Tunable dual-band perfect absorbers based on extraordinary optical transmission and Fabry-Perot cavity resonance.

Magnetic resonance is considered to be a necessary condition for metamaterial perfect absorbers, and dual-band absorbers can be composed of a pair of metallic layers with anti-parallel surface currents. We designed and fabricated a tunable dual-band perfect absorber based on extraordinary-optical-transmission (EOT) effect and Fabry-Perot cavity resonance. The idea and the mechanism are completely different from the absorber based on the near-field interaction. The important advantage of our structure is that we can switch a single-band absorber to a dual-band absorber by changing the distance between two metallic layers and/or incident angle. The peak originating from the EOT effect becomes significantly narrower, resulting in an increase of the Q-factor from 16.88 to 49. The dual-band absorber can be optimized to be insensitive to the polarization of the incident electromagnetic wave by slightly modifying the absorber structure.

[Effect of erythropoietin 3-enhancer on proliferation of pulmonary artery smooth muscle cells induced by hypoxia].

The effects of erythropoietin (EPO)3 -enhancer on endothelium-dependent and endothelium-independent proliferation caused by hypoxia in cultured porcine pulmonary artery smooth muscle cells (PASMCs) were investigated with MTT test, H(3)-TdR incorporation and flow-cytometry. The results showed that (1) PASMCs exposed to hypoxia for 24 h proliferated significantly, which was suppressed by pretransfecting wild type EPO3 -enhancer fragments into PASMCs, but not by protransfecting mutant fragments; and (2) the conditioned medium of pulmonary artery endothelial cells (PAECs) exposed to hypoxia for 24 h promoted the proliferation of PASMCs. This effect was abolished when wild type EPO3 -enhancer fragments were transfected, but it persisted when mutant fragments were transfected. The results suggest that (1) the conditioned medium of hypoxic PAECs induces proliferation of PASMCs. This may be because that not only PAECs are sensitive to hypoxia, but also PASMCs respond to hypoxia directly; and the hypoxic responses of both endothelial cells (ECs) and smooth muscle cells (SMCs) can be inhibited by exogenous EPO3 -enhancer fragments. (2) Since there is a HIF-1 binding site in EPO3 -enhancer, there may be a common pathway for HIF-1 hypoxia signal transduction in hypoxic responses of ECs and SMCs.

[Effects of L-arginine on pulmonary circulation and cerebral blood flow in acute and chronic hypoxic rats].

The effects of L-arginine (L-Arg) on pulmonary circulation and cerebral blood flow in acute and chronic hypoxic rats and their mechanism were studied. The results showed that bolus injection of L-Arg 400mg.kg-1 did not inhibit acute hypoxic pulmonary vasoconstriction (HPV), while 800mg.kg-1 could inhibit HPV. Neither of these two doses of L-Arg was found to have any influence on the change in cerebral blood flow during acute hypoxia. Long-term administration of L-Arg (300mg.kg-1/d) could attenuate chronic hypoxic pulmonary hypertension, the increase in pulmonary vascular resistance and right ventricular hypertrophy, and the HPV as well. It did not influence the cerebral blood flow. Since the inhibitor of NO synthetase, NG-nitro-L-arginine methyl ester, could antagonize the effect of L-Arg, it is suggested that an increase in the synthesis of NO might contribute to the effect of L-Arg.

Effect of cigarette smoking on hypoxic pulmonary vasoconstriction and its relation to animal species and period of smoking.

The alteration in hypoxic pulmonary vasoconstriction (HPV) induced by cigarette smoking was studied in Wistar rats, piglets and in humans. The percentage change of pulmonary vascular resistance (delta PVR%) and the amplitude of the systolic wave in impedance pneumorheogram (delta H%) were used to estimate the strength of HPV. It was observed that immediately after acute cigarette smoking, HPV in rats increased (delta PVR% from 55.0 +/- 15.6% to 102.3 +/- 12.4%), which is mainly mediated by leukotrienes (LTs); whereas HPV in piglets decreased (delta PVR% from 65.2 +/- 12.5% to 55.9 +/- 9.8%), which is mainly mediated by beta-adrenergic receptors, and HPV in humans also increased (delta H% from 20.6 +/- 2.6% to 31.1 +/- 4.1%), in which prostaglandins and leukotrienes may play the role of mediators. However, after one-month cigarette smoking, the HPV in rats fell significantly (delta PVR% 11.4 +/- 1.6%). An increase in synthesis of vasodilative prostaglandins and a decrease in leukotrienes synthesis may be the contributing factors to this alteration in HPV.

Effects of cigarette smoking on the function of metabolizing arachidonic acid and angiotensin I in the isolated perfused rat lungs.

The effects of acute and chronic cigarette smoking on the metabolism of exogenous arachidonic acid (AA) and angiotensin I (AI) in perfused isolated rat lungs were studied. The results showed that acute cigarette smoking did not alter the contents of 6-keto-PGF1 alpha (the stable metabolite of PGI2) and TXB2 (the stable metabolite of TXA2) in the effluent and the increment of pulmonary artery pressure (delta Ppa) caused by AA. The conversion of A I into A II was significantly increased (P < 0.01), while the delta Ppa induced by A I injection was obviously decreased as compared with controls (P < 0.05). After cigarette smoke exposure for 30 days, the delta Ppa caused by AA or A I did not differ from that of controls, but the contents of 6-keto-PGF1 alpha and A II increased more markedly than those in non-smoking rats (P < 0.05). It is suggested that acute and chronic cigarette smoking in rats can promote the lung function of converting A I into A II, chronic smoking can increase the lung function of metabolizing AA into PGI2.

Strain difference in pulmonary vascular responsiveness to hypoxia in rats.

The difference in pulmonary vascular response to hypoxia between Hilltop Sprague-Dawley (HT) rats and Wistar (W) rats was studied. Effects of inhibitor of leukotriene (LT) synthesis or prostaglandin (PG) synthesis on hypoxic pulmonary vasoconstriction (HPV) and chronic pulmonary hypertension were observed, and variations in plasma TXB2 and 6-keto-PGF1 alpha during hypoxia were determined. The results showed that in rats of both strains LTs are the major mediator of HPV, which is also mediated by vasoconstrictive PGs in HT rats, while modulated by vasodilative PGs in W rats. This might be the crucial mechanism responsible for the higher pulmonary vascular responsiveness in HT rats. Differences in the modulating effect of histamine and in the structural feature of pulmonary arteriole might be contributing factors as well.

Relation of TXA2 and PGI2 to the difference in hypoxic pulmonary vasoconstriction between different strains of rats.

TXB2 and 6-keto-PGF1 alpha levels in arterial and venous plasma of Wistar and Hilltop rats during hypoxia were measured to investigate the roles of TXA2 and PGI2 in hypoxic pulmonary vasoconstriction (HPV) and responsiveness difference of pulmonary vessels to hypoxia between different strains of rats. The results showed that PGI2 might play an important role in maintaining the low resistance in pulmonary circulation of these two strains of rats. Increased TXA2 during hypoxia may partially mediate HPV in Wistar rats, while augmented PGI2 during hypoxia may modulate HPV in Wistar rats. This might be the important mechanism responsible for more intensive responsiveness of pulmonary vessels to hypoxia in Hilltop rats than in Wistar rats.