Secondary ileal lymph node metastases from rectal cancer: a case report.

BACKGROUND: Colorectal cancer can invade adjacent organs, but rarely metastasizes to the regional lymph nodes (LNs) of the invaded organ. Herein, we report a case of rectal cancer invading the ileum and metastasized to the regional ileal LNs. CASE PRESENTATION: A 77-year-old male presented abdominal pain and anorexia, diagnosed with rectal cancer invading the small intestine and concurrently metastasized to the regional LN of the intestine and liver. High anterior resection and partial resection of the small intestine was performed, then, the patient was referred to our hospital for chemotherapy. We performed 17 cycles of systemic chemotherapy that achieved a partial reduction in size of the LN, followed by an ileocecal resection with ileal mesentery resection for regional LNs removal. Histopathological analysis of the resected ileal LNs and six liver lesions revealed a moderately differentiated tubular adenocarcinoma. The patient was discharged on postoperative day 18. Cancer recurrences developed in the lungs 5 months after the surgery, then to the liver and peritoneum, and further surgery and chemotherapy were performed. Despite the challenging presentation, the patient survived for 40 months after the first surgery. CONCLUSIONS: We report a rare case of a surgical resection of a secondary ileal LN metastasis from rectal cancer. The patient survives for a relatively long time after surgical resection. When colorectal cancer invades the small intestine, clinicians should consider the possibility of secondary LN metastasis in the invaded site.

How to do it: rescue duct-to-duct biliary reconstruction techniques to avoid severe biliary complications of hepatic resection for hepatocellular carcinoma.

There are few reports on duct-to-duct biliary reconstruction for complex liver resection with limited bile duct resection. We performed duct-to-duct biliary reconstruction in two patients undergoing limited bile duct resection where Roux-en-Y hepaticojejunostomy (HJ) was difficult. An external biliary drainage tube was placed routinely at the anastomotic site to prevent stenosis. In case 1, the tumor-infiltrated part of the left hepatic duct (LHD) was resected and the LHD was repaired using duct-to-duct reconstruction with interrupted sutures. In case 2, after the tumor-infiltrated part of the LHD and posterior hepatic duct (PHD) were resected, T-tube reconstruction was performed on the PHD, and the LHD was anastomosed using interrupted sutures for the posterior wall and a round ligament patch for the anterior wall. Our literature review suggests that an external biliary drainage tube with stenting over the anastomosis may reduce the risk of biliary complications.

Finite Element Modeling for Biomechanical Comparisons of Multilevel Transforaminal, Posterior, and Lateral Lumbar Approaches to Interbody Fusion Augmented with Posterior Instrumentation.

OBJECTIVE: Verifying the intervertebral stability of each intervertebral fusion procedure, including transforaminal, posterior, and lateral lumbar interbody fusion (TLIF, PLIF, and LLIF, respectively), and the ratio of stress on the rods and pedicle screws during initial fixation may help select a fixation procedure that reduces the risk of mechanical complications, including rod fracture and screw loosening. Thus, we aimed to assess whether these procedures could prevent mechanical complications. METHODS: Using the finite element method (FEM), we designed 4 surgical models constructed from L2-5 as follows: posterior lumbar fusion (PLF), TLIF, PLIF, and LLIF models. Bilateral rods and each pedicle screw stress were tracked and calculated as Von Mises stress (VMS) for comparison among the PLF and other 3 interbody fusion models during flexion, extension, and side-bending movements. RESULTS: The lowest rod VMS was LLIF, followed by PLIF, TLIF, and PLF in flexion and side bending movements. Compared with PLF, intervertebral fixation significantly reduced stress on the rods. No remarkable differences were observed in extension movements in each surgical procedure. A tendency for higher pedicle screw VMS was noted at the proximal and distal ends of the fixation ranges, including L2 and L5 screws for each procedure in all motions. Intervertebral fixation significantly reduced stress on the L2 and L5 screws, particularly in LLIF. CONCLUSIONS: Stress on the rods and pedicle screws in the LLIF model was the lowest compared with that induced by other intervertebral fusion procedures. Therefore, LLIF may reduce mechanical complications occurrence, including rod fracture and screw loosening.

Bowel perfusion demonstrated using indocyanine green fluorescence imaging in two cases of strangulated ileus.

