Arterial Pressure Oscillations Research Articles

Patterns of sympathetic neuron activity associated with Mayer waves.

Patterns of sympathetic neuron activity associated with Mayer waves.

Cardiovascular effects of cnidarian toxins: a comparison of toxins extracted from Chiropsalmus quadrigatus and Chironex fleckeri.

A comparison has been made of the pharmacologic properties of toxins isolated from Chiropsalmus quadrigatus and Chironex fleckeri. The effects of the toxins were studied in intact anaesthetized animals and in a number of isolated organ preparations. Toxin extracted from Chiropsalmus tentacle was found to resemble the previously reported Chironex cardiotoxin. However, it was less stable and its activity differed in onset and duration of effects. Toxin from Chiropsalmus caused an initial hypertensive response in animals due to direct vasoconstriction. This was followed by hypotension and cardiac irregularities. Arterial pressure oscillations were frequently seen prior to death. It was not possible to elicit a carotid occlusion reflex during the action of the toxins. Ganglion blocking drugs prevented oscillations by blocking the efferent arm of the vasomotor reflex arc. A stinging by either cnidarian should produce similar symptoms, but Chironex appears the more dangerous species for man.

Arterial pressure changes during spontaneous sleep in man

The systemic arterial pressure was measured continuously during spontaneous night sleep (using a catheter in the branhial artery) in eight normotensive subjects. The results can be summarized as follows: 1. 1. Arterial pressure decreased rapidly in the first part of the night and increased gradually in the second part. 2. 2. Pressure decreased progressively from when the subject was still awake to successive slow sleep stages: the difference in pressure between one stage and the next is significant. Pressure was slightly higher, but not to a significant degree, in REM stage than in stage 2. 3. 3. Variations of arterial pressure during a particular stage might be present both in stage 2 and in the REM stage. In stage 2, in some subjects, these variations became periodic from time to time, identifiable with the arterial pressure oscillations described by Sigmund Mayer; they were often accompanied by a respiratory periodicity. In the REM stage the increases in arterial pressure were more pronounced but not necessarily in relation to variations of arteriolar tone or of heart rate.

Cardiovascular effects of toxins isolated from the cnidarian Chironex fleckeri Southcott.

1. Two unstable high molecular weight toxins have been isolated from tentacles of Chironex fleckeri by exclusion chromatography. Both are cardiotoxic; the lower molecular weight fraction is also a potent haemolysin.2. Both toxins reduce the rate, amplitude of contraction and coronary flow in the isolated, perfused guinea-pig heart. Relative to the mouse lethal dose the haemolytic fraction is less potent in this preparation than the purely cardiotoxic fraction.3. Both toxins cause a rise in arterial pressure in anaesthetized rats and rabbits by a direct action on the vascular musculature. This is followed by hypotension, bradycardia and cardiac irregularity. An increase in respiratory rate is followed by apnoea of variable duration, which is associated with a rise in arterial pressure. Animals frequently show arterial pressure oscillations with periods of apnoea interspersed with hyperpnoea.4. The carotid occlusion reflex is depressed during hypotensive periods after both toxins, although (-)-noradrenaline can still elicit a marked pressor response. Bilateral cervical vagotomy has but little effect on the response to either toxin, save to prevent hyperpnoea, but radical denervation of sinoaortic afferents reduces the arterial pressure fall after the initial hypertensive response, suggesting that this fall is due to a combination of baroreceptor stimulation and a fall in cardiac output. Blood pressure oscillations are still seen, possibly due to central stimulation by hypercapnia.5. Interference with the efferent arm of the vasomotor reflex arc with hexamethonium, bretylium or phenoxybenzamine either abolishes or markedly reduces the blood pressure oscillations without affecting the initial hypertensive response.6. The cardiovascular effects of the two toxins are thought to be due to direct vasoconstriction, cardiotoxicity, baroreceptor stimulation and possibly depression of the vasomotor centre. The resultant disordering of the feed-back system regulating vasomotor tone leads to the characteristic arterial pressure oscillations.

Sympathetic unit activity associated with Mayer waves in the spinal dog.

Sympathetic unit activity associated with Mayer waves in the spinal dog.

Oscillatory behavior of the sympathetic system induced by picrotoxin.

