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In order to extend the service life of 45# steel and reduce production costs, coating NiCrBSi alloy powder on the surface of 45# steel can meet production requirements, avoid resource waste and achieve green manufacturing. Based on response surface method (RSM), the dilution rate, aspect ratio and contact angle were taken as the optimization goals, and the process parameters (laser power, scanning speed and powder feeding rate) were optimized and the optimal process parameters were determined. On this basis, the microstructure of Ni-based coating was characterized by the cladding experiment. The friction wear and corrosion resistance of the coating were tested, and the enhancement mechanism of the wear resistance and corrosion resistance of the coating was analyzed. The results show that the optimized coating has good corrosion resistance and wear resistance. It provides a reference for the optimization of process parameters in 45# steel repair work.

Cold exposure increases the risk of adverse events related to cardiovascular causes, especially in the elderly. In this review, we focus on recent findings concerning the impact of aging on the regulatory mechanisms of cold-induced cardiovascular responses. In response to cold exposure, the initial physiological thermoregulation in healthy young persons, such as cutaneous vasoconstriction to reduce heat loss, is attenuated in older individuals, resulting in a reduced ability of the older persons to maintain body temperature in cold environment. Impaired sympathetic skin response, reduced noradrenergic neurotransmitter synthesis, insufficient noradrenergic transmitters, and altered downstream signaling pathways inside the vascular smooth muscle may be among the underlying mechanisms for the maladaptive vasoconstrictive response to cold stress in the elderly. The increase in blood pressure during cold exposure in young persons may be further augmented in aging adults, due to greater central arterial stiffness or diminished baroreflex sensitivity with aging. Cold stress raises myocardial oxygen demand caused by increased afterload in both young and old adults. The elderly cannot adjust to meet the increased oxygen demand due to reduced left ventricular compliance and coronary blood flow with advancing age, rendering the elderly more susceptible to hypothermia-induced cardiovascular complications from cold-related diseases. These age-associated thermoregulatory impairments may further worsen patients' health risk with existing cardiovascular diseases such as hypertension, coronary artery disease, and heart failure. We searched PubMed for papers related to cold stress and its relationship with aging, and selected the most relevant publications for discussion.

Ca2+/calmodulin-dependent protein kinase II (CaMKII) is upregulated in congestive heart failure (CHF), contributing to electrical, structural, and functional remodeling. CaMKII inhibition is known to improve CHF, but its direct cardiac effects in CHF remain unclear. We hypothesized that CaMKII inhibition improves cardiomyocyte function, [Ca2+]i regulation, and β-adrenergic reserve, thus improving advanced CHF. In a 16-week study, we compared plasma neurohormonal levels and left ventricular (LV)- and myocyte-functional and calcium transient ([Ca2+]iT) responses in male Sprague-Dawley rats (10/group) with CHF induced by isoproterenol (170 mg/kg sq for 2 days). In rats with CHF, we studied the effects of the CaMKII inhibitor KN-93 or its inactive analog KN-92 (n = 4) (70 µg/kg per day, mini-pump) for 4 weeks. Compared with controls, isoproterenol-treated rats had severe CHF with 5-fold–increased plasma norepinephrine and about 50% decreases in ejection fraction (EF) and LV contractility [slope of LV end-systolic pressure–LV end-systolic volume relation (EES)] but increased time constant of LV relaxation (τ). They also showed significantly reduced myocyte contraction [maximum rate of myocyte shortening (dL/dtmax)], relaxation (dL/dtmax), and [Ca2+]iT. Isoproterenol superfusion caused significantly fewer increases in dL/dtmax and [Ca2+]iT. KN-93 treatment prevented plasma norepinephrine elevation, with increased basal and acute isoproterenol-stimulated increases in EF and EES and decreased τ in CHF. KN-93 treatment preserved normal myocyte contraction, relaxation, [Ca2+]iT, and β-adrenergic reserve, whereas KN-92 treatment failed to improve LV and myocyte function, and plasma norepinephrine remained high in CHF. Thus, chronic CaMKII inhibition prevented CHF-induced activation of the sympathetic nervous system, restoring normal LV and cardiomyocyte basal and β-adrenergic–stimulated contraction, relaxation, and [Ca2+]iT, thereby playing a rescue role in advanced CHF. SIGNIFICANCE STATEMENT We investigated the therapeutic efficacy of late initiation of chronic Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibition on progression of advanced congestive heart failure (CHF). Chronic CaMKII inhibition prevented CHF-induced activation of the sympathetic nervous system and restored normal intrinsic cardiomyocyte basal and β-adrenergic receptor–stimulated relaxation, contraction, and [Ca2+]i regulation, leading to reversal of CHF progression. These data provide new evidence that CaMKII inhibition is able and sufficient to rescue a failing heart, and thus cardiac CaMKII inhibition is a promising target for improving CHF treatment.

Background Angiotensin-(1–12) [Ang-(1–12)] is a renin-independent precursor for direct angiotensin-II production by chymase. Substantial evidence suggests that heart failure (HF) may alter cardiac Ang-(1–12) expression and activity; this novel Ang-(1–12)/chymase axis may be the main source for angiotensin-II deleterious actions in HF. We hypothesized that HF alters cardiac response to Ang-(1–12). Its stimulation may produce cardiac negative modulation and exacerbate left ventricle (LV) systolic and diastolic dysfunction. Methods and results We assessed the effects of Ang-(1–12) (2 nmol/kg/min, iv, 10 min) on LV contractility, LV diastolic filling, and LV-arterial coupling (AVC) in 16 SD male rats with HF-induced by isoproterenol (3 mo after 170 mg/kg sq. for 2 consecutive days) and 10 age-matched male controls. In normal controls, versus baseline, Ang-(1–12) increased LV end-systolic pressure, without altering heart rate, arterial elastance (EA), LV end-diastolic pressure (PED), the time constant of LV relaxation (τ) and ejection fraction (EF). Ang-(1–12) significantly increased the slopes (EES) of LV end-systolic pressure (P)-volume (V) relations and the slopes (MSW) of LV stroke wok-end-diastolic V relations, indicating increased LV contractility. AVC (quantified as EES/EA) improved. In contrast, in HF, versus HF baseline, Ang-(1–12) produced a similar increase in PES, but significantly increased τ, EA, and PED. The early diastolic portion of LV P V loop was shifted upward with reduced in EF. Moreover, Ang-(1–12) significantly decreased EES and MSW, demonstrating decreased LV contractility. AVC was decreased by 43%. Conclusions In both normal and HF rats, Ang-(1–12) causes similar vasoconstriction. In normal, Ang-(1–12) increases LV contractile function. In HF, Ang-(1–12) has adverse effects and depresses LV systolic and diastolic functional performance.

