On the VIP-ergic innervation of the uterotubal junction

Chronic ACTH treatment (3 IU/kg daily for 8 days) caused an increase in wet weight of the interscapular brown adipose tissue (ISBAT) in the rat without affecting the enzyme activities of the cardiac or skeletal muscles or of ISBAT. On the other hand, chronic β-blockade (alprenolol 10 mg/kg daily for 8 days) induced elevated activities in the oxidative enzymes of the ISBAT but not of the muscle tissues measured. Combined ACTH and alprenolol treatment also increased significantly the citrate synthase and malate dehydrogenase activities and protein concentration, but decreased the weight of ISBAT to normal. The results suggest that, although a direct antagonism between the β-blockers and ACTH has not been demonstrated, β-blockers can abolish the ACTH-induced weight gain of the ISBAT.     

大鼠脑底动脉的氮能神经支配

目的研究NOS阳性纤维和终末在大鼠脑底动脉的分布.方法采用NADPH-d组织化学的方法观察大鼠颈内动脉脑底段、大脑前、中、后动脉及基底动脉的NOS阳性纤维和终末分布.结果脑底动脉各段均有螺旋形NOS阳性神经纤维分布,且有数目不等的膨体,交织成网状,还可见许多点状的NOS阳性终末.结论以上提示这些氮能神经纤维及终末对脑底动脉具有调节作用.     

ALCOHOLICS WITH REDUCED DOPAMINE D2 RECEPTOR FUNCTION POSSESS NORMAL PLATELET MONOAMINE OXIDASE ACTIVITY

Platelet monoamine oxidase (MAO) activity, proposed to be amarker for central 5- hydroxytryptamine (5-HT) capacity, wasinvestigated in 14 severely alcohol-dependent subjects withreduced dopamine (DA) D₂ receptor function, as assessed by thegrowth hormone responses to apomorphine. Twelve healthy menwere used as controls. Platelet MAO activity in the alcohol-dependent subjects was not different from that in controls.The finding from this preliminary study suggests that severelyalcohol-dependent subjects with reduced DA D₂ receptor functionhave normal 5-HT capacity.     

Atrioesophageal Fistula After Cryoballoon Pulmonary Vein Isolation

Atrioesophageal Fistula After Cryoballoon PV Isolation . The risk of atrioesophageal fistula after cryoballoon pulmonary vein isolation is thought to be much lower than after radiofrequency ablation, seeing that no data exist on this complication so far. We report for the first time on the occurrence of an atrioesophageal fistula 4 weeks after cryoballoon ablation at the site of the left inferior pulmonary vein. We suggest that even when using cryothermal ablation technique, an imaging modality to assess the proximity of esophagus and left atrium should be routinely performed to avoid this fatal complication. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1254–1257, November 2012)     

Protection to Fasciola hepatica in the gut mucosa of immune rats is associated with infiltrates of eosinophils,IgG1 and IgG2a antibodies around the parasites

We investigated the immune effector mechanisms that underlie protection against F. hepatica in the gut wall of immune rats, using (immuno)histochemistry. In the lamina propria of immune Wistar rats, four weeks after oral infection, frequencies of IgE-positive cells, eosinophils and mucosal mast cells were significantly increased, compared with naïve rats. These factors represent the traditional effector mechanisms against helminths. No significant differences were detected between the two groups in frequencies of IgM-, IgG2a-, IgG1- and IgA- positive cells, CD4- and CD8-positive cells, NK cells, macrophages, neutrophils or goblet cells. Upon challenge of immune rats with F. hepatica in an ex vivo gut segment, NEJs that migrated through the (sub)mucosa were coated with IgG1 and IgG2a antibodies and surrounded by eosinophils. No IgE or IgA antibodies were detected on the parasites. The onset of these immune effector responses, two h after challenge, was related to the expression of protection. These results suggest that NEJs are killed by an eosinophil-mediated cytotoxic response involving IgG antibodies. These antibodies were not produced in the intestine, but infiltrated the gut upon challenge. The observed immune effector responses were not restricted to the site where the primary infection is located, namely the small intestine, but were also detected in the large intestine. The presence of the protective immune mechanisms in two other rat strains demonstrates the pivotal importance of these responses, irrespective the genetic background of the host.     

Abnormal Automaticity as Mechanism of Atrial Tachycardia in the Human Heart—Electrophysiologic and Histologic Correlation:

Abnormal Automaticity in Human Atrium, introduction: A 32-year-old woman was operated upon because of drug refractory atrial tachycardia.
Methods and Results: Electrophysiologic study was performed prior to operation. During surgery, epicardial mapping of the electrical activity of the left atrium was performed. The left atrial appendage was resected and studied in a tissue bath. Thereafter, histologic examination was performed. Polarity of the P wave in the surface ECG suggested that the tachycardia originated high in the left atrium. Epicardial mapping disclosed earliest activation in the apex of the left atrial appendage. Intracellular recordings from surgical specimen made at the site of origin, which was marked during surgery, revealed cells with phase 4 depolarization at cycle lengths ranging from 360 to 540 msec. Exit block prevented spread of activation from the spontaneously firing cells to surrounding tissue. Histology showed that spontaneous activity arose in an area with abnormal cells-characterized by an amorphous, pale eosinophilic staining cytoplasm and absence of nuclei-surrounded by normal myocytes.
Conclusion: The observations indicate that the mechanism of the atrial tachycardia was based on abnormal automaticity in an area consisting of a conglomeration of normal and abnormal myocytes.