We report the use of indocyanine green (ICG) fluorescence for intraoperative diagnosis in two cases of strangulated ileus. We successfully preserved the bowel and avoided postoperative complications by detecting adequate perfusion and no necrosis in the intestine's strangulated regions. In the first case, enhanced computed tomography (CT) revealed a closed loop intestine, which showed poor contrast, and we performed laparotomy with ICG fluorescence. In the second case, the CT scan revealed bowel obstruction without ascites. We conservatively treated the patient with the insertion of a long tube. The patient's condition did not improve, and we performed laparotomy using ICG fluorescence. In both of these cases, the visual observation during laparotomy showed that the ileum had dark-red discoloration. We demonstrated perfusion and preserved the ileum by injecting 2.5 mg of ICG intravenously; fluorescence was observed in the dark-red ileum using the PINPOINT system (Novadaq, Kalamazoo, MI, US). Both patients recovered successfully after the surgery with no adverse events. Our data suggest that ICG fluorescence imaging can be one of the decision-making modalities in patients with strangulated ileus.

Comparison of the Susceptibility to Implant Failure in the Lateral, Posterior, and Transforaminal Lumbar Interbody Fusion: A Finite Element Analysis.

OBJECTIVE: There are several techniques for lumbar interbody fusion, and implant failure following lumbar interbody fusion can be troublesome. This study aimed to compare the stress in posterior implant and peri-screw vertebral bodies among lateral lumbar interbody fusion (LLIF), posterior lumbar interbody fusion (PLIF), and transforaminal lumbar interbody fusion (TLIF) and to select the technique that is least likely to cause implant failure. METHODS: We created an intact L3-L5 model and simulated the LLIF, PLIF, and TLIF techniques at L4-L5 using finite element methods. All models at the lower portion of L5 were fixed and imposed a preload of 400 N and a moment of 7.5 Nm on the upper portion of L3 to simulate flexion, extension, lateral bending, and axial rotation. We investigated the peak stresses and stress concentration in the posterior implant and peri-screw vertebral bodies for the LLIF, PLIF, and TLIF techniques. RESULTS: The extension, flexion, bending, and rotation peak stresses and stress concentration in the posterior implant, as well as the peri-screw vertebral bodies, were the lowest in LLIF, followed by PLIF and TLIF. CONCLUSIONS: It was found that implant failure was least likely to occur in LLIF, followed by PLIF and TLIF. Hence, surgeons should be aware of these factors when selecting an appropriate surgical technique and be careful for implant failure during postoperative follow-up.

[A patient with autoimmune pancreatitis complicated by pancreatic pseudocyst that caused colonic perforation-induced gastrointestinal bleeding].

A 62-year-old male patient was referred to our hospital for jaundice and bloody feces. He had hyper-IgG4-emia. Computed tomography (CT) showed diffuse pancreatic enlargement, pancreatic pseudocyst, and hematoma of the splenic flexure of the colon. Magnetic resonance imaging (MRI) showed a fistula in the pancreatic pseudocyst and splenic flexure of the colon. Moreover, lower gastrointestinal endoscopy showed a fistula in the same region. Endoscopic retrograde cholangiopancreatography (ERCP) showed narrowing of the main pancreatic duct and stenosis of the lower bile duct. Following this, the patient was diagnosed with autoimmune pancreatitis-induced pancreatic pseudocyst and colonic perforation-induced gastrointestinal bleeding. The pancreatic pseudocyst and fistula were resolved through steroid treatment.

Laparoscopic hemostasis for abdominal brunt massive hemorrhage due to endometriosis.

In the gynecological literature, a limited number of studies have reported intraperitoneal bleeding due to abdominal blunt trauma. In this report, we describe a rare case of massive intraabdominal hemorrhage from the uterine artery triggered by a fall injury without apparent abdominal bruising in the presence of severe endometriosis and a uterine fibroid. A 28-year-old woman who fell from a railway platform was transported to an emergency hospital. Although she did not sustain abdominal bruising and initially had no abdominal symptoms, she complained of gradually worsening abdominal pain. Abdominal CT identified intraabdominal massive hematoma, and emergency exploratory laparoscopy revealed active bleeding from the right uterine artery eroded by endometriosis, which was treated with laparoscopic electrocoagulation. The cause of the intraabdominal bleeding was associated with avulsion of the endometriosis adhesion between the right perimetrium and the right uterine artery due to inertial forces of the uterus during the fall injury. A uterine fibroid discovered during laparoscopy was suspected to strengthen the inertial forces of the uterus. In the case of hemoperitoneum after trauma, gynecological sources of bleeding must be kept in mind, especially for patients with a known history of fibroids or endometriosis.

