Differential mode delay diagnostics for LP modes traversing a few-mode fiber.

We provide differential mode delay (DMD) diagnostics for linearly polarized (LP) modes traversing a few-mode fiber (FMF). We employ a modal interferometer method with a butt coupling mechanism to measure the DMD between any two modes guided in FMFs with step-index (SI) and depressed-cladding profiles. The measurement principle is based on investigating a transmitted spectrum through temporal decomposition by means of a Fourier transform. At least four different temporal waveforms are needed for an FMF supporting four LP modes to estimate the DMD between two different LP modes. A butt coupling mechanism with an air gap between an FMF and a dispersion-shifted fiber is employed for simultaneous DMD measurement. The present diagnostics requires some knowledge of the bending loss characteristics of the FMFs and the butt coupling properties of the circular symmetry modes or circular asymmetry modes in their electric fields. The DMD diagnostics are realized taking the bending loss and butt coupling characteristics into consideration. We present experimental results for the DMD and DMD slope as a function of the wavelength in a 1450-1625 nm telecommunication band.

Diagnosis of modal and chromatic dispersions for the LP01 and LP11 modes through temporal decomposition by means of Fourier transform.

We provide a novel approach for estimating the modal and chromatic dispersions of the LP01 and LP11 modes traversing a two-mode fiber (TMF). A modal interferometer is used to measure the differential group delay (DGD) and chromatic dispersion for the two modes in the 1260-1360 nm telecommunication band. The measurement principle is based on an investigation of a transmitted spectrum through temporal decomposition by means of a Fourier transform. The diagnosis of the DGD and chromatic dispersion for the two modes is discussed theoretically and experimentally. The experimental results obtained here exactly match those obtained previously. The salient feature of the present method is that the modal interferometer configuration makes it possible to measure both the DGD and chromatic dispersion and also estimate the shape of optical pulses traversing a TMF.

Space-division multiplexed transmission in the S-band over 55 km few-mode fibers.

Transmission of highly spectral efficient 24.5 GBaud quadrature phase shift keying and 16- and 64-quadrature amplitude modulated signals in the S-band between 1492 nm and 1518 nm wavelength is demonstrated over 55 km few-mode fibers. The carrier lines for S-band transmission were generated by a single wideband optical comb source with more than 120 nm optical bandwidth. While the three-mode fiber was originally optimized for C- and L-band transmission, we show that differential mode delay and mode-dependent loss show only a minor wavelength dependence within the measured S-band channels. However, the transceiver sub-system, including S-band optical amplifiers as well as a reduced optical signal-to-noise ratio of the comb source, leads to a significant Q-factor penalty for channels towards the edges of the S-band optical amplifiers below 1495 nm and above 1515 nm wavelength.

Optimal design of 4LP-mode multicore fibers for high spatial multiplicity.

High spatial multiplicity fiber designs are presented for homogeneous and heterogeneous 4LP-mode multicore fibers (MCFs) that support six spatial modes per core. The high-spatial-density 4LP-mode MCF design methodology is explained in detail. The influence of the number of cores on the cladding diameter (Dcl) and relative core multiplicity factor (RCMF) is investigated. The optimal core designs and MCF layouts with square and triangular lattices maintain glass fiber reliability (maximum Dcl = 250 µm). For homogeneous 4LP-mode MCFs, a 19-core triangular-lattice fiber gives the highest RCMF of 61.7. For heterogeneous 4LP-mode MCFs, an RCMF of 65.4 is obtained for a 21-core square-lattice fiber.

Preventive effect of chronic endothelin type A receptor antagonist on coronary microvascular spasm induced by repeated epicardial coronary artery endothelial denudation in pigs.

AIM: We investigated the role of endothelin-1 (ET-1) in coronary microvascular spasm in a porcine model. METHODS: A flowmeter was implanted around the left anterior descending coronary artery (LAD), and epicardial coronary artery endothelial denudation (ED) was performed just distal to the flowmeter every 2 weeks (W) until 6 W in 10 pigs (ED group). Ten pigs were chronically treated with endothelin type A receptor (ET(A)) antagonist (TA-0201, 0.1 mg/kg/day, ED+ET(A) group), while neither ED nor administration of ET(A) antagonist was performed in 12 pigs (Control group). We assessed changes in LAD blood flow and the denuded site diameter induced by acetylcholine (ACh, 0.05 microg/kg i.c.). RESULTS: In the ED group, administration of ACh to LAD induced zero flow without LAD diameter reduction at 8 W. In the ED+ET(A) group, the decrease in LAD blood flow response to ACh was suppressed. Chronic administration of TA-0201 suppressed ROS generation in the myocardium. Decreases of eNOS and intimal thickening were smaller in the TA-0201 administration group than the non-TA-0201 administration group. CONCLUSION: Chronic administration of ET(A) receptor antagonist is effective to prevent coronary microvascular spasm.

Antioxidant is a useful supportive agent for the treatment of coronary vasospasm with endothelial dysfunction in pig.