When laser cladding is used to repair parts, the interaction of parameters has a significant influence on equipment performance. In order to explore the process parameters and quality of Ni60PTA coating, the statistical relationship between the process parameters (laser power, scanning speed, and powder feeding rate) and the responses (dilution ratio, ratio of layer width to height, and contact angle) was established by experiments using the response surface method (RSM) and variance analysis. The results show that the laser power is the dominant factor affecting the dilution ratio. However, the scanning speed has the greatest influence on the ratio of layer width to height and contact angle. These experimental results show that the proposed model can predict the actual data. In addition, the microstructure and microhardness of the samples prepared with the optimum process parameters were characterized. The results show that the quality of the cladding layer is good without cracks, deformation, and pores. The microstructure of the cladding zone is mainly composed of γ (Ni), FeNi3, M (M = Fe, Ni, Cr)23C6, M7C3, and CrB. The average microhardness of the coating is about 620 HV0.2, which is about 3.1 times that of 45 steel substrate.

Acute myocardial infarction (AMI) is myocardial necrosis caused by the persistent interruption of myocardial blood supply, which has high incidence rate and high mortality in middle-aged and elderly people in the worldwide. Biomarkers play an important role in the early diagnosis and treatment of AMI. Recently, more and more researches confirmed that circRNA may be a potential diagnostic biomarker and therapeutic target for cardiovascular diseases. In this paper, a series of biological analyses were performed to find new effective circRNA biomarkers for AMI. Firstly, the expression levels of circRNAs in blood samples of patients with AMI and those with mild coronary stenosis were compared to reveal circRNAs which were involved in AMI. Then, circRNAs which were significant expressed abnormally in the blood samples of patients with AMI were selected from those circRNAs. Next, a ceRNA network was constructed based on interactions of circRNA, miRNA and mRNA through biological analyses to detect crucial circRNA associated with AMI. Finally, one circRNA was selected as candidate biomarker for AMI. To validate effectivity and efficiency of the candidate biomarker, fluorescence in situ hybridization, hypoxia model of human cardiomyocytes, and knockdown and overexpression analyses were performed on candidate circRNA biomarker. In conclusion, experimental results demonstrated that the candidate circRNA was an effective biomarker for diagnosis and therapy of AMI.

Background: Transgenic rats expressing the human angiotensinogen gene [TGR (hAogen) 1623] (hAogen) exhibit sustained hypertension and systolic dysfunction associated with altered cardiac renin-angiotensin system and β- adrenergic receptor (AR) signal transduction systems. We have shown previously, in contrast to β 1 - and β 2 -ARs, β 3 -ARs are linked to G i proteins, and stimulation of β 3 -ARs inhibits cardiac contraction and relaxation. Hypertension is associated with increased cardiac expression of G i proteins. This may alter β 3 -AR stimulation and play an important role in the cardiac functional impairment of this humanized model of hypertension. However, the alteration and functional effect of β 3 -AR activation in this model are unknown. We tested the hypothesis that high cardiac tissue Ang II content in hAogen may cause an up-regulation of cardiac β 3 -AR, which exacerbates myocyte dysfunction and impairs calcium regulation, thereby directly contributing to the cardiac dysfunction. Methods: We compared LV myocyte β 3 -AR expression and myocyte functional and [Ca 2+ ] i transient ([Ca 2+ ] iT ) responses to β- and β 3 -AR stimulation in myocytes obtained from 8 Sprague Dawley (SD) control and 8 hAogen male adult rats. Results: Versus SD, in hAGT rats, basal myocyte contraction (dL/dt max , 107.1 vs 138.8 μm/s), relaxation (dR/dt max , 94.0 vs 103.9 μm/s) and [Ca 2+ ] iT (0.15 vs 0.21) were depressed. A non-selective β-AR agonist, isoproterenol (ISO) (10 -8 M) produced significantly smaller increases in dL/dt max , (42% vs. 61%), dR / dtmax (35% vs. 51%), and [Ca 2+ ] iT (20% vs. 30%). Moreover, versus SD, in hAogen rats, LV myocyte β 3 -AR protein level increased by 32% (0.29 vs 0.22) with resulted significantly altered myocyte functional response to β 3 -AR stimulation. Compared with the changes in SD myocytes, in hAogen myocytes, BRL (10 -8 M) produced a significantly greater decreases in dL/dt max , (27% vs 12%), dR/dt max (28% vs 11%), and [Ca 2+ ] iT (17% vs 10%). Conclusions: TGR (hAogen) 1623, this humanized model of hypertension is associated with an up-regulation of LV myocyte β 3 -AR, which enhances β 3 -AR-caused inhibition of myocyte contractile, relaxation and [Ca 2+ ] iT and exacerbates β-AR desensitization, thereby directly contributing to the cardiac dysfunction.

Background: The negative inotrope and up-regulation of β 3 -adrenergic receptors (AR) in human and animal failing hearts suggest a direct and contributing role of cardiac β 3 -AR activation on the progression of congestive heart failure (CHF). However, its precise role is still being debated. We hypothesize that up-regulation of cardiac β 3 -AR is detrimental and chronic β 3 -AR blockade may prevent CHF-caused intrinsic defects of left ventricular (LV) myocyte force-generating capacity and relaxation and improve β-AR regulation, thereby limiting the progression of CHF. Methods: We compared the alterations of LV and myocyte functional responses and [Ca 2+ ] i transient ([Ca 2+ ] iT ) in SD rats divided into 3 groups (8/group): 1) CHF 3 months after isoproterenol (ISO) (170 mg/kg, sq, for 2 days); 2) ISO/β 3 -ANT , 2 months after receiving ISO, a selective β 3 -AR antagonist (ANT), L-748,337, was initiated (10 -7 M/kg/day, sq. by mini-pump) and was given for 1 month; and 3) Sham controls . Results: Compared with controls, the animals that received ISO treatment had CHF onset at 1 month and progressed to severe HF at 3 months after ISO. Plasma norepinephrine (NE) (1295 vs 259 pg/ml) increased 5-fold; whereas, stroke volume (SV) (39 vs 91 μl) and ejection fraction (EF) (39 vs 62%) significantly decreased, and LV end-diastolic pressure (P ED ) (13.9 vs 6.0 mmHg) was doubled. These changes were paralleled with about 50% reductions in cell contraction (dL/dt max , 93 vs 186 μm/s) and relaxation (dR/dt max , 96 vs 159 μm/s) associated with a significant decrease in the peak systolic [Ca 2+ ] iT , (0.17 vs 0.26). In addition, superfusion of ISO (10 -8 M) caused much less increases in dL/dt max (39 vs 68%), dR/dt max (23 vs 54%), and [Ca 2+ ] IT (14 vs 28%). Treatment with β 3 -ANT increased SV (89 μl) and EF (60%), decreased P ED more than 90% from ISO-treated values, and corrected the elevation of plasma NE (301 pg/ml), dL/dt max (184 μm/s), dR/dt max (152 μm/s), and [Ca 2+ ] iT (0.24). ISO-induced increase in dL/dt max and [Ca 2+ ] iT also returned close to control levels. Conclusion: Chronic β 3 -ANT treatment after CHF significantly improves LV and myocyte contractile function and [Ca 2+ ] i regulation and limits the development of CHF. Thus, β 3 -AR blocker may provide a new therapeutic strategy for the treatment of CHF.