Detailed anatomy and procedure of celiac artery decompression in median arcuate ligament syndrome.

PURPOSE: Median arcuate ligament (MAL) syndrome is a clinical syndrome caused by the compression of the celiac artery (CA) by the MAL. This study aimed to present the detailed anatomy and a step-by-step procedure of CA decompression for MAL syndrome. METHODS: The CA decompression procedure involves exposing the diaphragmatic crura and aorta, taping the left gastric artery, and dividing the compressive tissues. The MAL and ganglionic tissue, which form a broad band with multiple layers overlying the CA, comprise the compressive tissues. Therefore, the compressive tissues overlying the CA are encircled and divided one by one until the CA stenosis is released. CA decompression is confirmed with intraoperative duplex ultrasonography of the CA, with a return to normal peak systolic velocities without variation between deep inspiration and expiration. CONCLUSION: This report presents the detailed anatomy and procedural steps for CA decompression in MAL syndrome.

Arterial communication around the pancreatic tail enabled division of the gastroduodenal artery during pancreaticoduodenectomy in patient with complete celiac artery occlusion: a case report.

BACKGROUND: Stenosis or obstruction of the celiac artery (CA) is known as celiac artery stenosis (CAS) and is usually accompanied by the formation of arterial anastomosis between the superior mesenteric artery (SMA) system and the CA system. Arterial bypass is mainly achieved through the gastroduodenal artery (GDA); therefore, the division of the GDA during pancreaticoduodenectomy (PD) could pose a problem in patients with CAS. CASE PRESENTATION: We reported a case of PD presenting complete occlusion of the CA, in which perfusion to organs in the CA system was maintained via peri-pancreatic arterial communication. There were complicated arterial anastomoses around the pancreas, which were clearly visualized on a three-dimensional reconstruction of the arterial system using multi-detector computed tomography. Among these complicated anastomoses, one well-developed anastomosis between the SMA and the splenic artery through the dorsal pancreatic artery (DPA) was identified. The DPA was considered to work as a potential collateral pathway from the SMA to organs in the CA system after division of the GDA. During surgery, Doppler ultrasonography detected hepatopetal arterial flow even after the GDA clamping; therefore, we performed typical PD with division of the GDA. The postoperative course of the patient was uneventful, and there was no sign of ischemic complications in the CA system organs including the liver, stomach or spleen. CONCLUSIONS: Three-dimensional reconstruction of the arterial system using multi-detector computed tomography and the intraoperative GDA clamping test were useful to determine whether it was possible to divide the GDA in PD, in the case of CAS.

Prostatic ischemia induces ventral prostatic hyperplasia in the SHR; possible mechanism of development of BPH.

In the light of increasing evidence that benign prostatic hyperplasia is associated with cardiovascular disease, we have investigated the relationship between prostatic blood flow and prostatic hyperplasia in the spontaneously-hypertensive-rat (SHR). Twelve-week-old male SHRs were treated with nicorandil for six weeks. Wistar-Kyoto rats were used as controls. Six weeks after nicorandil treatment, blood pressure and the prostatic blood flow were estimated, and tissue levels of malondialdehyde, HIF-1α, TGF-ß1, bFGF, dihydrotestosterone, and α-SMA were measured. SHRs showed significant increases in blood pressure, tissue levels of malondialdehyde, HIF-1α, TGF-ß1, bFGF, α-SMA and a significant decrease in the prostatic blood flow. Although treatment with nicorandil failed to alter the blood-pressure and α-SMA, it significantly ameliorated the increased levels of malondialdehyde, HIF-1α, TGF-ß1, and bFGF. There were no significant differences in tissue levels of dihydrotestosterone among any groups. These data indicate that development of prostatic hyperplasia may be associated with prostatic hypoxia, which nicorandil prevents via its effect to increase the blood flow.

Olmesartan ameliorates urinary dysfunction in the spontaneously hypertensive rat via recovering bladder blood flow and decreasing oxidative stress.