OBJECTIVES: Recently, many antioxidants have been tested in cardiovascular disease. The effect of antioxidants on alleviation of coronary vasospasm, however, remains unclear. We investigated whether chronic administration of ascorbic acid and glutathione prevents coronary vasospasm in pigs. MATERIALS AND METHODS: Balloon-induced endothelial injury in the left anterior descending coronary artery was performed every 2 weeks until 6 weeks (0, 2, 4, 6 weeks). Ten micrograms per kilogram serotonin-induced vasoconstriction was assessed before each endothelial injury and at eighth week by coronary angiography. RESULTS: In endothelial injury without antioxidant group (ED group, n=12), serotonin-induced left anterior descending coronary artery vasoconstriction was augmented from 7+/-4% (0 week) to 88+/-8% (8th week, P<0.01) with electrocardiogram-ST elevation, and an increase of cyclooxygenase-2 expression and a decrease of endothelial nitric oxide synthase expression was observed at the spasm portion removed from the endothelial denuded site. In the endothelial injury group with oral administration of ascorbic acid 3 g/day and glutathione 1 g/day after the first endothelial injury (ASC+GSH group, n=12), serotonin-induced vasoconstriction was suppressed (8th week, 60+/-6%, P<0.01 vs. ED group) and endothelial nitric oxide synthase expression was fairly well maintained. Intimal thickening was observed at the left anterior descending artery spasm portion in the endothelial injury without antioxidant group but not at the corresponding portion in the ASC+GSH group. CONCLUSION: Antioxidant therapy was partially effective to prevent coronary vasospasm, whereas intimal thickening after endothelial injury was nearly restored. From these results, chronic antioxidant therapy may well be a useful supportive therapy for the treatment of coronary vasospasm, although it has limited availability despite amelioration of endothelial dysfunction.

Differing effects of metoprolol and propranolol on large vessel and microvessel responsiveness in a porcine model of coronary spasm.

OBJECTIVES: The purpose of this study is to assess the effect of beta1-selective blocker on coronary vasospasm. MATERIALS AND METHODS: Balloon epicardial coronary artery endothelial denudation was performed at the left anterior descending coronary artery every 2 weeks for a total of 4 times in pigs. Changes in denuded site diameter and left anterior descending coronary artery blood flow caused by acetylcholine or serotonin were assessed before each endothelial denudation and at week 8 in untreated pigs (ED group) and in those treated with metoprolol (Meto group) or propranolol (Pro group). RESULTS: In the ED group, decreased blood flow response to acetylcholine enhanced from -20+/-10% before the first ED to -100% (i.e. zero flow) at week 8 without denuded site narrowing, suggesting microvascular spasm, and serotonin-induced left anterior descending coronary artery diameter reduction at week 8 was -92+/-15%. In the Pro group, blood flow reduction by acetylcholine and left anterior descending coronary artery diameter reduction by serotonin did not change compared with those of the ED group. In the Meto group however, blood flow reduction by acetylcholine (week 8, -70+/-16%) and left anterior descending coronary artery diameter reduction by serotonin (week 8, -64+/-15%) were blunted (P<0.01) compared with those of ED and Pro groups. CONCLUSION: The beta1-selective blocker metoprolol was effective to prevent coronary vasospasm.

Effects of antioxidants on coronary microvascular spasm induced by epicardial coronary artery endothelial injury in pigs.

OBJECTIVES: The effect of oxidative stress on coronary microvascular disease is unknown. We investigated whether chronic administration of ascorbic acid (ASC) or glutathione (GSH) prevents microvascular dysfunction and remodeling induced by upstream repeated coronary artery endothelial injury. METHODS: Balloon endothelial injury was repeated at the left anterior descending coronary artery (LAD), just distal to an implanted flow meter, every 2 weeks for 6 weeks in pigs. Changes in LAD blood flow induced by acetylcholine (ACh) and 5-hydroxytryptamine were assessed before each endothelial injury and at 8 weeks after the first endothelial injury in pigs without treatment (endothelial injury group, n = 12) and in pigs treated with oral ASC (3 g/day) (ASC group, n = 12) and ASC (3 g/day) plus GSH (1 g/day) (ASC + GSH group, n = 12). RESULTS: In the endothelial injury group, reduced blood flow in response to ACh was augmented from a decrease of 18 +/- 17% to a decrease of 100% (that is, zero flow, 8 weeks, P < 0.01), accompanied by an increase of ascorbyl free radicals (AFRs) in coronary sinus blood. In contrast, in the ASC + GSH group, blood flow response to ACh was altered to a decrease of 45 +/- 17% (8 weeks, P < 0.01 compared with the endothelial injury group), coronary sinus blood AFRs did not change (8 weeks, 21.4 +/- 12.5 signal intensities, P < 0.01 compared with the endothelial injury group) and the rate of platelet aggregation induced by adenosine diphosphate was small (8 weeks, 56 +/- 17%, P < 0.01 compared with the endothelial injury group). CONCLUSIONS: Chronic administration of antioxidants suppressed microvascular hypercontraction, suggesting that it may be a promising therapeutic strategy for treating coronary microvessel disorders, including microvascular angina.

Repeated epicardial coronary artery endothelial injuries lead to a global spontaneous coronary artery spasm.

OBJECTIVES: This study was conducted to develop a spontaneous coronary spasm model. MATERIALS AND METHODS: Balloon endothelial denudation was carried out in the epicardial left anterior descending coronary artery (LAD) every 2 weeks, for a total of four times, in 12 pigs. Changes in the denuded site diameter and LAD blood flow caused by acetylcholine or serotonin were assessed before each denudation and at week 8. Blood pressure, electrocardiogram (ECG) from the LAD area and LAD blood flow were monitored continuously in conscious and unrestrained pigs. RESULTS: Spontaneous ECG ST depression with a decrease in LAD blood flow appeared at around 2 weeks. In accordance with this, 0.5 microg/kg acetylcholine induced similar ECG and LAD blood flow changes without denuded site narrowing, suggesting microvascular spasm. Thereafter, ECG ST depression or elevation by serotonin via a denuded site spasm was found after 6 weeks and spontaneous ECG ST changes due to epicardial coronary artery spasm were observed. CONCLUSION: Epicardial coronary artery endothelial injury may induce spontaneous vasospasticity in the downstream coronary microvessels as well as in the denuded portion, suggesting functional abnormality through the entire coronary arterial tree.