine support. RESULTS: The recovery rates of CO and +/-LVdP/dt were significantly (P < 0.05) higher in the FK-treated dogs than in the controls (CO: 93 +/- 6 versus 66% +/- 4%; +LVdp/dt: 125 +/- 8 versus 77 +/- 10%; and -LVdp/dt: 81 +/- 7 versus 52 +/- 6%; for FK-treated versus control dogs, respectively). The recovery rate of LVP was higher in the FK-treated dogs than in the controls (90 +/- 5 versus 72 +/- 5%), but this difference was not statistically significant. Immunohistochemical staining revealed that COX-2 expression was reduced significantly in the myocardium of FK-treated dogs compared with controls. CONCLUSION: Hemodynamic parameters following transplantation were improved significantly in dogs treated with FK3311. Therefore, the inhibition of COX-2 improves transplanted cardiac function following long-term preservation.

Expression of new human inorganic pyrophosphatase in thyroid diseases: its intimate association with hyperthyroidism.

Inorganic pyrophosphatase (PPase) controls the level of inorganic pyrophosphate produced by biosynthesis of protein, RNA, and DNA. Thus, PPase is essential for life. PPase expression is unclear in the thyroid. We cloned a new human PPase, phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPPase), and established a rabbit polyclonal anti-LHPPase antibody. This is the first study to determine the PPase expression by immunohistochemistry and Western blot. Intranuclear LHPPase expression of thyrocytes was enhanced most prominently in Graves' disease and autonomously functional thyroid nodule. To estimate a regulating factor of subcellular localization of LHPPase, we examined its expression of Graves' disease-derived thyrocytes in vitro with the disease-originated serum. Nuclear expression of LHPPase was lost in cultured thyrocytes even with the serum, while its cytoplasmic expression was retained. The data suggest that increased expression of LHPPase is associated with hyperthyroidism. Intranuclear expression of LHPPase may not be regulated by Graves' disease-derived serum factors.

Immunohistochemical analysis of bcl-2, Bax and Bak expression in thyroid glands from patients with Graves' disease.

In order to clarify the role of apoptosis and the expression of Bcl-2 family proteins in the pathology of Graves' disease (GD), we evaluated the apoptosis by in situ end-labeling of fragmented DNA and the expression of Bcl-2, Bax and Bak by immunohistochemistry in thyroid tissues from 20 patients with GD and in normal thyroid tissues from 6 patients with follicular adenoma (N). Apoptotic nuclei were found in thyrocytes and in germinal center of lymphoid follicles. Bcl-2 was strongly expressed in both GD and N thyrocytes. Bax was not expressed in either GD or N thyrocytes. Bak was expressed in thyrocytes from 5 of 20 patients with GD, while it was detected in all N thyrocytes. In lymphoid follicles Bcl-2 was expressed in the mantle zone, while Bax and Bak were both expressed in the germinal center. The percentage of apoptotic nuclei in GD thyrocytes was low (0~3.6%), and negatively correlated with the weight of the thyroid glands resected (rs = -0.43, P<0.05). It was greater in Bak-positive GD thyrocytes than in Bak-negative ones (mean +/- SD; 1.7 +/- 0.7% vs. 0.7 +/- 0.9%, P<0.05). These findings suggest that the differential expression of Bcl-2 family proteins in both thyrocytes and lymphoid follicles may be involved in the pathology of GD.

Effects of adding P38 mitogen-activated protein-kinase inhibitor to celsior solution in canine heart transplantation from non-heart-beating donors.

BACKGROUND: The activation of p38 mitogen-activated protein kinase (MAPK) plays an important role in ischemia-reperfusion injury. This study evaluated the effects of p38 MAPK inhibition using FR167653, a novel p38 MAPK inhibitor, as an additive to Celsior solution in canine heart transplantation from non-heart-beating donors (NHBDs). METHODS: Donor hearts were left in situ for 20 minutes after cardiac arrest, which was induced by rapid exsanguination. Twelve donor-recipient pairs of mongrel dogs were divided into two groups: the control and FR167653 (FR) groups (n=6 each). In both groups, the grafts were subjected to coronary flushing and immersed in Celsior solution for 4 hours with or without FR167653. Orthotopic heart transplantation was then performed. Cardiac output (CO), left ventricular pressure (LVP), and end-systolic maximal elastance (Emax) were measured 2 hours after weaning from cardiopulmonary bypass (CPB), and the hearts were then harvested for histopathologic study. The activation of p38 MAPK was evaluated in another 20 mongrel dogs. RESULTS: In the FR group, CO, LVP recovery rate, and Emax were significantly (P<0.05) higher 2 hours after weaning from CPB, histopathologic damage was attenuated, and the activation of p38 MAPK was significantly (P<0.05) inhibited 10 minutes after reperfusion compared with the control group. CONCLUSIONS: The addition of FR167653 to Celsior solution improved heart-graft viability, probably by way of the inhibition of p38 MAPK activation, which may attenuate ischemia-reperfusion injury in heart transplantation from NHBDs.