PURPOSE: As hypertension (HT) is one of the risk factors for lower urinary tract symptoms, we investigated the effect of an angiotensin II type I receptor blocker, olmesartan, on bladder dysfunction in the spontaneously hypertensive rat (SHR). MATERIALS AND METHODS: Twelve-week-old male SHRs were administered perorally with olmesartan (0, 1, or 3 mg/kg/day) or nifedipine (30 mg/kg/day) for 6 weeks. Wistar rats were used as normotensive controls. The effects of olmesartan or nifedipine on blood pressure (BP), bladder blood flow (BBF), urodynamic parameters, tissue levels of malondialdehyde (MDA), nuclear factor erythroid 2-related factor 2 (Nrf2), and nerve growth factor (NGF) were measured in the bladder. Localization of 4-hydroxy-2-nonenal (4-HNE), Nrf2, and NGF in the bladder was shown by immunohistochemistry. RESULTS: The SHRs showed significant increase in BP, micturition frequency, and expression of MDA, 4-HNE, Nrf2, and NGF when compared to the control Wistar rats. Conversely, there was a decrease in BBF and single voided volume in SHRs when compared to Wistar rats. Treatment with olmesartan and nifedipine significantly improved BP. However, only olmesartan significantly ameliorated urodynamic parameters and oxidative damage compared to the non-treated SHR. The immunoreactivities of 4-HNE, Nrf2, and NGF in SHR urothelium and blood vessels were increased compared to the control. Treatment with a high dose of olmesartan decreased the expressions of 4-HNE, Nrf2, and NGF in the bladder. CONCLUSION: Our data suggest that BP, BBF, and oxidative stress may be responsible for the functional changes in HT-related bladder dysfunction. Olmesartan significantly ameliorated this bladder dysfunction.

Characterization of silodosin and naftopidil in the treatment of bladder dysfunction in the spontaneously hypertensive rat.

PURPOSE: As increasing evidence suggest that α(1)-blockers prevent benign prostatic hyperplasia related overactive bladder and nocturia in the human, we investigated the effects of silodosin and naftopidil on hypertension-related bladder dysfunction in the spontaneously hypertensive rat (SHR) model. MATERIALS AND METHODS: Twelve-week-old male SHRs received no treatment or treatment with silodosin (100 µg/kg, p.o.) or naftopidil (10 or 30 mg/kg, p.o.) once daily for 6 weeks. Wistar rats were used as normotensive controls. After 6-week treatment, voiding functions were estimated by metabolic cages (dark- and light-cycle separately) and cystometric studies. Furthermore, the bladder blood flow (BBF) was measured employing the hydrogen clearance method. RESULTS: SHRs showed significant increases in micturition frequency, and decreases in BBF and single voided volume in both metabolic cages and cystometrograms compared to the Wistar group. Treatment with silodosin normalized the decreased BBF, and treatment with naftopidil increased the BBF in a dose-dependent manner in the SHR group. Although treatment with silodosin and the high dose of naftopidil significantly inhibited micturition frequency in one day, only treatment with the high dose of naftopidil significantly inhibited micturition frequency and urine production in the light-cycle compared to the non-treated SHRs. Although treatment with silodosin and the high dose of naftopidil significantly increased single voided volume, only treatment with silodosin significantly inhibited non-voiding contractions in the cystometrgrams. CONCLUSION: Our data suggest that both silodosin and naftopidil improve hypertension-related bladder dysfunction in the SHR, and naftopidil but not silodosin improves urinary frequency in the light-cycle due to inhibition of urine production.

Decreased susceptibility to salt-induced hypertension in subtotally nephrectomized mice lacking the vasopressin V1a receptor.

