A Square Wave Electromagnetic Flowmeter for Application to Intact Blood Vessels

SUMMARY Present methods for measurement of stroke volume from die aortic pressure pulse are not suitable for beat-to-beat determinations during non-steady state conditions because these methods assume that each systolic ejection is equal to the peripheral runoff during the same beat We bare tested a new method which allows determination of an aortic pressure-volume conversion factor over a wide range of pressures during transient changes in stroke volume and infusions of vasoactive drugs in 6 dogs with chronically implanted aortic electromagnetic flowmeters. Each aortic diastolic pressure decay is approximated by an exponential the time constant of which is used to calculate the pressure loss during systole due to blood flow into the periphery. The total increment in aortic pressure due to systolic ejection, if there were no flow from the aorta during systole, then is calculated. The total systolic increment (AP 3V ) is assumed to describe the pressure-volume characteristics during systole and is related to stroke volume by a constant multiplier that is derived from the indicator-dilution measurements of cardiac output. The values for beat-to-beat variations that were determined by use of the aortic electromagnetic flowmeter and by this aortic pressure pulse method were found to be within the range of measurement errors of stroke volume determined from individual aortic electromagnetic flow pulses.

Section: Methods For Averaging Successive Diastolic Decaysmentioning

confidence: 99%

Continuous determination of beat to beat stroke volume from aortic pressure pulses in the dog.

Bourgeois

Gilbert²,

Bernuth

et al. 1976

“…The technique used in this study is similar to that described by Denison, Bardhanabaedya and Green. 3 The studies were done on openchested mongrel dogs given morphine sulfate, 2 mg./Kg. subcutaneously, followed in one half hour by 0.25 ml./Kg.…”

mentioning

confidence: 99%

Effects of Autonomic Nerves and Their Mediators on the Coronary Circulation and Myocardial Contraction

Denison

Green

Dawson

et al. 1958

Self Cite

Mean and phasic coronary flows were recorded simultaneously by an electromagnetic meter, and peripheral coronary pressure was recorded distally from the temporarily occluded descending branch of the left coronary artery. From the results of these studies we conclude that: 1. The sympathetic cardiac nerves, as does levarterenol, increase myocardial contraction, (indicated by a shorter, more abrupt systole and more rapid isometric relaxation), and cause a slight degree of coronary arteriolar dilation. 2. Parasympathetic fibers exert no significant effect, although acetylcholine diminishes coronary arteriolar tone and may slightly diminish ventricular contraction. 3. That measurements of mean coronary flow and resistance are relatively satisfactory for indicating changes in coronary arteriolar tone, but are of relatively little value in evaluating myocardial contraction.C ONFLICTING reports have appeared in the literature regarding the sympathetic control of the coronary circulation; direct constrictor and dilator effects have been described as well as indirect dilator effects resulting from altered contraction. Very little information is available as to whether or not a true parasyrnpathetic control exists. The available reports are conflicting but the general consensus in the published data is that vagal parasympathetic stimulation would, if it had any effect, cause constriction of the coronary arterioles. Most of the early investigators measured only mean flow. Heart rate, aortic pressure, and strength of contraction were usually not evaluated, nor was arteriolar resistance calculated. These various variables may have led to contradictory interpretations. It appeared that a clearer interpretation of these effects could be made if the various flow determining factors could be evaluated separately.

“…Artificial respiration was given throughout each experiment. The rate of blood flow was measured with the electromagnetic flowmeter of Denison, Spencer and Green 10 and recorded in the superior (cranial) mesenteric artery; lateral pressures in the mesenteric artery and the portal vein were measured with strain gages using technic similar to those described previously. 8 The pressure drop across the flowmeter cannula and connecting tubing was 0.179 mm.…”

mentioning

confidence: 99%

Comparison of Changes in Mesenteric Resistance Following Splanchnic Nerve Stimulation with Responses to Epinephrine and Norepinephrine

Déal

Green

1956

Self Cite

This is a study of the characteristics of the splanchnic nerve supply to the mesenteric vascular circuit. The flow and pressure responses in the dog's superior mesenteric artery to splanchnic nerve stimulation and to intraarterial injections of epinephrine and norepinephrine, before and during various levels of adrenergic blockade, are analyzed. The results suggest that the splanchnic nerve contains only vasoconstrictor fibers, the mediator of which is probably norepinephrine, but that it also contains fibers which induce the release of epinephrine from the adrenal gland. Xo evidence for the presence of cholinergic dilator fibers was found.V ON BASCH 1 claimed in 1873 that the inhibitory action on the gut which resulted from splanchnic nerve stimulation was dependent upon coincident vasoconstiiction. Xo difference in the response was obtained with the right and the left splanchnic nerves. 2 Bayliss and Starling 8 reported that section of the splanchnic nerves resulted in vascular dilation in the intestine; they felt that the vasoconstriction obtained on stimulation was independent of the inhibitory action observed. In connection with experiments on hepatic blood flow, Burton-Opitz 4 also reported a drop in blood flow from the intestine after stimulation of the greater splanchnic nerve. These results, in general, have been supported by other investigators. 6 -' Richins 7 reported that direct microscopic observations of the small vessels of the intestinal wall revealed a dilation after the administration of ergotoxine phosphate (0.5 ml. of a 1/1000 solution), thus suggesting the possibility of a tonic sympathetic vasoconstrictor activity.An earlier paper from this laboratory 8 compared the effects of intra-arterial sympathomimetic amines and of ischemia on the blood vessels of the canine mesenteric vascular bed with those of skeletal muscle, cutaneous and venal beds before and during adrenergic blockade. A recent paper 9 reported the effects of sympathetic nerve stimulation before and during adrenergic blockade on the vasculature of canine skeletal muscle. The present paper reports results of a similar study on the mesentery, and compares the results with those obtained in skeletal muscle which was shown to be supplied by both adrenergic constrictor fibers and cholinergic dilator fibers by way of the lumbar sympathetic chain. METHODSFourteen dogs, weighing 13.0 to 24.5 Kg. (average 1S.5) were anesthetized with 30 ing./Kg. of sodium pentobarbital intravenously and received 40 mg./ Kg. of Mepesulfate initially plus 20 mg./Kg. every half hour thereafter to prevent coagulation. Artificial respiration was given throughout each experiment. The rate of blood flow was measured with the electromagnetic flowmeter of Denison, Spencer and Green 10 and recorded in the superior (cranial) mesenteric artery; lateral pressures in the mesenteric artery and the portal vein were measured with strain gages using technic similar to those described previously. 8 The pressure drop across the flowmeter cannula and connecting tubing was 0....