Background: Natriuretic peptides (NPs) play a crucial role in maintaining cardiovascular homeostasis. NPs stimulate the production and release of cGMP, leading to the vasodilating and natriuretic actions. In heart failure (HF), circulating and cardiac ANP, BNP, and CNP are increased and exhibit a range of actions. However, although they serve as therapeutic agents, their direct cardiac effects in HF are uncertain due to the confounding influence of NPs-produced changes in loading condition on conventional measures of LV function. We test the hypothesis that equal hypotensive 3 NPs may have different inotropic effects on LV contractility and relaxation in HF. Methods: We assessed the cardiac effects of intravenous infusion (20 min) of ANP (2 μg/kg plus 0.5 μg/kg/min), BNP (2 μg/kg plus 0.04 μg/kg/min) and CNP (2 μg/kg plus 0.4 μg/kg/min) on different days in 6 instrumented conscious dogs with pacing-induced HF by using pressure (P)-volume (V) analysis, a load-independent measure of LV contractility. Results: Versus baselines, 3 NPs produced arterial vasodilation with similar and significant decreases in LV end-systolic pressure (10 to 12 mmHg) with relatively unchanged heart rate. ANP caused significant reductions (13%) of E ES (4.2 vs 4.8 mmHg/ml) and M SW (54.6 vs 62.8 mmHg). The time constant of LV relaxation (τ, 45.1 vs 37.6 ms) was lengthened. The LV-arterial coupling, E ES / E A (arterial elastance) (0.57 vs 0.58) was unaltered. The peak mitral flow, dV/dt max was only increased by 7% (178 vs 166 ml/s). With BNP, there were no significant changes in E ES (5.1 vs 4.9 mmHg/ml) and M SW, but E ES /E A was improved 30% (0.74 vs 0.57) due to decreased E A . τ (33.4 vs 37.9 ms) was significantly shortened and dV/dt max increased 15% (189 vs 165 ml/s). In contrast, CNP produced significant increases (~30%) in E ES (6.3 vs 4.8 mmHg/ml) and M SW (80.5 vs 62.4 mmHg) with enhanced increase in E ES /E A (50%, 0.87vs 0.58), but decrease in τ (25%, 28.4 vs 38.1 ms) and significantly greater augmented dV/dt max (25%, 205 vs 164 ml/s). Similar observations of NPs were made at constant heart rate, or after autonomic blockade. Conclusion: In conscious dogs with HF, equal hypotensive ANP, BNP and CNP have negative, no effect, and positive inotropic effects on LV contractility and relaxation, respectively.

Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is upregulated in congestive heart failure (CHF), contributing to electrical, structural, and functional remodeling. CaMKII inhibition is known to improve CHF, but its direct cardiac effects in CHF remain unclear. We hypothesized that CaMKII inhibition improves cardiomyocyte function, [Ca(2+)](i) regulation, and β-adrenergic reserve, thus improving advanced CHF. In a 16-week study, we compared plasma neurohormonal levels and left ventricular (LV)- and myocyte-functional and calcium transient ([Ca(2+)](iT)) responses in male Sprague-Dawley rats (10/group) with CHF induced by isoproterenol (170 mg/kg sq for 2 days). In rats with CHF, we studied the effects of the CaMKII inhibitor KN-93 or its inactive analog KN-92 (n = 4) (70 µg/kg per day, mini-pump) for 4 weeks. Compared with controls, isoproterenol-treated rats had severe CHF with 5-fold–increased plasma norepinephrine and about 50% decreases in ejection fraction (EF) and LV contractility [slope of LV end-systolic pressure–LV end-systolic volume relation (E(ES))] but increased time constant of LV relaxation (τ). They also showed significantly reduced myocyte contraction [maximum rate of myocyte shortening (dL/dt(max))], relaxation (dL/dt(max)), and [Ca(2+)](iT). Isoproterenol superfusion caused significantly fewer increases in dL/dt(max) and [Ca(2+)](iT). KN-93 treatment prevented plasma norepinephrine elevation, with increased basal and acute isoproterenol-stimulated increases in EF and E(ES) and decreased τ in CHF. KN-93 treatment preserved normal myocyte contraction, relaxation, [Ca(2+)](iT), and β-adrenergic reserve, whereas KN-92 treatment failed to improve LV and myocyte function, and plasma norepinephrine remained high in CHF. Thus, chronic CaMKII inhibition prevented CHF-induced activation of the sympathetic nervous system, restoring normal LV and cardiomyocyte basal and β-adrenergic–stimulated contraction, relaxation, and [Ca(2+)](iT), thereby playing a rescue role in advanced CHF. SIGNIFICANCE STATEMENT: We investigated the therapeutic efficacy of late initiation of chronic Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) inhibition on progression of advanced congestive heart failure (CHF). Chronic CaMKII inhibition prevented CHF-induced activation of the sympathetic nervous system and restored normal intrinsic cardiomyocyte basal and β-adrenergic receptor–stimulated relaxation, contraction, and [Ca(2+)](i) regulation, leading to reversal of CHF progression. These data provide new evidence that CaMKII inhibition is able and sufficient to rescue a failing heart, and thus cardiac CaMKII inhibition is a promising target for improving CHF treatment.

