[Usage of New Device to Prevent Sternum Separation after Median Sternotomy in 140 Cases].

While minimally invasive cardiac surgery (MICS) has become increasingly popular recently even in the field of cardiovascular surgery, the conventional full median sternotomy is still the main approach to the mediastinum, especially for cases which cannot be applied for MICS or in the facilities where MICS is not performed. It has been known that sternal instability is one of the leading causes of sternal infection after median sternotomy. Therefore, we have sought for an additional product to secure strong sternal stability. Since August in 2018, we used a new type of corrugated plate( Super Fixsorb Wave) which is placed inside the sternum in addition to regular sternal wires for 140 patients who had full median sternotomy. Up to now, we have no complications regarding sternotomy including mediastinitis. We believe that additional use of Super Fixsorb Wave enables firm sternal stability and prevents mediastinitis following full median sternotomy.

[Cardiac Rehabilitation in Minimally Invasive Cardiac Surgery Coronary Artery Bypass Grafting].

OBJECTIVES: A purpose is to compare the in-hospital rehabilitation progress after minimally invasive cardiac surgery coronary artery bypass grafting (MICS CABG) with that after off pump coronary artery bypass grafting( OPCAB). METHODS: We analyzed 60 patients who underwent coronary artery bypass grafting surgery from January 2015 to December 2016. Fourteen patients underwent MICS CABG (MICS CABG group) and 46 patients underwent OPCAB (OPCAB group). The post-operative days to start standing position and independent walking, and hospitalization duration were analyzed between the 2 groups. RESULTS: There were no significant differences between the groups:standing position(1.2 vs 1.2 days) and independent walking(4.8 vs 4.9 days). Hospitalization duration was shorter in MICS CABG group(14.3 vs 17.5 days). CONCLUSION: MICS CABG may shorten hospitalization length compared with OPCAB, however, further research will be needed.

[Rupture of Saccular Brachiocephalic Artery Aneurysm after One Year and Seven Months from Coil Embolization;Report of a Case].

A 52-years-old man, who had undergone coil embolization of saccular aneurysm of the brachiocephalic artery, presented with right back discomfort. Diagnosis by computed tomography was difficult because of an artifact from the coils. Angiography, on the other hand, revealed a rupture of the aneurysm, and emergency surgery was performed. A Y-shaped graft was anastomosed to the ascending aorta under partial clamp. Then, one of its branches was anastomosed to the common carotid artery also under partial clamp in an end-to-side fashion. The cerebral blood flow monitored by a regional oximetry system (INVOS) remained stable. The other branch was anastomosed to the subclavian artery in end-to end fashion. No postoperative neurologic complications occurred. Angiography was useful in diagnosis of brachiocephalic artery aneurysm rupture after coil embolization. INVOS was also useful for monitoring the cerebral blood flow during surgery.

[Minimally Invasive Coronary Artery Bypass Grafting Using Proximal Anastomoses Device;Report of a Case].

A 68-years-old male with diabetes mellitius (HbA1c 6.5%) was referred for coronary artery bypass grafting(CABG). Preoperative coronary angiography (CAG) signed 3-vessels coronary disease[#2 75 %,#4 posterior descending (PD) 75%,#6 90%,#14 90%]. Minimally invasive coronary artery grafting (MICS CABG) was selected because of faster postoperative recovery than off-pump CABG via a 10 cm left 5th thoracotomy approach. In situ bilateral internal thoracic artery(BITA) and saphenous vein (SVG) was harvested by special manner using long type Harmonic. Bypass graft design was in situ right internal thoracic artery-LAD, in situ left internal thoracic artery-left circumtlex#14, and aorta-SVG-#4PD-#4atrio-ventricular. BITA, the ascending aorta for proximal anastomoses, and all coronary targets were directly accessed with off-pump technique. Heartstring III Proximal Seal System was used to anastomose SVG to the ascending aorta. There were no major postoperative complications. Postoperative CAG revealed all grafts patent and postoperative hospital stay was 14 days. This case was the 1st usage of Heartstring III Proximal Seal System in our clinic. We believe that the usage of Heartstring III Proximal Seal System in MICS CABG is realistically possible, and providing good quality;however, further research will be needed.

[Minimally Invasive Coronary Artery Bypass Grafting Using Bilateral In Situ Internal Thoracic Arteries].

