Photoinduced reactions of chloroacetone in solid Ar: Identification of CH2=COCICH3

The UV light-induced reactions of chloroacetone in a cryogenic Ar matrix were investigated using infrared spectroscopy. The photoinduced isomerisations of gauche-chloroacetone to syn-chloroacetone and hypochlorous acid 1-methylethenyl ester were confirmed by comparing the experimental and calculated spectra. In addition, the photolysis products were found to be CH2double bond; length as m-dashCdouble bond; length as m-dashO and a cyclopropanone⋯HCl complex. The cyclopropanone⋯HCl complex was further decomposed into CH2double bond; length as m-dashCH2, CO and HCl. The hypochlorous acid 1-methylethenyl ester was further isomerized to 2-chloro-2-methyloxirane.ArticleCHEMICAL PHYSICS LETTERS. 614:258-262 (2014)journal articl

Low Cardiac Output Leads Hepatic Fibrosis in Right Heart Failure Model Rats.

BACKGROUND:Hepatic fibrosis progresses with right heart failure, and becomes cardiac cirrhosis in a severe case. Although its causal factor still remains unclear. Here we evaluated the progression of hepatic fibrosis using a pulmonary artery banding (PAB)-induced right heart failure model and investigated whether cardiac output (CO) is responsible for the progression of hepatic fibrosis. METHODS AND RESULTS:Five-week-old Sprague-Dawley rats divided into the PAB and sham-operated control groups. After 4 weeks from operation, we measured CO by echocardiography, and hepatic fibrosis ratio by pathological examination using a color analyzer. In the PAB group, CO was significantly lower by 48% than that in the control group (78.2±27.6 and 150.1±31.2 ml/min, P<0.01). Hepatic fibrosis ratio and serum hyaluronic acid, an index of hepatic fibrosis, were significantly increased in the PAB group than those in the control group (7.8±1.7 and 1.0±0.2%, P<0.01, 76.2±27.5 and 32.7±7.5 ng/ml, P<0.01). Notably, the degree of hepatic fibrosis significantly correlated a decrease in CO. Immunohistological analysis revealed that hepatic stellate cells were markedly activated in hypoxic areas, and HIF-1α positive hepatic cells were increased in the PAB group. Furthermore, by real-time PCR analyses, transcripts of profibrotic and fibrotic factors (TGF-β1, CTGF, procollargen I, procollargen III, MMP 2, MMP 9, TIMP 1, TIMP 2) were significantly increased in the PAB group. In addition, western blot analyses revealed that the protein level of HIF-1α was significantly increased in the PAB group than that in the control group (2.31±0.84 and 1.0±0.18 arbitrary units, P<0.05). CONCLUSIONS:Our study demonstrated that low CO and tissue hypoxia were responsible for hepatic fibrosis in right failure heart model rats

Impairment of Excitation-Contraction Coupling in Right Ventricular Hypertrophied Muscle with Fibrosis Induced by Pulmonary Artery Banding

<div><p>Interstitial myocardial fibrosis is one of the factors responsible for dysfunction of the heart. However, how interstitial fibrosis affects cardiac function and excitation-contraction coupling (E-C coupling) has not yet been clarified. We developed an animal model of right ventricular (RV) hypertrophy with fibrosis by pulmonary artery (PA) banding in rats. Two, four, and six weeks after the PA-banding operation, the tension and intracellular Ca²⁺ concentration of RV papillary muscles were simultaneously measured (n = 33). The PA-banding rats were clearly divided into two groups by the presence or absence of apparent interstitial fibrosis in the papillary muscles: F+ or F- group, respectively. The papillary muscle diameter and size of myocytes were almost identical between F+ and F-, although the RV free wall weight was heavier in F+ than in F-. F+ papillary muscles exhibited higher stiffness, lower active tension, and lower Ca²⁺ responsiveness compared with Sham and F- papillary muscles. In addition, we found that the time to peak Ca²⁺ had the highest correlation coefficient to percent of fibrosis among other parameters, such as RV weight and active tension of papillary muscles. The phosphorylation level of troponin I in F+ was significantly higher than that in Sham and F-, which supports the idea of lower Ca²⁺ responsiveness in F+. We also found that connexin 43 in F+ was sparse and disorganized in the intercalated disk area where interstitial fibrosis strongly developed. In the present study, the RV papillary muscles obtained from the PA-banding rats enabled us to directly investigate the relationship between fibrosis and cardiac dysfunction, the impairment of E-C coupling in particular. Our results suggest that interstitial fibrosis worsens cardiac function due to 1) the decrease in Ca²⁺ responsiveness and 2) the asynchronous activation of each cardiac myocyte in the fibrotic preparation due to sparse cell-to-cell communication.</p></div

General parameters in tissues from sham (Sham), hypertrophy without fibrosis (F-), and hypertrophy with fibrosis (F+).

<p>General parameters in tissues from sham (Sham), hypertrophy without fibrosis (F-), and hypertrophy with fibrosis (F+).</p

Data set of tension and Ca²⁺ in papillary muscles using the aequorin method.

<p>Data set of tension and Ca²⁺ in papillary muscles using the aequorin method.</p

Excitation-contraction coupling in papillary muscle with and without fibrosis.

<p>Tension and Ca²⁺ transients in papillary muscles simultaneously measured by the aequorin method. A: Representative traces in tension (upper) and intracellular Ca²⁺ (lower) in each sample. B: Summarized data of peak value in each sample. C: Summarized data of the peak time of tension and intracellular Ca²⁺. D: Summarized data of relaxation time. E: Summarized data of tension divided by the cross-sectional area of the muscle in each sample.Values are means ± SE; n = 28 in Sham (S), n = 23 in hypertrophy without fibrosis (F-), and n = 10 in hypertrophy with fibrosis (F+).</p

Myocardial stiffness in papillary muscle with and without fibrosis.

<p>The relationship between muscle stretch and resting tension in papillary muscle. On the x-axis, each muscle length was normalized by Lmax, at which papillary muscle developed maximum active tension. On the y-axis, muscle resting tension was normalized by maximum active tension at Lmax. Filled squares: Sham; open circles: F- (hypertrophy); and gray triangles: F+ (hypertrophy with fibrosis). Values are means ± SE; n = 21 in Sham, n = 17 in F-, and n = 4 in F+.</p

List of primer sequences used for QRT-PCR.

<p>List of primer sequences used for QRT-PCR.</p

Correlation coefficient of physical and biological data to % of fibrosis.

<p>Correlation coefficient of physical and biological data to % of fibrosis.</p

Reduced intercalated disks and connexin 43 expression in hypertrophy with fibrosis.

<p>A: Representative photos of Masson’s trichrome staining (M-T; upper) and connexin 43 immunohistochemistry staining (Cx43; lower) in the long-axis sections of papillary muscles obtained from Sham (S), hypertrophy without fibrosis (F-), and hypertrophy with fibrosis (F+). Arrows represent intercalated disks. In F+, intercalated disks were invaded with fibrosis and the Cx43 expression level was reduced. B; Expression of Cx43 mRNA was measured by QRT-PCR. Values are means ± SE; n = 21 in Sham, n = 19 in F-, and n = 6 in F+. C: Expression of Cx43 proteins was measured by the western blot technique. Values are means ± SE; n = 6 each.</p