AIMS: G protein-coupled estrogen receptor 30 (GPR30) activation by its agonist, G1, exhibits beneficial actions in female with heart failure (HF). Recent evidence indicates its cardiovascular benefits may also include male as well. However, whether and how GPR30 activation may limit HF progression and have a salutary role in males is unknown. We hypothesized that chronic G1 treatment improves LV and cardiomyocyte function, [Ca(2+)](i) regulation and β-adrenergic reserve, thus reversing HF progression in male. MAIN METHODS: We compared left ventricle (LV) and myocyte function, [Ca(2+)](i) transient ([Ca(2+)](iT)) and β-AR modulation in control male mice (12/group) and isoproterenol-induced HF (150 mg/kg s.c. for 2 days). Two weeks after isoproterenol injection, HF mice received placebo, or G1 (150 μg/kg/day s.c. mini-pump) for 2 weeks. KEY FINDINGS: Isoproterenol-treated mice exhibited HF with preserved ejection fraction (HFpEF) at 2-weeks and progressed to HF with reduced EF (HFrEF) at 4-weeks, manifested by significantly increased LV time constant of relaxation (τ), decreased EF and mitral flow (dV/dt(max)), which were accompanied by reduced myocyte contraction (dL/dt(max)), relaxation (dR/dt(max)) and [Ca(2+)](iT). Acute isoproterenol-superfusion caused significantly smaller increases in dL/dt(max), dR/dt(max) and [Ca(2+)](iT). G1 treatment in HF increased basal and isoproterenol-stimulated increases in EF and LV contractility of E(ES). Importantly, G1 improved basal and isoproterenol-stimulated dL/dt(max), dR/dt(max) and [Ca(2+)](iT) to control levels and restored normal cardiac β-AR subtypes modulation. SIGNIFICANCE: Chronic G1 treatment restores normal myocyte basal and β-AR-stimulated contraction, relaxation, and [Ca(2+)](iT), thereby reversing LV dysfunction and playing a rescue role in a male mouse model of HF.

Background: Atrial fibrillation (AF) is an important and growing clinical problem. Current pharmacological treatments are unsatisfactory. Electrical remodeling has been identified as one of the principal pathophysiological mechanisms that promote AF, but there are no effective therapies to prevent or correct electrical remodeling in patients with AF. In AF, cardiac production and circulating levels of B-type natriuretic peptide (BNP) are increased. However, its functional significance in AF remains to be determined. We assessed the hypotheses that chronic BNP treatment may prevent the altered electrophysiology in AF, and preventing AF-induced activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) may play a role. Methods and Results: Forty-four rabbits were randomly divided into sham, rapid atrial pacing (RAP at 600 beats/min for 3 weeks), RAP/BNP, and sham/BNP groups. Rabbits in the RAP/BNP and sham/BNP groups received subcutaneous BNP (20 μg/kg twice daily) during the 3-week study period. HL-1 cells were subjected to rapid field stimulation for 24 hours in the presence or absence of BNP, KN-93 (a CaMKII inhibitor), or KN-92 (a nonactive analog of KN-93). We compared atrial electrical remodeling-related alterations in the ion channel/function/expression of these animals. We found that only in the RAP group, AF inducibility was significantly increased, atrial effective refractory periods and action potential duration were reduced, and the density of I Ca, L and I to decreased, while I K1 increased. The changes in the expressions of Cav1.2, Kv4.3, and Kir2.1 and currents showed a similar trend. In addition, in the RAP group, the activation of CaMKIIδ and phosphorylation of ryanodine receptor 2 and phospholamban significantly increased. Importantly, these changes were prevented in the RAP/BNP group, which were further validated by in vitro studies. Conclusions: Chronic BNP therapy prevents atrial electrical remodeling in AF. Inhibition of CaMKII activation plays an important role to its anti-AF efficacy in this model.

Background Whether chronic obstructive sleep apnea ( OSA ) could promote epicardial adipose tissue ( EAT ) secretion of profibrotic adipokines, and thereby contribute to atrial fibrosis, and the potential therapeutic effects of metoprolol remain unknown. Methods and Results A chronic OSA canine model was established by repeatedly clamping the endotracheal tube for and then reopening it for 4 hours every other day for 12 weeks. In a metoprolol treatment group, metoprolol succinate was administered daily for 12 weeks. The EAT infiltration and left atrial fibrosis were examined. The expressions of adipokines secreted by EAT and hypoxic 3T3‐L1 adipocytes were detected. The changes in collagen synthesis, transforming growth factor‐β1 expression, and cell differentiation and proliferation in cardiac fibroblasts induced by hypoxic 3T3‐L1 adipocyte‐derived conditioned medium were further analyzed. Chronic OSA induced infiltration of EAT into the left atrium. OSA enhanced the profibrotic effect of EAT on the adjacent atrial myocardium. Moreover, OSA induced profibrotic cytokine secretion from EAT . We also found that hypoxia induced adipokine secretion in cultured adipocytes, and the medium conditioned by the hypoxic adipocytes increased collagen and transforming growth factor‐β1 protein expression and cell proliferation of cardiac fibroblasts. More importantly, metoprolol attenuated infiltration of EAT and alleviated the profibrotic effect of EAT by inhibiting adipokine secretion. Metoprolol also inhibited hypoxia‐induced adipokine secretion in adipocytes and thereby blocked the hypoxic adipocyte–derived conditioned medium–induced fibrotic response of cardiac fibroblasts. Conclusions Chronic OSA enhanced the profibrotic effect of EAT on the neighboring atrial myocardium by stimulating the secretion of profibrotic adipokines from EAT , which was significantly attenuated by metoprolol. This study gives insights into mechanisms underlying OSA ‐induced atrial fibrillation and also provides experimental evidence for the protective effects of metoprolol.

In heart failure (HF), the impaired left ventricular (LV) arterial coupling and diastolic dysfunction present at rest are exacerbated during exercise. C-type natriuretic peptide (CNP) is elevated in HF; however, its functional effects are unclear. We tested the hypotheses that CNP with vasodilating, natriuretic, and positive inotropic and lusitropic actions may prevent this abnormal exercise response after HF. We determined the effects of CNP (2 μg/kg plus 0.4 μg/kg per minute, i.v., 20 minutes) on plasma levels of cGMP before and after HF and assessed LV dynamics during exercise in 10 chronically instrumented dogs with pacing-induced HF. Compared with the levels before HF, CNP infusion caused significantly greater increases in cGMP levels after HF. After HF, at rest, CNP administration significantly reduced LV end-systolic pressure (PES), arterial elastance (EA), and end-diastolic pressure. The peak mitral flow (dV/dtmax) was also increased owing to decreased minimum LVP (LVPmin) and the time constant of LV relaxation (τ) (P < 0.05). In addition, LV contractility (EES) was increased. The LV-arterial coupling (EES/EA) was improved. The beneficial effects persisted during exercise. Compared with exercise in HF preparation, treatment with CNP caused significantly less important increases in PES but significantly decreased τ (34.2 vs. 42.6 ms) and minimum left ventricular pressure with further augmented dV/dtmax. Both EES, EES/EA (0.87 vs. 0.32) were increased. LV mechanical efficiency improved from 0.38 to 0.57 (P < 0.05). After HF, exogenous CNP produces arterial vasodilatation and augments LV contraction, relaxation, diastolic filling, and LV arterial coupling, thus improving LV performance at rest and restoring normal exercise responses after HF.

