Biomedical subjects
Publications and source records attributed to M J Duff.
We show that the recently demonstrated absence of the usual discontinuity for massive spin 2 with a Lambda term is an artifact of the tree approximation, and that the discontinuity reappears at one loop.
Vagal ganglia that innervate the canine sinoatrial node (SAN) have been localized to a fat pad overlying and surrounding the right pulmonary vein complex (PVFP). The ventral epicardial surface of the right atrium was mapped in seven dogs anesthetized with alpha-chloralose after beta-blockade (timolol) and cardiac sympathetic and parasympathetic decentralization. A small, concentric bipolar exploring electrode was used to stimulate (during the atrial refractory period and using trains of five to eight stimuli per beat) systematically in the epicardial regions between the PVFP and the SAN. Changes in SAN rate with stimulation were measured, and the anatomic location was identified on a 150-point grid fitted to conform to size and shape of the atrium. Mapping was performed before and after local (PVFP) and systemic ganglionic blockade (hexamethonium). Data reveal that the primary vagal postganglionic pathways to the sinoatrial nodal region are subepicardial and adjacent to the SAN artery along the sulcus terminalis. Hexamethonium in the PVFP abolishes SAN inhibition during preganglionic vagal excitation, without interrupting vagal suppression of atrioventricular conduction. However, SAN slowing (with varying attenuation) continued to occur after hexamethonium (either PVFP or systemically) when the exploring electrode was applied directly over intramural postganglionic fibers between PVFP and sinus node. Attention is directed to existence of a very few synapses closer to SAN, probably in isolated ganglia immersed in fatty connective tissues along the sulcus terminalis.
The maximum atrial paced rate with 1:1 atrioventricular conduction (Rmax) was compared before and after selective parasympathectomy of the atrioventricular nodal region (AVNR). Each animal was instrumented with right atrial and right ventricular bipolar electrodes. Rmax was determined (1) under quietly resting, control conditions, (2) following beta-adrenergic blockade, (3) following muscarinic blockade, and (4) following combined beta-adrenergic and muscarinic blockade. During a second surgical procedure approximately two weeks later, parasympathectomy was achieved by dissection and topical application of phenol to the fat pad and underlying epicardium at the inferior left atrial junction with the inferior vena cava; completeness of AVNR parasympathectomy was tested at surgery by supramaximal stimulation of right and left cervical vagi, with and without rapid atrial pacing. AVNR sympathetic innervation remained intact. All studies were conducted while the animals were conscious and quietly resting. Before parasympathectomy, Rmax under control conditions averaged 136 +/- b4 beats per minute (bpm). Following beta-blockade, Rmax was 126 +/- 5 bpm; while with muscarinic blockade, Rmax averaged 373 +/- 4 bpm (P less than 0.001, with control). With combined beta- and muscarinic blockade, Rmax was 300 +/- 14. After AVNR parasympathectomy, although the resting heart rate was unchanged, the Rmax under control conditions was 342 +/- 10 bpm. beta-Blockade reduced this significantly (P less than 0.001) to 278 +/- 15 bpm. With muscarinic blockade, Rmax averaged 346 +/- 11 bpm, which was not different from the control Rmax after AVNR parasympathectomy. Combined beta- and muscarinic blockade produced an Rmax of 280 +/- 14 bpm.(ABSTRACT TRUNCATED AT 250 WORDS)
Histamine caused a triphasic response of human pulmonary artery strips in vitro, consisting of a small initial contraction followed by pronounced relaxation preceding a second contractile response. These characteristics were not seen with other contractile stimuli including 5-hydroxytryptamine, leukotriene D4, and KCl. The relaxant component of this response was ablated by removal of endothelium from the vascular strips or by pretreatment of the tissue with 1 microM indomethacin. Measurement of the PGI2 degradation product 6-keto-PGF1 alpha in supernatants from histamine-challenged tissues confirmed the synthesis of PGI2. Supernatants from unstimulated or leukotriene-challenged tissues contained no detectable amounts of 6-keto-PGF1 alpha. The histamine H1 antagonist diphenydramine inhibited both the contractile and relaxant responses to histamine whereas the H2 antagonist cimetidine affected neither component. The released PGI2 significantly altered the dose-response curve to histamine without inhibiting the maximal contractile responses. We conclude that histamine induces PGI2 formation from pulmonary arterial endothelium via an H1 receptor.