AIMS: By examining vasopressin V1a receptor (V1aR) knockout (KO) mice, we previously found that the V1aR is critically involved in the regulation of normal blood pressure. The present study was undertaken to elucidate the role of the V1aR in salt-induced hypertension. METHODS AND RESULTS: We compared haemodynamic responses induced by subtotal nephrectomy + salt loading in V1aR KO mice with those of wild-type (WT) controls. The time course of changes in the systolic blood pressure and heart rate during the salt loading was attenuated in the KO mice compared with that for the WT mice. The elevation of the plasma norepinephrine level caused by the subtotal nephrectomy + salt loading was also reduced in the V1aR KO mice. A V1aR antagonist markedly lowered the arterial blood pressure in the salt-loaded WT mice but not in the normotensive WT mice or in the salt-loaded or normotensive V1aR KO mice. Whereas arginine vasopressin (AVP) administered to the lateral ventricle of the brain induced pressor and tachycardiac responses accompanied by sympathetic activation in the WT mice, these events were completely abolished in the V1aR KO mice. Also, pressor and tachycardiac responses induced by intraventricularly administered hypertonic saline in the WT mice were diminished in the V1aR KO mice. Moreover, the pressor response induced by intraventricularly administered AVP was reduced in alpha(1d) adrenoceptor KO mice, whereas the tachycardiac response did not differ from that of the WT mice. CONCLUSION: These results suggest that the V1aR is involved in the elevation of arterial blood pressure caused by dietary salt and that a V1aR antagonist, in particular regarding its effect in the brain, could have significant therapeutic potential in the treatment of hypertension.

Vasopressin promotes cardiomyocyte hypertrophy via the vasopressin V1A receptor in neonatal mice.

[Arg8]-vasopressin (AVP) is an essential hormone for maintaining osmotic homeostasis and is known to be a potent vasoconstrictor that regulates the cardiovascular system. In the present study, cardiomyocytes were isolated from neonatal mice and used to investigate the effects of AVP on cardiac hypertrophy. Reverse transcription polymerase chain reaction (RT-PCR) analysis revealed that vasopressin V1A receptor mRNA, but not V1B or V2 receptor mRNA, was expressed in primary cultured neonatal mouse cardiomyocytes. By exposing the cultured neonatal cardiomyocytes to AVP for 24 h, cell surface areas were significantly increased, suggesting that AVP could induce cardiomyocyte growth. We then investigated the expression level of the atrial natriuretic peptide (ANP), which is a marker of cardiac hypertrophy. Stimulation with AVP increased the expression of cardiomyocyte ANP mRNA in a dose- and time-dependent manner. Immunocytochemical studies showed that stimulation with AVP significantly increased the expression of the ANP protein as well. Furthermore, AVP administration activated extracellular signal-regulated kinase (ERK)1/2 in cardiomyocytes. The effects of AVP on these parameters were significantly inhibited by a selective vasopressin V1A receptor antagonist, OPC-21268, and were not observed in cardiomyocytes from mice lacking the vasopressin V1A receptor. In vivo cardiac hypertrophy in response to pressure overload was attenuated in vasopressin V1A receptor-deficient (V1AR-KO) mice. Taken together, our data suggest that AVP promotes cardiomyocyte hypertrophy via the vasopressin V1A receptor, which is in part regulated by the pathway of ERK1/2 signaling.

Vasopressin V1A receptor enhances baroreflex via the central component of the reflex arc.

The neurohypophyseal peptide [Arg(8)]-vasopressin (AVP) exerts its physiological actions via 3 distinct receptor isoforms designated V1A, V1B, and V2. We recently showed that V1A receptor was involved in the baroreflex control of heart rate using V1A receptor knockout mice. The present study was undertaken to further clarify this finding. In conscious mice, resting blood pressure of the knockout group was lower than that of the wild-type group (wild-type, 108+/-2.0 mm Hg; knockout, 98+/-3.8 mm Hg; n=6-7) without notable change in heart rate. Although phenylephrine and nitroprusside-induced changes in blood pressure did not differ in these strains, the subsequent bradycardia and tachycardia were markedly blunted in the knockout mice (mean slopes for baroreflex curve after phenylephrine treatment; wild-type, -5.65+/-0.30 bpm/mm Hg; knockout, -3.97+/-0.52 bpm/mm Hg; those after nitroprusside treatment; wild-type, -0.51+/-0.10 bpm/mm Hg; knockout, -0.18+/-0.05 bpm/mm Hg; n=6-7). Under urethane anesthesia (1.0-1.2 g/kg, i.p.), electrical stimulation of the vagal afferent nerve evoked frequency-dependent hypotension and bradycardia in the wild-type mice. In contrast, in the knockout mice such stimulation induced a pressor, not a depressor, response and diminished bradycardia. Moreover, electrical stimulation-induced hemodynamic changes through the vagal afferent nerve in the wild-type mice were significantly attenuated by pretreatment with intravenously administered V1A receptor antagonist d(CH(2))(5)Tyr(Me)AVP. Electrical stimulation of the vagal efferent nerve-induced hemodynamic changes (depressor and bradycardia) and chronotropic responses to adrenergic and cholinergic stimuli were not different between the 2 strains. These results suggest that the V1A receptor in the central nervous system is involved in the regulation of the heart rate via the baroreflex arc.