Background Angiotensin-(1–12) [Ang-(1–12)] is a chymase-dependent source for angiotensin II (Ang II) cardiac activity. The direct contractile effects of Ang-(1–12) in normal and heart failure (HF) remain to be demonstrated. We assessed the hypothesis that Ang-(1–12) may modulate [Ca 2+ ] i regulation and alter cardiomyocyte contractility in normal and HF rats. Methods and results We compared left ventricle (LV) myocyte contractile and calcium transient ([Ca 2+ ] iT ) responses to angiotensin peptides in 16 SD rats with isoproterenol-induced HF and 16 age-matched controls. In normal myocytes, versus baseline, Ang II (10 −6 M) superfusion significantly increased myocyte contractility (dL/dt max : 40%) and [Ca 2+ ] iT (29%). Ang-(1–12) (4 × 10 −6 M) caused similar increases in dL/dt max (34%) and [Ca 2+ ] iT (25%). Compared with normal myocytes, superfusion of Ang II and Ang-(1–12) in myocytes obtained from rats with isoproterenol-induced HF caused similar but significantly attenuated positive inotropic actions with about 42% to 50% less increases in dL/dt max and [Ca 2+ ] iT . Chymostatin abolished Ang-(1–12)-mediated effects in normal and HF myocytes. The presence of an inhibitory cAMP analog, Rp-cAMPS prevented Ang-(1–12)-induced inotropic effects in both normal and HF myocytes. Incubation of HF myocytes with pertussis toxin (PTX) further augmented Ang II-mediated contractility. Conclusions Ang-(1–12) stimulates cardiomyocyte contractile function and [Ca 2+ ] iT in both normal and HF rats through a chymase mediated action. Altered inotropic responses to Ang-(1–12) and Ang II in HF myocytes are mediated through a cAMP-dependent mechanism that is coupled to both stimulatory G and inhibitory PTX-sensitive G proteins.

Objective: Recent evidence has shown that, in heart failure (HF), clinically relevant concentrations of angiotensin-(1-7) [Ang-(1-7)] counteracts angiotensin II induced cardiac depression and produces positive inotropic effects in both left ventricle (LV) and myocytes. However, the underlying electrophysiological mechanism is unclear. We investigated the role and mechanism of Ang-(1-7) on LV myocyte L-type calcium current (ICa,L) responses in normal state and in HF. Method: We compared the effect of Ang-(1-7) (10−5 M) on ICa,L responses in isolated LV myocytes obtained from 11 rats with isoproterenol (ISO) induced HF (3 months after 170 mg/kg subcutaneous for 2 days) and from 8 age-matched normal control rats by patch clamp technique. Results: In normal myocytes, compared with baseline, superfusion of Ang-(1-7) caused no significant changes in ICa,L (8.2 ± 0.2 versus 8.0 ± 0.3 pA/pF, p= not significant). In HF myocytes, the baseline ICa,L was significantly reduced (5.3 ± 0.1 versus 8.0 ± 0.3 pA/pF, p < 0.01). Ang-(1-7) produced a 21% increase in ICa,L (6.4±0.1 versus 5.3±0.1 pA/pF, p < 0.01). Pretreatment of HF myocytes with a nitric oxide (NO) synthase inhibitor (L-NAME, 10−5 M) resulted in a significantly greater increase in ICa,L (28%, 8.4 ± 0.1 versus 6.5 ± 0.1 pA/pF, p < 0.01) during Ang-(1-7) superfusion. In contrast, during incubation with the bradykinin (BK) inhibitor HOE 140 (10−6 M), Ang-(1-7) induced increase in ICa,L was significantly decreased. The Ang-(1-7) induced increase in ICa,L was abolished by [D-Ala7]-Ang-(1-7) (A-779, 10−5 M). Conclusions: HF alters the response of ICa,L to Ang-(1-7). In normal myocytes, Ang-(1-7) has no significant effect on ICa,L. However, in HF myocytes, Ang-(1-7) increases ICa,L. These effects are mediated by the Ang-(1-7) Mas receptors and involve activation of NO/BK pathways.

Background: In addition to its well-known vasodilating and natriuretic actions, C-type natriuretic peptide (CNP), has been viewed as an endogenous inhibitor of the renin-angiotensin system, but its...

A new squaraine dye Bis(4-N,N-dicarboxymethyl-2-hydroxyphenyl)squaraine (SQ) which could be used as organic photovoltaic materials, was synthesized, and its molecular structure was fully characterized by elemental analysis, IR, 1H NMR and MS. SQ exhibits strong absorption band over 600–700 nm. Addition of TiO2 colloids to the ethanol solution of SQ resulted in the increase of optical density, quenching of fluorescence and shortened fluorescence lifetime. The apparent association constant between the sensitizer and semiconductor as measured from the fluorescence quenching data, was 2427 M−1. Fluorescence lifetime measurements gave the rate constant for the electron injection process from the excited singlet of SQ to the conduction band of TiO2 nanoparticles as 2.55 × 10 8 s−1. In addition, SQ doped SiO2 gel glass slices were prepared and characterized by absorption and emission spectra.

Background . In heart failure (HF), circulating levels of arginine vasopressin (AVP) are elevated and there is direct relationship between a rise in AVP levels and increased morbidity and mortality. Recent observations further demonstrated the increased AVP 1A receptor (V1AR) expression in failing human hearts and suggested that these alterations may alter cardiac contractile behavior in HF. However, the direct cardiac effects of V1AR in normal and HF remain undetermined. The cellular basis for AVP-associated adverse clinical consequences in HF is unclear. We assessed the hypothesis that in HF, AVP may produce negative modulation on [Ca 2+ ] i regulation and cause direct depression in cardiomyocyte contractile performance. Methods . We assessed LV myocyte functional and calcium transient ([Ca 2+ ] iT ) responses to AVP (10 -7 M) in 8 control and 12 SD rats with isoproterenol (ISO) induced HF (2 months after 170 mg/kg sq for 2 days) in the absence and presence of selective V1AR blockade ([Pmp1, Tyr (OMe) 2, Arg 8 ] AVP, 10 -6 M), or pretreatment of myocytes with G i inhibitor (PTX, 2 μg/ml, 6 hrs). Results . Compared with controls, ISO-treated rats had established HF after ISO at 2 months with significant LV dilatation and decreased ejection fraction (EF, 31% vs 61%). In normal myocytes, versus baselines, AVP superfusion caused no significant changes in myocyte contraction (dL/dt max ) (130.6 vs 136.8 μm/s), relaxation (dR/dt max ) (99.5 vs 103.5 μm/s) and [Ca 2+ ] iT (0.24 vs 0.24). In contrast, in HF, myocyte function was impaired and further depressed by AVP. Versus HF baselines, AVP resulted significantly decreases in dL/dt max (24%, 57.2 vs 75.4 μm/s) and dR/dt max (20%, 39.3 vs 49.0 μm/s) accompanied by reduced [Ca 2+ ] iT (17%, 0.14 vs 0.17). In HF myocytes, these AVP mediated effects were abolished by prior exposure of myocytes to V1AR blockade or PTX. Conclusions . HF alters AVP cardiac effects. In HF, AVP exacerbates the dysfunctional [Ca 2+ ] i homeostasis, producing decreased the peak systolic [Ca 2+ ] iT . AVP causes direct inhibitions of LV myocyte contraction and relaxation, These effects are coupled with the activation of V1AR and are likely to be mediated through the PTX-sensitive G protein pathway and may thus play an important role in promoting functional impairment in HF.