A 73-year-old male with diabetes mellitius was referred to our hospital for coronary artery bypass grafting (CABG). Preoperative coronary angiography revealed three-vessel coronary disease. Minimally invasive coronary artery grafting (MICS CABG) via left thoracotomy was selected to decrease surgical site infection due to severe diabetes. In situ bilateral internal thoracic arteries (BITA) were harvested using a long type Harmonic scalpel. In situ right internal thorac artery( RITA)-left anterior descending artery (LAD), in situ left internal thorac artery( LITA)-high lateral branch (HL), and aorta-saphenous vein graft (SVG)-#4 posterior descending artery were performed. BITA, the ascending aorta for proximal anastomosis, and all coronary targets were directly accessed with off-pump technique. There were no major postoperative complications. Postoperative 3D-computed tomography angiography (CTA) revealed all grafts were patent. We believe that use of BITA in MICS CABG is feasible, and can provide satisfactory quality. Further research however, will be needed.

[New Intracoronary Shunt Cannula in Off-pump Coronary Artery Bypass Grafting].

In off-pump coronary artery bypass grafting(OPCAB), a bloodless operative field has great influence on the quality of anastomosis. In addition, maintenance of distal coronary flow during anastomosis stabilizes hemodynamics. We introduced a new intracoronary shunt cannula, Mini Shunt Pro (MSP). MSP adopts the step-tip, which allows easy insertion and reduces the risk of intimal injury. The distal and proximal sides of the tips of MSP are 0.25 mm different in diameter, which improves its fitness to the coronary artery and enhances a bloodless operative field. This new shunt cannula is considered to be safe and useful for high-quality anastomosis in OPCAB.

Is hyperuricemia a risk factor for arteriosclerosis? Uric acid and arteriosclerosis in apolipoprotein e-deficient mice.

Although hyperlipidemia, high blood pressure, and diabetes increase the risk of arteriosclerosis, it is not clear whether hyperuricemia increases the risk of arteriosclerosis or not. We examined the effects of uric acid and curative drugs for hyperuricemia on atherosclerosis-susceptible C57BL/6J apolipoprotein E-deficient (apoE(-/-)) mice. Male apoE(-/-) mice (age: 6 weeks) were fed a normal diet (normal diet group) or a uric acid-enriched diet. Mice fed the uric acid-enriched diet were divided into three groups and administered a drinking vehicle (high uric acid diet group), allopurinol (20 mg·kg(-1)·d(-1)), or benzbromarone (20 mg·kg(-1)·d(-1)) for 10 weeks. Serum uric acid concentrations were higher in the high uric acid diet group than in the normal diet group, and concentrations in the allopurinol and benzbromarone groups were lower than in the high uric acid diet group. Serum total cholesterol and triglyceride levels were lower in the allopurinol group than in the high uric acid diet group. Oxidative stress was lower in the benzbromarone group than in the high uric acid diet group. Atherosclerotic lesion areas were smaller in the allopurinol and benzbromarone groups than in the high uric acid diet group. Thus, hyperuricemia may not be an independent risk factor for arteriosclerosis; however, the administration of allopurinol and benzbromarone prevented the development of atherosclerosis in apoE(-/-) mice fed a uric acid-enriched diet. The anti-atherosclerotic effect was in part due to lower total cholesterol and oxidative stress in the serum. Other possible mechanisms underlying this effect should be investigated.

Fibrin Hydrogel Layer-Anchored Pericardial Matrix Prevents Epicardial Adhesion in the Severe Heart Adhesion-Induced Miniature Pig Model.

Postoperative adhesion is a very common and serious complication that occurs frequently in cardiac surgery. The purpose of this study was to evaluate the efficacy of a fibrin hydrogel layer-anchored decellularized pericardial matrix in preventing pericardial adhesions in a miniature pig model with a myocardial injury. Fibrin hydrogel layer-anchored decellularized pericardial matrix was prepared by spraying a mixture of fibrinogen and thrombin on a fibrinogen-doped decellularized pericardium. Cardiac injury was generated by abrading and desiccating the epicardial surface of a miniature pig to induce severe postoperative adhesions. The adhesion between the epicardial surface and fibrin hydrogel layer-anchored decellularized pericardial matrix in three different regions (left outer, front, and right outer) was evaluated macroscopically one month after surgery. The fibrin hydrogel layer-anchored decellularized pericardial matrix showed significantly less adhesion than an autologous pericardium (0.2 ± 0.7 in DPM-FHG0.5 and 0.4 ± 0.8 in DPM-FHG1, p < 0.01) and expanded polytetrafluoroethylene (ePTFE) (1.6 ± 0.5, p < 0.05). The fibrin hydrogel concentration had no effect on preventing postoperative adhesion. A thinner fibrin hydrogel layer was observed on the decellularized pericardial matrix one month after surgery; however, the inside of the matrix was filled with fibrin hydrogel. Fibrin hydrogel layer-anchored decellularized pericardial matrix prevented postoperative epicardial adhesions in a miniature pig model. Our findings suggest that pericardial closure using a fibrin hydrogel layer-anchored decellularized pericardial matrix is a promising method for preventing adverse outcomes in reoperative surgeries.

