This study investigated the role of prostaglandins (PGs) and leukotrieres (LTs) in hypoxic pulmonary vasoconstriction (HPV) and in cigarette smoking-induced changes in hemodynamics and HPV in Wistar rats. Selective LTD4-LTE4 receptor antagonist LY-171883 (LY) inhibited HPV by 71.8%, while cyclooxygenase inhibitor indomethacin (IND) augmented HPV. The results indicate that LTs mediate HPV in Wistar rats. Smoking increased the level of TXB2 over control by 143.6% in plasma and 69.2% in lung tissue, concomitantly, pulmonary and systemic vascular resistance (PVR and SVR) were increased by 38.7% and 46.7%, respectively. Both LY and IND prevented the smoking-induced increase of PVR and SVR. After smoking HPV increased twofold. The increase of HPV was abolished by LY, but not by IND. Our results suggest that smoking leads to pulmonary and systemic vasoconstriction partly mediated by TXA2 and LTs; smoking also leads to an augmentation of HPV, and LTs play an important role in it.

To investigate the effects of prostaglandins (PGs) and leukotrienes (LTs) on hypoxic pulmonary vasoconstriction (HPV), in vivo rats experiment and in vitro perfused lung experiment were conducted. The effect of hypoxia on hemodynamics, concentrations of TXB2 and 6-keto-PGF1 alpha in serum and lung tissue during hypoxia and effects of PGs and LTs on HPV were observed. The results showed that pulmonary arterial pressure (Ppa) and pulmonary vascular resistance were increased during hypoxia, but cardiac output and systemic arterial pressure were decreased. There were increases of the concentrations of TXB2 and 6-keto-PGF1 alpha and their ratio in serum and lung tissue during hypoxia. After use of cyclooxygenase inhibitor (indomethacin) in vivo and in vitro, HPV was augmented respectively, but after use of lipoxygenase inhibitor (diethylcorbamazine) or leukotriene receptor blocker (LY-171883), HPV was attenuated. It was suggested that LTs mediated pulmonary vasoconstriction, PGs inhibited pulmonary vasoconstriction and they played a modulating role during hypoxia.

The role of allergens in asthmatic inflammation is not clearly understood. To elucidate the mechanism of cockroach allergen (CRa)-induced airway disease, we studied three groups of Hartley guinea-pigs sensitized to control, ovalbumin (OA) or CRa. Parameters measured were anaphylactic antibodies by allergy skin test (AST), PCA assay and Western blot, changes in specific airway resistance (SRaw), analysis of bronchoalveolar lavage (BAL) and contracture responses of tracheal muscle (TSM) to non-specific and specific stimuli, in vitro. Both OA and CRa animals showed a similar allergic sensitization (AST and PCA), while Western blot identified several reaginic bands in CRa group compared to a single band in OA group. SRaw illustrated that CRa induce dual-asthmatic responses (4/6) in the CRa group, whereas OA induce only an early asthmatic response (3/6) in the OA group (P<0.01). The average total leukocytes in BALF of the CRa were 27.0x10(6), mostly neutrophils and eosinophils, while those of the OA showed 3.5x10(6), mostly eosinophils, respectively (P<0.0001). TSM responses to non-specific stimuli were similar in both groups (P>0.1), while the antigen-specific TSM contractions were more brisk in the OA group than those of CRa group (P<0.001). Thus, the study indicates that both CRa and OA sensitize guinea-pigs, yet CRa induces more severe and persistent late-phase inflammation than OA. This appears to be related to an influx of neutrophils rather than anaphylactic bronchospasm.

The first step of the sensory systems is to construct the meaning of the information they receive from the senses. They do this by generating random noise and then filtering the noise with adaptive filters. We simulate the operation with the solutions of matrices of ordinary differential equations that predict bifurcations between point and limit cycle attractors. The second step is integration of the outputs from the several sensory systems into a multisensory percept (gestalt), which in the third step is consolidated and stored as knowledge. Simulation of the second step requires use of landscapes of non-convergentchaoticattractors. This is not deterministic chaos, which is much too brittle owing to the infinite sensitivity to initial conditions. It is a hybrid form we callstochastic chaos, which is stabilized by additive noise modeled on noise sources in the sensory systems. Thus bifurcation and chaos theory provides tools for succinct empirical models of cortical dynamics performing the most basic cognitive operations: generalization, abstraction, and categorization in constructing knowledge. The descriptions are in a form that is suitable for more advanced modeling using analog VLSI, neuropercolation from random graph theory, non-equilibrium dissipative thermodynamics, and macroscopic many-body physics. This review concludes with a summary of the applications of stochastic chaos in pattern classification and some prescriptions for neurobiologists on what to look for in large-scale anatomical formations. 

The Neiguan and Lingdao were stimulated by electroacupuncture in anesthetized Wistar rats. We observed that the value of ventricular fibrillation threshold (VFT) was increased significantly in 30 min of electro-acupuncturing (P less than 0.01) and in 15 min of stopping the acupuncturing (P less than 0.05). Although the value of VFT was increased until 30 min of stopping acupuncture, it was not significantly different compared with its basic value. The control group were dealt with the same way as the experimental group except electroacupuncture. The value of VFT measured in control group were not significantly different compared with its basic value.