Background. The negative inotrope and upregulation of β 3 -adrenergic receptors (AR) in failing human and animal hearts suggest a direct and contributing role of cardiac β 3 -AR activation on heart failure (HF) progression. However, its precise role is still being debated. We hypothesize that up-regulation of β 3 -AR is detrimental and chronic β 3 -AR blockade may limit or prevent the progression of HF. Methods. We determined Left ventricular (LV) and myocyte functional response and β 1 - and β 3 -AR expressions in 3 groups of rats (6/group) for a period of 4 months: 1) Isoproterenol (ISO)-treated, 4 months after receiving ISO (170 mg/kg, sq, for 2 days); 2) ISO/β 3 -ANT, two months after receiving ISO, L-748,337, a selective β 3 -AR antagonist (β 3 -ANT) (10 -7 M/kg/day by implanted osmotic mini pump) was initiated after established HF and was given for 2 months; and 3) sham controls. Results. Compared with controls, ISO-treated rats had HF onset at one month after ISO and progressed to severe HF at 4 months. Plasma norepinephrine (NE, 1482 vs 247 pg/ml) increased 6 fold. Both stroke volume (SV) and ejection fraction (EF, 32% vs 61%) decreased more than 48%, and LV end-diastolic pressure (P ED , 15.4 vs 6.0 mmHg) doubled, parallel with 48% reductions in cell contraction (dL/dt max, 78 vs 149 μm/s) and relaxation (dR/dt max , 66 vs 128 μm/s) and a much less increase in dL/dt max (30% vs 74%) in response to superfusion of ISO (10 -8 M). These changes were associated with significantly decreased β 1 -AR mRNA (0.30 vs 0.64) and protein levels (0.36 vs 0.62), but increased β 3 -AR mRNA (1.29 vs 0.52) and protein levels (0.35 vs 0.18). Treatment with β 3 -ANT significantly decreased P ED and plasma NE (191 pg/ml). Both SV and EF (59%) increased to more than 76% from ISO-treated values. The signal ratios of β 1 -AR mRNA (0.61) and β 3 -AR mRNA (0.59) remained close to control levels. ISO-induced increase in dL/dt max (75%) was also significantly augmented. Conclusion. Chronic β 3 -ANT prevented plasma norepinephrine elevations and causes normalization of β 1 - and β 3 -AR gene expression, restores normal responsiveness of myocyte to β-AR stimulation, and leads to regression of LV and myocyte dysfunction in a rat model of progressive HF. Thus, β 3 -AR blocker may provide a new therapeutic strategy for the treatment of HF.

Background: There is substantial evidence supporting oxidative stress as an important mechanism to age-related cardiac dysfunction and altered β 3 -adrenergic receptor (AR)-activated nitric oxide synthase (NOS) pathway contributing to this process. However, the NOS isoforms involved are controversial. The mechanism of how β 3 -AR stimulation impacts ROS, SERCA2a, and cardiac function in cardiac aging (CA) is unclear. We tested the hypothesis that oxidative stress from up-regulation of cardiac β 3 -AR-activated iNOS uncoupling promotes CA. Methods: We compared myocyte subtypes of β-ARs, three NOS, peroxynitrite (NT), NADPH, GTPCH and SERCA2a expressions and myocyte contractile and [Ca 2+ ] i transient ([Ca 2+ ] iT ) responses to β-AR stimulation with isoproterenol (ISO, 10 -8 M). LV myocytes were isolated from 2 young (Y) (~4 to 6 m) and 2 aged (A) (~28 to 31 m) groups (5/group) of wild-type (WT) and β 3 -AR knockout (β 3 KO) mice. Results: Compared to YWT, AWT myocytes had significantly increased protein levels of β 3 -AR (0.31 vs 0.16) and iNOS (0.48 vs 0.21) accompanied with increased oxidative stress indicated by significant increases in NT formation (increased 102%) and NADPH (P67 -phox , 35% and p22 -phox , 28%), but decreased GTPCH expression (41%, 0.48 vs 0.82) and activity. AWT myocytes had significantly decreased β 1 -AR protein (0.38 vs 0.59), SERCA2a (0.26 vs 0.72) and the ratios of SERCA2a/PLB. These changes were associated with reduced basal cell contraction (dL/dt max, 76.4 vs 122.8 μm/s), relaxation (dR/dt max , 58.9 vs 94.3 μm/s), and [Ca 2+ ] iT (0.16 vs 0.24) accompanied by diminished β-AR-stimulated positive inotropic response. Importantly, in contrast to age-caused changes in AWT, versus Yβ 3 KO, in Aβ 3 KO myocytes, there were no significant alterations in iNOS (0.19 vs 0.16), NT (increased 9%), β 1 -AR (0.60 vs 0.62), and SERCA2a (1.2 vs 1.4). Aβ 3 KO myocytes had normal cell contraction and relaxation with preserved ISO-stimulated positive inotropic response. Conclusions: Myocardial aging is associated with up-regulation of cardiac β 3 -AR-activated iNOS pathway, which leads to imbalance in NO/superoxide production, favoring subsequent iNOS uncoupling and directly contributes to age-associated deficits in LV myocyte function and [Ca 2+ ] i regulation.