V1a vasopressin receptors maintain normal blood pressure by regulating circulating blood volume and baroreflex sensitivity.

Arginine-vasopressin (AVP) is a hormone that is essential for both osmotic and cardiovascular homeostasis, and exerts important physiological regulation through three distinct receptors, V1a, V1b, and V2. Although AVP is used clinically as a potent vasoconstrictor (V1a receptor-mediated) in patients with circulatory shock, the physiological role of vasopressin V1a receptors in blood pressure (BP) homeostasis is ill-defined. In this study, we investigated the functional roles of the V1a receptor in cardiovascular homeostasis using gene targeting. The basal BP of conscious mutant mice lacking the V1a receptor gene (V1a-/-) was significantly (P < 0.001) lower compared to the wild-type mice (V1a+/+) without a notable change in heart rate. There was no significant alteration in cardiac functions as assessed by echocardiogram in the mutant mice. AVP-induced vasopressor responses were abolished in the mutant mice; rather, AVP caused a decrease in BP, which occurred in part through V2 receptor-mediated release of nitric oxide from the vascular endothelium. Arterial baroreceptor reflexes were markedly impaired in mutant mice, consistent with a loss of V1a receptors in the central area of baroreflex control. Notably, mutant mice showed a significant 9% reduction in circulating blood volume. Furthermore, mutant mice had normal plasma AVP levels and a normal AVP secretory response, but had significantly lower adrenocortical responsiveness to adrenocorticotropic hormone. Taken together, these results indicate that the V1a receptor plays an important role in normal resting arterial BP regulation mainly by its regulation of circulating blood volume and baroreflex sensitivity.

Possible involvement of calpain activation in pathogenesis of chronic heart failure after acute myocardial infarction.

Changes in proteolytic activity of the myocardium during the development of heart failure after left coronary artery ligation (CAL) of rats were examined. Hemodynamics of the rats at the eighth week (8w-CAL rat), but not at the second week (2w-CAL rat), after CAL showed the symptoms of chronic heart failure. Contents of mu-calpin and m-calpain, but not an intrinsic calpain inhibitor calpastatin, in the viable left ventricular muscle (viable LV) and the right ventricular muscle (RV) of the 2w-CAL and 8w-CAL rats were increased, which was associated with an elevation of intrinsic activities of leupeptin-sensitive, Ca(2+)-activated proteolysis in the cytosolic fractions of the viable LV and RV. Oral administration of 3 mg/kg/d trandolapril or 1 mg/kg/d candesartan from the second to eighth week after CAL improved the hemodynamics of 8w-CAL rats. The drug treatment attenuated the increases in mu-calpain and m-calpain contents and the elevation of the proteolytic activity of the viable LV and RV in the 8w-CAL rat. The drug treatment increased calpastatin content of the RV in the 8w-CAL rat. These results suggest that sustained activation of calpain is involved in the development of chronic heart failure and that trandolapril and candesartan prevent the activation of calpains after CAL.

Effects of angiotensin I-converting enzyme inhibitor and angiotensin II type 1 receptor blocker on the right ventricular sarcoglycans and dystrophin after left coronary artery ligation.

We examined the effects of trandolapril and candesartan on changes in the levels of sarcoglycans and dystrophin in the right ventricle of rats with the left coronary artery ligation. Hemodynamic and morphological alterations suggested the development of hypertrophy of the right ventricle and chronic heart failure by the 8th week. By the end of the 8th week, alpha- and beta-sarcoglycans and dystrophin were decreased. Increases in mu- and m-calpains in the hypertrophied right ventricle were associated with an elevation of casein-proteolytic activity in the cytosolic fraction. Oral administration of 3 mg/kg/day trandolapril or 1 mg/kg/day candesartan from the 2nd to 8th week after the left coronary artery ligation attenuated decreases in alpha-sarcoglycan and dystrophin and reduced the increased proteolytic activity. The results suggest that attenuation of decreases in sarcoglycans and dystrophin is a possible mechanism underlying trandolapril- and candesartan-mediated improvement of structural and functional alterations of the right ventricle in the coronary artery-ligated rat.