Abstract-Indomethacm treatment or removal of the venular endothehum will attenuate functional artenolar vasodllatlon m the hamster cremaster muscle We tested the hypothesis that prostanold release from venular endothehal cells was responsible for the finctlonal vaso&latlon of the paired artenole The hamster cremaster muscle was prepared for m vlvo nucroscopy and stimulated for 1 mmute (lOV, 40 psec, 1 Hz) Before a second muscle stimulation, the venular endothehum was removed by perfismg the venule with several air bubbles A third muscle snmulatlon was performed during prostaglandm mhlbltlon (28 pmol/L mdomethacm superfusion) Artenoles (n=9, 551-5 pm) ddated 25+4% dunng the mltlal muscle stnnulatlon After removal of the endothehum from the paired venules, there was no effect on resting artenolar hameters (5324 pm)), but the functional artenolar dllatlon was attenuated to 1555% (PC 05) The ad&tlonal mdomethacm treatment had a q&cant effect on resting diameter (30+4 pm) but did not alter the magnitude of the fimctlonal vasodllatlon (11?4%, P> 05) In a second set of expenments, the order of the experimental protocol was reversed Muscle stlmulatlon resulted m a 2352% increase m dlametel (47+-2 to 57+2 pm) Indomethacm treatment qlgmficantly attenuated the functional dilation to 8t3% (4522 to 48?2 pm) Artenolar diameter was slgmficantly smaller after disruption of the venular endothehum with air bubbles (4022 pm), but there was no effect on the functlonal vasodllatlon, 8?3"% increase m diameter (to 4322 pm) These results suggest that the artenolar dilatory response to muscle stimulation IS mehated, m part, by prostanold release from the venular endothehum (Hypertension. 1998;31[part 2]:213-217.)Key Words: endothehum n prostaglandms n venule n arteriole n hyperemla N umerous studies have shown a functional role for the arterial endothehum m the control of arterlolar diameter and thus the control of blood flow On the arterial Tide of the clrculatlon, the endothellum ha3 been shown to regulate artenolar tone m response to changes In flow and in response to changes m oxygen tension 'G' More recently, studies have focused on the role of the venular endothehum m the regulation of arterlolar diameter On the venular side of the clrculatlon, it has been shown that vasoactlve substances can diffuse from the venule to affect the tone of the adjacent artenoles " Falcone and Bohlen" have shown that apphcatlon of acetylcholme to a venule will cause dllatlon of its paired arteriole resulting from the release of a venular endothehalderived relaxing factor More recently, Boegehold' has shown that acute increases m venular shear rate will cause paired artenolar dilation as the result of a release of a venular endothehal relaxing factor Fmally, we have shown that m the absence of an intact endothehum, the functional hyperemlc response of the paired arteriole IS slgnlficantly attenuated, a result suggesting a role for the venular endothehumIn the regulation of artenolar diameter during exercise aThe identity of the diffusible substance re...

No abstract

A B S T R A C T The effect of acutely induced hypoxia, hypercapnic acidosis, and the combination of the two on the amount of acetylstrophanthidin (AS) required to produce cardiac arrhythmias was determined in anesthetized dogs. Each animal was studied during ventilation with room air and again during ventilation with gas mixtures of appropriate concentrations; 24 hr separated the study periods. AS was infused intravenously at a rate of 5 ptg/kg per min.Significantly less AS was required to produce arrhythmias during hypoxia and hypercapnic acidosis together than during the period with normal arterial Po,, Pco2, and pH (10 animals). Included in this group were two animals which had undergone previous bilateral adrenalectomy and four animals in which heart rate was maintained at the same frequency during both study periods. A significant reduction in the toxic dose of AS also was demonstrated in eight animals, two with constant heart rate, during hypoxia with normal arterial Pco2 and pH. Hypercapnic acidosis alone (eight animals) did not significantly alter the toxic dose of AS. After the administration of propranolol (six animals) or hexamethionium (six animals), no significant difference was observed between the toxic dose of AS during hypoxia and that during ventilation with room air. Thus although hypoxia and hypercapnic acidosis together do reduce the amount of AS required to produce arrhythmias, it is the hypoxia which exerts the

The effect of 250 mg of diphenylhydantoin, administered intravenously, on left ventricular function was determined during cardiac catheterization in nine patients with heart disease. Five minutes after drug administration, left ventricular end-diastolic pressure rose in each patient from an average of 6.0 mm Hg to 10.0 mm Hg. Concurrently, stroke work and stroke power indices decreased in each patient by an average of 22.0% and 22.2%, respectively. Stroke volume index decreased in seven patients and maximum left ventricular dp/dt fell in eight patients. Over the next 25 minutes, all parameters returned to control values. Cardiac index was unchanged, whereas generally small and insignificant changes were observed in heart rate and systemic arterial pressure throughout the study. Although this study has demonstrated that diphenylhydantoin depresses myocardial function, the effect may have limited clinical significance since it was relatively short-lived and did not reduce cardiac output or greatly elevate ventricular end-diastolic pressure. Furthermore, the absence of a significant systemic hypotensive effect is of distinct clinical importance.

The effect of reducing the force of right atrial contraction on right ventricular stroke volume was determined in anesthetized open-chest dogs. Atrial contractile force, measured directly with a strain-gauge arch, was decreased by electrical stimulation of the right vagus nerve; right ventricular stroke volume was measured with an electro-magnetic flowmeter. Heart rate was maintained constant by electrical stimulation of the right atrium.