Angiotensin-(1-12) [Ang-(1-12)] functions in rodents and humans as a tissue substrate for the direct generation of Ang II via chymase. Since its direct cardiac effect have not been studied, the importance of this renin-independent mechanism for Ang II paracrine/intracrine actions in modulating cardiac contractility were determined in freshly isolated myocytes from 11 normal SD rats. Systolic amplitude (SA), peak velocity of shortening (dL/dtmax), the peak velocity of relengthening (dR/dtmax), and changes in the peak calcium transient ([Ca2+]i) were evaluated before and following exposure to Ang II (10-6 M), Ang-(1-12) delivered alone (range: 2x10-6 to 4x10-6 M) or after 1 h incubation with human recombinant chymase (10 μg protein/mL at 37°C). Both Ang II and the mixture of Ang-(1-12) with chymase elicited positive inotropic responses in freshly isolated cardiac myocytes associated with significant increases in peak systolic [Ca2+]i (Figure) while superfusion of Ang-(1-12) alone elicited an increase in dL/dtmax without significant changes in [Ca2+]i. The increases in contractility elicited by Ang II or the Ang-(1-12)/chymase mixture were abolished by prior exposure of the myocytes to losartan (10-5 M) or the chymase inhibitor chymostatin (8x10-5 M). We conclude that in single adult rat myocytes Ang-(1-12) stimulates contractile function through a chymase mediated action and by mechanisms that implicate a paracrine/intracrine activation of intracellular calcium.

Background: Sildenafil (SIL), a selective inhibitor of cGMP-specific PDE5 has been shown to exert profound cardioprotection in various cardiac pathologies. This beneficial action has been attributed to its selective vasodilatation effect. However, recent studies indicate that SIL may augment cGMP signaling and produce direct cardiac inotropic modulation, thus affords its cardioprotection in heart failure (HF). Whether SIL plays a role in cardiac contractile behavior in HF remains undetermined. SIL has been reported variably to have a positive, negative or no inotropic effect on cardiac contractility in HF. These disparate observations may be due to the confounding effects of loading conditions and dosage of SIL. We tested the hypothesis that SIL evokes positive modulation on cardiac contractility which importantly contributes to its beneficial action in HF. Methods: We measured Left ventricular (LV) contractility changes after SIL (0.4 mg/kg, iv), and compared myocyte contractile and [Ca 2+ ] i transient ([Ca 2+ ] iT ) responses to SIL (10 -6 M) in 8 rats with isoproterenol (ISO)-induced HF (3 months after 170 mg/kg sq for 2 days). LV contractility was measured by pressure-volume analysis. Results: Compared with normal controls, ISO-treated rats had established HF after ISO at 3 months with significantly elevated plasma norepinephrine, LV dilatation, and decreased ejection fraction (EF, 29% vs 61%). Compared with baseline, acute administration of SIL caused no change in LV systolic blood pressure and heart rate, but increased EF (43% vs 29 %). LV time constant of relaxation (t) (12.2 vs 15.1 ms) decreased. The slopes of LV pressure-volume relations of E ES (49%, 0.92 vs 0.61 mmHg/μl) and M SW (42%, 97.4 vs 68.6 mmHg) were increased, indicating significantly enhanced LV contractility. These responses were accompanied with about 24% increases in cell contraction (dL/dt max , 97.1 vs 78.3 μm/s) and relaxation (dR/dt max , 63.7 vs 51.5 μm/s) and relatively unchanged [Ca 2+ ] iT (0.149 vs 0.137), while myocyte Ca 2+ sensitivity was enhanced. Conclusions: In HF, positive inotropic effect is induced by acute inhibiting PDE5 with clinically-relevant concentrations of SIL. The cardiostimulatory and vasodilatory actions of SIL make it suitable for the treatment of HF.

Background: We have shown that Sildenafil (SIL), a selective PDE5 inhibitor reversed left ventricular (LV) dysfunction and β- adrenergic receptors (AR) desensitization in heart failure (HF). However the mechanism is not yet clear. Recent evidence suggests that normal myocardial performance depend on the balance in cardiomyocyte β 3 -, β 1 -, and β 2 -AR. Pivotal restructuring of β-AR system resulting in decline of β-adrenergic reserve plays a crucial role in the development of HF. We assessed the hypothesis that chronic SIL would prevent HF-induced abnormalities of β-AR subtype-stimulated regulation on intrinsic LV myocyte function and [Ca 2+ ] i regulation, thus restoring cardiac function. Methods: Studies were conducted in 3 groups (10/group) of rats: 1) HF, 12 weeks (W) after receiving isoproterenol (ISO) (170 mg/kg sq for 2 days); 2) HF/SIL, 8W after receiving ISO, SIL (70 μg/kg/day sq via mini pump) was initiated and given for 1 M; and 3) controls. After 12W, we compared LV myocyte contractile and [Ca 2+ ] iT responses to β-AR subtype stimulation by random exposure of myocytes to ISO (10 -8 M) or a selective β 1 -, β 2 -, or β 3 -agonist, Norepinephrine (NE, 10 -7 M), Zinterol (ZIN, 10 -5 M) and BRL-37,344 (BRL, 10 -8 M), respectively, during drug superfusion. Results: Only ISO-treated rats had HF showed 46% decreased LV contractility (E ES ) and extensive LV myocardium fibrosis. Compared with normal myocytes (N), in HF myocytes, basal cell contractility (dL/dt max , HF: 77 vs N: 136 μm/s), relaxation and [Ca 2+ ] iT all significantly decreased. ISO-stimulated dL/dt max (31% vs 67%) was attenuated accompanied by a diminished NE-mediated increase in dL/dt max (13% vs 49%), but enhanced BRL-induced decreases in dL/dt max (-29% vs -16%).The response of dL/dt max (25% vs 15%) to ZIN was increased. Importantly, in HF/SIL myocytes, the basal dL/dt max (139 μm/s) and [Ca 2+ ] iT remained close to control values with preserved β-stimulated positive modulation on cell contraction. The increases in dL/dt max in response to ISO (70%) and NE (44%) were similar as in normal myocytes, but repose to ZIN (27%) was enhanced. Conclusions: Chronic SIL reverses β-adrenergic signaling defects, resensitizing the β-AR subtype system modulation on LV myocytes function, thus playing a salutary role in HF.

