In vivo effect of naftidrofuryl on 5-hydroxytryptamine-mediated constriction in rat peripheral microcirculation.

Naftidrofuryl is commonly used in treatment of peripheral vascular disease. Its vasodilator action has been partly explained by its inhibitory effect of 5-HT2 receptors on peripheral arteries in vitro. The purpose of this study was to test in vivo whether naftidrofuryl selectively inhibits 5-hydroxytryptamine (5-HT)-mediated constriction of large arterioles in the peripheral microcirculation. This constriction appears to be 5-HT2 receptor-mediated. Three separate protocols were used to test the effects of naftidrofuryl: chronic injection (15 mg/kg, i.p., twice daily for 5-6 days; n = 7), acute intravenous (i.v.) infusion (15 mg/kg over 30 min; n = 7), or topical application (5 x 10(-8) M, n = 6; 5 x 10(-7) M, n = 5; 5 x 10(-6) M, n = 5; 10(-5) M, n = 7). Male Sprague-Dawley rats (145-185 g body weight) were anesthetized with sodium pentobarbital (50 mg/kg) and the cremaster muscle was prepared for intravital video microscopy. Diameter response of arterioles (70-120 microns) to increasing concentrations of locally applied 5-HT (10(-8)-10(-4) M) was assessed. In rats receiving no drug treatment, 5-HT caused vasoconstriction of arterioles beginning at 10(-6) M and reaching approximately 40% constriction at 10(-4) M. These vasoactive responses were not altered by chronic daily doses or an acute infusion of naftidrofuryl. 5-HT responses obtained with and without naftidrofuryl applied directly into the cremaster-bath also had little effect on the arteriole response at each of the four concentrations tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship between endocardial activation of SA valve and right atrium in domestic fowl.

We mapped endocardial activation in the isolated, perfused chicken heart to determine how excitation spreads from the sinoatrial (SA) valve, the avian pacemaker structure, to the atrioventricular (AV) ring. We found activity originating from one of three sites on the right valvule with the upper half of this valvule being the dominant origin. Only one heart exhibited an origin lower on the right valvule. We never observed activity originating from the left valvule. Depending on the valvular origin, two patterns of atrial activation were observed. The dominant pattern emerged from an upper to middle origin on the right valvule and involved two preferential conduction pathways. One pathway followed the right transverse arch and pectinate muscle medially to depolarize the AV ring from a posterior medial direction. Activation along the second pathway traveled caudally along the right valvule and then followed the sinus septum to approach the AV ring from an anterior lateral direction. An atypical pattern resulted from one heart exhibiting a lower origin on the right valvule. In this case, preferential atrial conduction only followed the lower pathway. This could represent an entrance block located cranially in the right valvule preventing normal activation of the right transverse arch and pectinate muscle.

Changes in conduction within the diffuse sinoatrial node of the chicken following premature atrial stimulation.

Premature atrial stimulation was used to estimate sinoatrial conduction within the diffuse sinoatrial node of the bird (chicken), and compare its conduction with that reported for mammals. While sinoatrial conduction could not be determined in the chicken because reset did not occur, the premature wavefront did have an effect on the sinoatrial node because the recovery interval following the premature stimulus became less than compensatory with shortening of the premature stimulus interval. This less than compensatory non-reset recovery interval is interpreted as a conduction dependent response in which the intrinsic wavefront leading to the first recovery atrial activation conducts out of the node faster than normal. This conduction dependent recovery interval is seen infrequently in mammals (rabbit, dog and man). The absence of reset and the presence of a less than compensatory non-reset response in the chicken suggests that while the general organization of the sinoatrial node of the chicken is similar to that in mammals, a larger transitional cell network in the chicken prevents a premature wavefront from reaching the pacemaker cells and resetting them.