The effect of short-term coronary perfusion using a perfusion apparatus on canine heart transplantation from non-heart-beating donors.

BACKGROUND: We investigated the effects of briefly perfusing hearts from non-heart-beating donors (NHBDs) with a Celsior solution before cardiac transplantation. METHODS: Donor hearts were left in situ for 20 minutes after cardiac arrest was induced by rapid exsanguination. Twelve donor-recipient pairs of mongrel dogs were divided into 2 groups, the simple immersion (SI, n = 6) group and the coronary perfusion (CP, n = 6) group. Both groups underwent coronary flushing with Celsior, after which hearts from the SI group were stored using simple immersion for 4 hours and hearts from the CP group underwent 1 hour of further perfusion followed by storage for 3 hours. Orthotopic transplantation was then performed. We measured cardiac output, end-systolic maximal elastance (E(max)), left ventricular pressure, and rate pressure product 1 and 2 hours after weaning from cardiopulmonary bypass (CPB). Two hours after weaning from CPB, the hearts were harvested for histopathologic study and to determine the percentage of water content. RESULTS: The cardiac output (CO) recovery rate was significantly higher in the CP group than in the SI Group 1 hour after weaning from CPB (p < 0.05). The CO recovery rate, E(max), and rate pressure product were significantly higher and the percentage of water content was significantly lower in the CP group than in the SI Group 2 hours after weaning from CPB (p < 0.05). Histopathologic damage was more severe in the SI group. CONCLUSIONS: The results of this study suggest that short-term coronary perfusion with a Celsior solution may be useful for heart transplantation from NHBDs.

Thyrocytes, but not C cells, actively undergo growth and folliculogenesis at the periphery of thyroid tissue fragments in three-dimensional collagen gel culture.

In the thyroid, new follicle formation from preexisting follicles (mother follicle-derived folliculogenesis) has been poorly understood. To address this issue, we analyzed mother follicle-derived folliculogenesis, using a thyroid tissue-organotypic culture that retains three-dimensional follicles with both thyrocytes and C cells over a long period. Three types of mother follicle-derived folliculogenesis occurred only at the periphery of the tissue fragments embedded in collagen gel: (1) solid nest, (2) budding and (3) lumen-dividing types. Immunohistochemistry showed that neogenic follicles rarely had calcitonin-positive C cells. Electron microscopy showed that their component thyrocytes expressed normal polarity. In growth, bromodeoxyuridine uptake of thyrocytes at the tissue periphery was about 5 times the uptake that occurred at the center. C cells had no uptake. Thyrotropin (TSH, 10 mU/ml) and free calcium (0.17~1.95 mM), which are associated with the biological behavior of thyrocytes and C cells, respectively, did not affect the events described above. The data indicate that thyrocytes, but not C cells, actively undergo growth and three types of mother follicle-derived folliculogenesis at the tissue periphery in a TSH- or free calcium-independent manner. This suggests that the tissue periphery, which may escape from contact inhibition of cell growth, is the regenerative site.

A new organotypic culture of thyroid tissue maintains three-dimensional follicles with C cells for a long term.

Thyroid follicles embedded in extracellular matrix (ECM) seem to be supplied enough oxygen by a dense network of capillaries in vivo. Air exposure (AE) causes cells to increase oxygen availability in vitro. We speculated that three-dimensional (3D) environment of ECM together with AE may be applied to a thyroid tissue-organotypic culture, simply simulating such a microenvironment of follicles. To address the issue, we performed 3D collagen gel culture of minced thyroid tissues with or without AE. Most follicles in the tissues without AE died within 7 days. In culture with AE, most of the follicles with calcitonin-positive C cells were kept for over one month. Immunohistochemistry showed that thyrocytes displayed thyroglobulin, thyrotropin receptor, thyroid transcription factor-1 (TTF-1), and pendrin, which are all crucial for thyroid function. C cells expressed calcitonin gene-related peptide and TTF-1. Our study is the first demonstration that 3D collagen gel culture with AE retains 3D thyroid follicles with C cells for a long term. This suggests that ECM and oxygen supply together may be crucial for maintenance of 3D follicle structure and function. Our method will possibly open a new path to the study of thyrocyte-C cell interaction and thyroid biology.