Background: Accumulating evidence suggests that Angiotensin (A)-(1-7) exhibits cardiovascular effects that are in opposition to that of AII, thus providing protection against heart diseases. However, the exact means by which A-(1-7) affords cardioprotection are unclear. Its direct cardiac effect is not well understood. We previously showed that in heart failure (HF), AII decreases left ventricle (LV) contractility. Whether A-(1-7) may antagonize AII-induced cardiac depression, thereby contributing to its beneficial actions in HF remains to be determined. We assessed the hypothesis that A-(1-7) may produce positive modulation on [Ca 2+ ] i regulation and LV and myocyte contraction via A-(1-7) receptors, coupled with nitric oxide (NO)/bradykinin (BK)-mediated mechanism. Methods: We measured LV contractility changes after A-(1-7) (650 ng/kg, iv), which produced a 20-fold increase in plasma A-(1-7) levels, mimicking the elevations caused by angiotensin-converting enzyme inhibitor therapy in HF, and compared myocyte contractile, [Ca 2+ ] i transient ([Ca 2+ ] iT ) and I Ca,L responses to A-(1-7) (10 -5 M) in 14 rats with isoproterenol induced HF (3 months after 170 mg/kg sq for 2 days). In the subsets of cell contractile study, myocytes were pretreated to inhibit NO synthase (L-NAME, 10 -5 M), BK (HOE 140, 10 -6 M) or A-(1-7) receptor [D-Ala 7 ]-A-(1-7), 10 -5 M) followed with A-(1-7) exposure. Results: Compared with baseline, after A-(1-7), E ES (47%, 1.0 vs 0.68 mmHg/μl) and M SW (49%, 94.3 vs 62.8 mmHg) were increased, indicating enhanced LV contractility. In HF myocytes, A-(1-7) increased myocyte percent shortening (28%, 6.8% vs 5.3%), the velocity of contraction (31%, 106.4 vs 74.5 μm/sec) and relengthening (41%, 74.7vs 50.1 μm/sec) accompanied by significantly-increased [Ca 2+ ] iT (27%, 0.19 vs 0.15 pA/pF) and I Ca,L (24%, 6.3 vs 5.1pA/pF). L-NAME increased, HOE 140 decreased, and A-(1-7) receptor blockade prevented myocyte contractile responses to A-(1-7). Conclusion: In HF, clinically-relevant concentrations of A-(1-7) counteracted AII-induced cardiac depression, increased [Ca 2+ ] iT and I Ca,L , and produced positive inotropic effects in both LV and myocytes. These effects are coupled with A-(1-7) receptors and involve activation of NO/BK pathways.

Background: Sildenafil (SIL), a selective inhibitor of PDE5 has been shown to exert profound beneficial effects in heart failure (HF). Recently we further found that SIL caused regression of cardiac dysfunction in a rat model with isoproterenol (ISO)-induced progressive HF. However, the molecular basis is unclear. We hypothesized that reversal of HF-induced detrimental alterations on the expressions of cardiac SR Ca 2+ -ATPase (SERCA2a), β-adrenergic receptors (AR) and nitric oxide synthase (NOS) isoforms by SIL may play a key role for its salutary role in HF. Methods: Left ventricular (LV) and myocyte function and the protein levels of myocyte β 1 - and β 3 - AR, SERCA2a, phospholamban (PLB) and three NOS were simultaneously evaluated in 3 groups of male rats (6/group): HF , 3 months (M) after receiving ISO (170 mg/kg sq for 2 days); HF/SIL , 2 M after receiving ISO, SIL (70 μg/kg/day sq via mini pump) was initiated and given for 1 M; and Controls (C). Results: Compared with controls, ISO-treated rats progressed to severe HF at 3 M after ISO followed by significantly decreased LV contractility (E ES , HF: 0.7 vs C: 1.2 mmHg/μl) and slowed LV relaxation, reductions in the peak velocity of myocyte shortening (77 vs 136 μm/sec), relengthening (62 vs 104 μm/sec) and [Ca 2+ ] iT (0.15 vs 0.24) accompanied by a diminished myocyte inotropic response to β-AR agonist, ISO (10 -8 M). These abnormalities were associated with concomitant significant decreases in myocyte protein levels of β 1 -AR (0.23 vs 0.64), SERCA2a (0.46 vs 0.80), PLB Ser16 /PLB ratio (0.24 vs 0.40) and eNOS (0.28 vs 0.46), but significantly increases in protein levels of β 3 -AR (0.29 vs 0.10) and iNOS (0.18 vs 0.08) with relatively unchanged nNOS. Chronic SIL prevented the HF-induced decreases in LV and myocyte contraction, relaxation, peak [Ca 2+ ] iT , and restored normal myocyte contractile response to ISO stimulation. With SIL, protein levels of myocyte β 1 - and β 3 -AR, SERCA2a were restored close to control values, but eNOS was significantly elevated than controls (0.77). Conclusions: Chronic SIL prevents HF-caused downregulation of cardiac β 1 -AR and reverse contrast changes between iNOS and β 3 -AR with SERCA 2a and eNOS expression, leading to the preservation of LV and myocyte function, [Ca 2+ ] iT , and β-adrenergic reserve.

The photoelectrochemical behavior of mercapto-substituted hypocrellin B (MSHB), deposited on SnO2 optically transparent electrodes by means of the Langmuir–Blodgett technique, have been investigated. Addition of electron donors leads to a remarkable enhancement of the photocurrents and photovoltages. Effects of the electron donor concentration, LB film layers, and illumination time on the magnitude of the photocurrent were studied in detail. The usefulness of hypocrellin derivatives as efficient organic photoelectrical conversion materials is suggested.

Two strong fluorescent amphiphilic europium-dibenzoylmethane complexes, hexadecyltrimethyl ammonium tetrakis (dibenzoylmethane) europium (A) and octadecyltriethyl ammonium tetrakis (dibenzoylmethane) europium (B), were synthesized and characterized by FT-IR, UV-vis, DTA-TG analysis and X-ray diffraction. Both of them could form stable Langmuir films at the air-water interface and the Langmuir film of A can be easily transferred onto hydrophilic substrates to build up Langmuir-Blodgett (LB) films. The LB film of A has a good layered structure, as confirmed by its low-angle X-ray diffraction. The fluorescence spectra and fluorescence lifetimes of the LB films were quite different from those of their corresponding solid powders and solutions.

An amphiphilic zinc phthalocyanine (AmZnPc) containing long alkyl chains covalently attached to the positively charged macroring was synthesized. A monolayer of AmZnPc with equimolar meso-tetrakis-(4-tolyl)porphine (TTP) was spread on water from chloroform solution and transferred onto CaF 2 slides. Multilayers were also built up on these substrates. Surface pressure-area isotherms and UV—visible absorption spectra showed that the porphyrin molecules are arranged in the cavity between the long alkyl chains of AmZnPc in one layer of the Langmuir—Blodgett film. Polarized UV—visible spectroscopy indicated that there is no anisotropy in the layer plane and the AmZnPC macroring plane lies nearly parallel to the substrate surface.

Photoinduced anisotropy of a photochromic pyrrylfulgide/PMMA film was investigated by using two linearly polarized beams. Excitation by linearly polarized light induces into the film an optical axis that has the same polarization as the excitation beam. This causes a change of the transmittance and of the polarization state of the detection beam. With a microscope a matrix of 4x4 light spots with different polarizations were recorded in the pyrrylfulgide/PMMA film. If readout with non-polarized light, the matrix of light spots show no information pattern. However, when readout with differently polarized lights, different patterns can be displayed. The experiment demonstrates that pyrrylfulgide/PMMA films can be used to hide two differently polarized patterns, which may be applied in camouflage technology.