Association of computed tomography-derived muscle mass and quality with delayed acquisition independent walking after cardiovascular surgery.

BACKGROUND: In the context of cardiovascular surgery, the foremost concern lies in delayed functional recovery, as typified by the acquisition of independent walking after surgery, among older patients with decline in skeletal muscle mass and quality. Computed tomography (CT), which is typically employed for the preoperative assessment of pathological conditions in patients undergoing cardiovascular surgery, is also suitable for screening for potential decline in skeletal muscle mass and quality. The aim of this study was to examine the predictive capabilities of CT-derived parameters such as muscle mass and muscle quality for the delayed acquisition of independent walking in the postoperative period. METHODS: This retrospective study enrolled consecutive Japanese patients who underwent elective cardiovascular surgery between May 2020 and January 2023. In total, 139 patients were included in the analyses. Based on the preoperative CT image, the psoas muscle volume index (PMVI) and psoas muscle attenuation (PMA) were calculated. Information on patient characteristics, including preoperative physical fitness such as handgrip strength/body mass index (GS/BMI), short physical performance battery (SPPB), and 6-min walking distance (6MWD), were obtained from the medical records. We defined delayed acquisition of independent walking after surgery as the inability to walk 100 m within 4 days after surgery. RESULTS: The median age of the patients was 72 (interquartile: 64-78) years, and 74.8% (104/139) were men; 47.5% corresponded to the delayed group. The areas under the curves of SPPB, GS/BMI, 6MWD, PMVI, and PMA against delayed acquisition of independent walking after surgery were 0.68 [95% confidence interval (CI): 0.59 to 0.77], 0.72 (95% CI: 0.63 to 0.80), 0.73 (95% CI: 0.65 to 0.82), 0.69 (95% CI: 0.60 to 0.78), and 0.78 (95% CI: 0.70 to 0.85), respectively. In the multivariate logistic regression analysis, low PMA was significantly associated with delayed acquisition of independent walking even after adjustment for patient characteristics including physical fitness [model 1: SPPB (OR, 1.14; 95% CI: 1.03-1.25), model 2: GS/BMI (OR, 1.13; 95% CI: 1.03-1.25), and model 3: 6MWD (OR, 1.14; 95% CI: 1.03-1.25)], but PMVI was not. CONCLUSIONS: Our study revealed a strong association between PMA, a marker of CT-derived muscle quality, and the postoperative delay in achieving independent walking in patients who underwent cardiovascular surgery. The technique to obtain information on muscle quality during the time period before surgery may be an option for timely therapeutic intervention in patients who may have delayed acquisition of independent walking after surgery.

Ecklonia cava polyphenol protects the liver against ethanol-induced injury in rats.

BACKGROUND: The development of alcoholic liver disease is a complex process that involves both the parenchymal and non-parenchymal cells of the liver. We examined the effect of an Ecklonia cava extract on ethanol-induced liver injury. METHODS: Isolated hepatocytes and hepatic stellate cells (HSCs) were incubated with ethanol. Ecklonia cava polyphenol (ECP) was added to the cultures that had been incubated with ethanol. Male Wistar rats were fed a diet that included 0.02% or 0.2% ECP or no ECP. For a period of 3 weeks, the animals were given drinking water containing 5% ethanol and were also treated with carbon tetrachloride (CCl4) (0.1 ml/kg of body weight). RESULTS: In the cultured hepatocytes, the ECP treatment suppressed the ethanol-induced increase in cell death by maintaining intracellular glutathione (GSH) levels. In HSCs, ECP treatment suppressed the ethanol-induced increases in type I collagen and α-smooth muscle actin expression by maintaining intracellular levels of reactive oxygen species and GSH. We examined the effects of ECP on serum AST and ALT activity, as well as the progression of liver fibrosis in rats treated with ethanol and CCl4. ECP treatment suppressed plasma AST and ALT activities in the ethanol- and CCl4-treated rats. ECP treatment fully protected the rats against ethanol- and CCl4-induced liver injury. GENERAL SIGNIFICANCE: ECP may be a candidate for preventing ethanol-induced liver injury.

