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W L Porges

Publications and source records attributed to W L Porges.

23 records · Page 2Linked to original sources

Central nervous system opiate and 5-hydroxytryptamine influences on baroreflex control of the coronary circulation.

The effect of intravenous infusion of fentanyl (an opiate receptor agonist, 0.55 microgram kg-1 min-1) on the control of the circumflex coronary circulation was examined in unsedated dogs at rest and during baroreceptor stimulation evoked by acute rises in aortic pressure (balloon inflation in thoracic aorta). Circumflex flow was measured using Doppler flow transducers in dogs with experimental complete heart block and with ventricles paced at a constant rate. Studies were also performed before and one week after intracisternal injection of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT), to examine the role of CNS 5-hydroxytryptamine (5-HT) in any sympathetic vasoconstrictive effects. Fentanyl infusion caused after a few minutes a progressive rise in resting aortic pressure and a significant fall in circumflex conductance; circumflex flow usually fell. Atrial rate also fell. The gain of the baroreflex control of circumflex conductance was enhanced by fentanyl. One week after intracisternal 5,7-DHT, the gain of the baroreflex in each dog was diminished. When fentanyl was infused into these preparations, no consistent changes in resting atrial rate, aortic pressure and circumflex conductance could be observed, but all dogs showed a recovery of the coronary baroreflex gain towards values observed before intracisternal 5,7-DHT. These data suggest that the gain control of coronary baroreflexes is influenced by CNS opiate and 5-HT dependent mechanisms.

5,7-Dihydroxytryptamine↗

Baroreflex control of coronary blood flow varies regionally in awake dogs.

1. Baroreflex responses to changes in aortic pressure were measured simultaneously in three main coronary regions of awake dogs. 2. Pulsed Doppler flow probes were mounted at prior surgery on the right, circumflex and anterior descending coronary arteries; the animals were placed in complete heart block and the left ventricle was paced. After 2-4 weeks recovery, baroreflexes were evoked by inflating a balloon catheter placed in the mid-thoracic aorta via the femoral arteriotomy. Flow and pressure data were collected at rest, and during acute (8s) and steady-state (25s) baroreflex challenge. 3. Changing ventricular rate alone caused a fall in aortic pressure at low rates; however, over the range 60 to 180 b.p.m., circumflex and anterior descending coronary flow and conductance changed directly with ventricular rate, but right coronary flow and conductance remained unchanged. 4. Acute aortic pressure elevation increased flow at 8s in all beds at all rates. Conductance effects at 60 b.p.m. were negligible in all three beds, but rose at 100 and 180 b.p.m. in the right and circumflex beds. 5. Sustained aortic pressure elevation (25s) caused flow to return towards control in all beds ventricular rates, but in the right coronary at 60 b.p.m. flow fell below control. Conductance at this time was unchanged at all rates in the anterior descending bed, fell modestly in the circumflex, and decreased to below resting in the right coronary bed. 6. Baroreflex control of coronary flow and conductance thus varies between territories, and within territories, depending on ventricular rate. The right coronary bed appears to be regulated by a bidirectional, baroreflex-linked mechanism, which is functionally opposite in action to that found in most vascular beds.

Animals↗