Neuroprotective effect of (-)-epigallocatechin-3-gallate in rats when administered pre- or post-traumatic brain injury.

Our previous study indicated that consuming (-)-epigallocatechin gallate (EGCG) before or after traumatic brain injury (TBI) eliminated free radical generation in rats, resulting in inhibition of neuronal degeneration and apoptotic death, and improvement of cognitive impairment. Here we investigated the effects of administering EGCG at various times pre- and post-TBI on cerebral function and morphology. Wistar rats were divided into five groups and were allowed access to (1) normal drinking water, (2) EGCG pre-TBI, (3) EGCG pre- and post-TBI, (4) EGCG post-TBI, and (5) sham-operated group with access to normal drinking water. TBI was induced with a pneumatic controlled injury device at 10 weeks of age. Immunohistochemistry and lipid peroxidation studies revealed that at 1, 3, and 7 days post-TBI, the number of 8-Hydroxy-2'-deoxyguanosine-, 4-Hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells, and levels of malondialdehyde around the damaged area were significantly decreased in all EGCG treatment groups compared with the water group (P < 0.05). Although there was a significant increase in the number of surviving neurons after TBI in each EGCG treatment group compared with the water group (P < 0.05), significant improvement of cognitive impairment after TBI was only observed in the groups with continuous and post-TBI access to EGCG (P < 0.05). These results indicate that EGCG inhibits free radical-induced neuronal degeneration and apoptotic death around the area damaged by TBI. Importantly, continuous and post-TBI access to EGCG improved cerebral function following TBI. In summary, consumption of green tea may be an effective therapy for TBI patients.

Appearance of neural stem cells around the damaged area following traumatic brain injury in aged rats.

We have previously reported free radical production after traumatic brain injury (TBI), which induces neural stem cell (NSC) degeneration and death. However, the effects of aging on NSC proliferation around the damaged area following TBI have not been investigated. Therefore, in this study, we used 10-week (young group) and 24-month-old (aged group) rat TBI models to investigate the effects of aging on NSC proliferation around damaged tissue using immunohistochemical and ex vivo techniques. Young and aged rats received TBI. At 1, 3 and 7 days after TBI, immunohistochemical and lipid peroxidation studies were performed. Immunohistochemistry revealed that the number of nestin-positive cells around the damaged area after TBI in the aged group decreased significantly when compared with those in the young group (P < 0.01). However, the number of 8-hydroxy-2'-deoxyguanosine-, 4-hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells and the level of peroxidation around the damaged area after TBI significantly increased in the aged group, compared with those in the young group (P < 0.01). Furthermore, almost all ssDNA-positive cells in young and aged groups co-localized with NeuN and nestin staining. Ex vivo studies revealed that neurospheres, which differentiated into neurons and glia in culture, could only be isolated from injured brain tissue in young and aged groups at 3 days after TBI. These results indicate that, although there were fewer NSCs that have the potential to differentiate into neurons and glia, these NSCs escaped free radical-induced degeneration around the damaged area after TBI in the aged rat brain.

Continual Gram-negative bacterial challenge accelerates stroke onset in stroke-prone spontaneously hypertensive rats.

This study examined the effects of continual Gram-negative bacterial challenge on stroke onset. Stroke onset occurred significantly earlier in stroke-prone spontaneously hypertensive rats (SHRSP) injected with a bacterial cell suspension of Gram-negative rods or lipopolysaccharides (LPSs) than in uninjected controls. Paralysis of the hindlimb, piloerection, hypokinesis, and hyperkinesis were observed in LPS-injected SHRSP but not in uninjected controls during stroke onset. The serum levels of NOx, thiobarbituric acid reactive substance, and 8-hydroxydeoxyguanosine increased in LPS-injected SHRSP. These results suggest that continual Gram-negative bacterial challenge induces accelerated stroke onset in SHRSP, probably caused by oxidative stress responses derived from LPSs.

Myofibroblasts: Biochemical and proteomic approaches to fibrosis.

Fibrosis is a state, in which excess amounts of extracellular matrix are deposited in the tissue. Fibrosis can occur in various organs, including the liver, lung, kidney and heart. The progression of fibrosis involves interstitial hypercellularity, accumulation of extracellular matrix, and atrophy of epithelial structures, resulting in a loss of normal function. Myofibroblasts play a crucial role in the development and progress of fibrosis. When stimulated, myofibroblasts actively synthesize connective tissue components and cause organ fibrosis. As a result, the process and the mechanism of myofibroblast activation represent a target for antifibrotic treatment. As yet, however, an effective treatment has not been developed, and new treatment modalities are expected. Because activation of myofibroblasts is a key event during fibrosis development, there is great interest in identifying and characterizing proteins whose expression is changed after this activation. In this review, fibrosis is outlined and the role of myofibroblasts in this disorder is described. Furthermore, the search for candidate proteins to target for treatment and the prospects of antifibrotic therapy are discussed.

Delay of stroke onset by milk proteins in stroke-prone spontaneously hypertensive rats.

BACKGROUND AND PURPOSE: There is an inverse association between dairy food consumption and the incidence of stroke in observational studies. However, it is unknown whether the relationship is causal or, if so, what components in milk are responsible for reducing the incidence of stroke. METHODS: Stroke-prone spontaneously hypertensive rats were fed diets comprising amino acids, proteins from different sources (casein, whey, soybean, or egg white), or fats from different sources (butter, beef tallow, or cocoa butter) and the onset of stroke and lifespan were examined. RESULTS: Increasing the amount of dietary casein (5% to 55% of caloric intake) markedly delayed the onset of stroke. However, when stroke-prone spontaneously hypertensive rats were fed diets containing 55% of caloric intake as protein, rats fed casein or whey protein, a major component of milk, displayed a delayed onset of stroke compared with rats fed soybean or egg white protein. Rats fed an amino acids diet containing the same amino acids composition as casein did not have a delay in the onset of stroke. Increasing dietary fats, including butter as well as beef tallow and cocoa butter, did not affect the onset of stroke. All diets did not affect blood pressure in the early stage. CONCLUSIONS: These data suggest that the inverse association between dairy food consumption and incidence of stroke in epidemiological studies is causal and that peptides in milk protein, but not fat, might be responsible for this effect.

Interleukin-1ß accelerates the onset of stroke in stroke-prone spontaneously hypertensive rats.

High blood levels of inflammatory biomarkers and immune cells in stroke lesions have been recognized as results of stroke. However, recent studies have suggested that inflammation occurs prior to stroke onset. In this study, we aimed to clarify the role of inflammation in stroke onset among stroke-prone spontaneously hypertensive rats (SHRSP). At 4 weeks of age (before stroke onset), the plasma level of IL-1ß was significantly higher in SHRSP (153.0 ± 49.7 pg/ml) than in Wistar Kyoto rats (WKY) (7.7 ± 3.4 pg/ml, P < 0.001 versus SHRSP) or spontaneously hypertensive rats (SHR) (28.0 ± 9.1 pg/ml, P < 0.001 versus SHRSP) (n = 6 per strain). Stimulated IL-1ß signal was also observed in cerebrovascular endothelial cells of SHRSP. Gene expressions of IL-1ß, IL-1 receptors, caspase-1, and downstream genes (MCP-1 and ICAM-1), which associated with immune cell recruitment, were significantly greater in SHRSP than in WKY or SHR, coincident with greater NFκB protein levels in SHRSP compared to WKY or SHR. In addition, continuous administration of IL-1ß (2 µg/day) using an osmotic pump slightly increased the incidence of stroke in SHR (P = 0.046) and significantly accelerated the onset of stroke in SHRSP (P = 0.006) compared to each control (n = 10 per group). These results suggest that a stimulated IL-1ß signal might be a cause of stroke onset when concomitant with severe hypertension.

[Bioprosthetic valve endocarditis associated with rapid progression of valvular stenosis;report of a case].

Long-term durability and stability of the hemodynamic performance of commercially available 2nd generation Carpentier-Edwards stented bovine pericardial aortic bioprostheses (Perimount valve) is reported based on echocardiographic follow-up examinations. Prosthetic valve deterioration of the Perimount valve usually occurs late and is age-dependent. We describe bioprosthetic valve deterioration of a Perimount valve with severe stenotic change 1 month postoperatively that developed in an infective endocarditis patient. Although preoperative echocardiography showed no signs of valve dehiscence or vegetation on the prosthesis, valve stenosis alone had progressed extremely rapidly during 2 weeks of febrile symptom. The valve leaflet was found at explant to be infiltrated with a cellular material fibrin other than bacteria or leukocytes. This rare occurrence needs to be reported in the literature to forewarn clinicians of an early manifestation of endocarditis that may not be recognized yet.

Dietary protein, but not carbohydrate, is a primary determinant of the onset of stroke in stroke-prone spontaneously hypertensive rats.

BACKGROUND AND PURPOSE: Previously, an inverse association has been found between the dietary proportion of protein or fat and incidence of intracerebral hemorrhage. A positive association has been found with respect to carbohydrate intake. To examine what changes in macronutrient intake are causative, animal studies were conducted. METHODS: Stroke-prone spontaneously hypertensive rats (SHRSP) were fed diets with varying ratios of macronutrients ad libitum, and the onset of stroke was examined. RESULTS: When 10% of calories were from fat, rats fed a high-protein/low-carbohydrate diet (55% calories from protein) had a delayed onset of stroke, whereas rats fed a low-protein/high-carbohydrate diet (5% calories from protein) had an accelerated onset of stroke. When 30% of calories were from carbohydrate, a marked delay in the onset of stroke was observed when the diet was high in protein. When 85% of calories were from carbohydrate, rats fed 7.5% of calories as protein displayed an accelerated onset of stroke. When 20% of calories were from protein, increased fat content did not affect the onset of stroke. However, with a fat-free diet, when 20% of calories were from protein, the onset of stroke was delayed, whereas when 10% of calories were from protein, the onset of stroke was accelerated. CONCLUSIONS: The amount of protein, but not of carbohydrate and fat, is a primary determinant of the onset of stroke. However, when calories from protein are relatively low in the diet (10%), fat is necessary to delay the onset of stroke in SHRSP.

Immunohistochemical analysis of brain lesions using S100B and glial fibrillary acidic protein antibodies in arundic acid- (ONO-2506) treated stroke-prone spontaneously hypertensive rats.

Stroke-prone spontaneously hypertensive rats (SHRSP) used as a model of essential hypertension cause a high incidence of brain stroke on the course of hypertension. Incidences and sizes of brain lesions are known to relate to the astrocyte activities. Therefore, relation between brain damage and the expression profile of the astrocytes was investigated with morphometric and immunohistochemical analyses using astrocyte marker antibodies of S100B and glial fibrillary acidic protein (GFAP) with or without arundic acid administration, a suppressor on the activation of astrocytes. Arundic acid extended the average life span of SHRSP. An increase in brain tissue weight was inhibited concomitant with a lower rate of gliosis/hemosiderin deposit/scarring in brain lesions. S100B- or GFAP-positive dot and filamentous structures were decreased in arundic acid-treated SHRSP, and this effect was most pronounced in the cerebral cortex, white matter, and pons, and less so in the hippocampus, diencephalon, midbrain, and cerebellum. Blood pressure decreased after administration of arundic acid in the high-dose group (100 mg/kg/day arundic acid), but not in the low-dose group (30 mg/kg/day). These data indicate that arundic acid can prevent hypertension-induced stroke, and may inhibit the enlargement of the stroke lesion by preventing the inflammatory changes caused by overproduction of the S100B protein in the astrocytes.

Decreased expression of catechol-O-methyltransferase in the renal cortex of malignant spontaneously hypertensive rats.

Essential hypertension is a disease of unknown pathogenesis, although renal function has been implicated as an important factor in its cause. Stroke-prone spontaneously hypertensive (SHRSP) rats provide an animal model of essential hypertension. To understand the cause of hypertension, identifying proteins that are differentially expressed between hypertensive and normotensive rats may provide a key. Here, proteins in the renal cortex from SHRSP rats, malignant stroke-prone spontaneously hypertensive (M-SHRSP) rats, and Wistar Kyoto (WKY) rats as a normotensive control were subjected to two-dimensional difference gel electrophoresis (2D-DIGE). After in-gel digestion by trypsin, proteins were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOFMS). Several proteins showed differential expression patterns between hypertensive and normotensive rats. Among them, we focused on catechol-O-methyltransferase (COMT) because this enzyme inactivates catecholamines, possibly affecting blood pressure. To confirm the differential expression of COMT in each animal, we conducted Western blot analysis, which revealed that the expression of COMT is lower in M-SHRSP rats than in control and SHRSP rats, indicating that blood pressure and expression of COMT are related. In fact, the blood pressure of M-SHRSP rats was significantly higher than that of SHRSP rats at age of 10 weeks. Immunohistochemical and immunofluorescence studies showed that COMT in renal cortex is localized in tubular epithelial cells. The expression of COMT is lower in the renal cortex tubular epithelium of M-SHRSP rats than in normotensive rats. These results suggest that the decreased expression of COMT may be an important factor leading to the development of hypertension.