In cats anesthetized with sodium pentobarbital, paralyzed with gallamine, atropinized, and artificially ventilated, an intravenous injection of picrotoxin (dose between 2 and 5 mg/kg) consistently induced sustained oscillations of arterial blood pressure (BP). Because of their form, and regularity of repetition (range: 0.3 to 4 cycles/min), these oscillations can be considered analogous to vasomotor waves (Mayer waves), which are known to occur in conditions such as hemorrhage, metabolic acidosis, and cerebral ischemia. The BP oscillations characteristic of picrotoxin intoxication have the following properties: (i) they are generated in the CNS since they are abolished by ventral root block; (ii) they are accompanied in most cases by oscillations of the nictitating membrane tension of the same frequency; and (iii) they occur in animals with complete transection of the spinal cord at a cervical level and in those with sectioned ninth and tenth nerves; hence they are not dependent upon afferent impulse traffic arising in baro- and chemo-receptors. Furthermore, nictitating membrane tension oscillation has been seen when BP was maintained stable. The latter observations indicate that for maintaining the oscillation in the sympathetic system the concomitant hemodynamic changes are not essential. It would appear that the oscillation is the result of epileptiform activity of sympathetic neurons. Perhaps some types of spontaneously occurring vasomotor waves have a similar origin.

Frequency-response characteristics of vascular resistance vessels.

Frequency-response characteristics of vascular resistance vessels.

Characteristics of viscerosympathetic reflexes in the spinal cat.

ARTICLESCharacteristics of viscerosympathetic reflexes in the spinal catDN Franz, MH Evans, and ER PerlDN Franz, MH Evans, and ER PerlPublished Online:01 Dec 1966https://doi.org/10.1152/ajplegacy.1966.211.6.1292MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByMonoaminergic Modulation of Spinal Viscero-Sympathetic Function in the Neonatal Mouse Thoracic Spinal Cord5 November 2012 | PLoS ONE, Vol. 7, No. 11The autonomic response to human esophageal acidification and the development of hyperalgesia4 June 2012 | Neurogastroenterology & Motility, Vol. 24, No. 7Correlated multisecond oscillations in firing rate in the basal ganglia: modulation by dopamine and the subthalamic nucleusNeuroscience, Vol. 117, No. 2Inhibitory and indirect excitatory effects of dopamine on sympathetic preganglionic neurones in the 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third thoracic segment of the catJournal of the Autonomic Nervous System, Vol. 13, No. 3Spinal cord substance P mediates bicuculline-induced activation of cardiovascular responses from the ventral medullaJournal of the Autonomic Nervous System, Vol. 13, No. 1Localization of the cells of origin for primary afferent fibers supplying the gallbladder of the catExperimental Neurology, Vol. 84, No. 3Cardiovascular reflexes arising from the gallbladder and pancreas in spinal and in decerebrate catsBrain Research, Vol. 299, No. 2Responses of T2–T4 spinal neurons to stimulation of the greater splanchnic nerves of the catExperimental Neurology, Vol. 83, No. 2Differential sensitivity of four central sympathetic pathways to depression by clonidineEuropean Journal of Pharmacology, Vol. 78, No. 1Cardiovascular sympathetic afferent fibers21 June 2005Stabilization of the discharge rate of sympathetic preganglionic neuronsJournal of the Autonomic Nervous System, Vol. 5, No. 1Renal chemoreceptorsJournal of the Autonomic Nervous System, Vol. 3, No. 2-4Nervous Control of the Viscera—Afferent SystemSupraspinal regulation of spinal reflex discharge into cardiac sympathetic nervesBrain Research, Vol. 142, No. 3Somatic Sources of Afferent Input as Factors in Aberrant Autonomic, Sensory and Motor FunctionDepression of Sympathetic Preganglionic Neurons by Clonidine: Evidence for Stimulation of 5-HT Receptors3 July 2009 | Clinical and Experimental Hypertension, Vol. 1, No. 1A theoretical consideration of a model simulating the functional organization of the thoraco-lumbar sympathetic subsystem of the spinal cordJournal of Theoretical Biology, Vol. 67, No. 1L-Dopa-Induced Hypotension: Depression of Spinal Sympathetic Neurons by Release of 5-Hydroxytryptamine27 June 2012Conduction velocity and excitability of A and C fibers of cat mesenteric nervesNeurophysiology, Vol. 7, No. 3Spinal organization of sympathetic inhibition by spinal afferent volleysBrain Research, Vol. 87, No. 2-3Reflex responses of sympathetic preganglionic neurones initiated by different cardiovascular receptors in spinal animalsBrain Research, Vol. 68, No. 2The adrenergic innervation of the gastrointestinal tract23 June 2010Convergence in the lumbar spinal cord of pathways activated by splanchnic nerve and hind limb cutaneous nerve stimulationExperimental Neurology, Vol. 38, No. 2Dorsal Horn ElectrophysiologyOpposite Effects of L-Dopa and 5-HTP on Spinal Sympathetic ReflexesNature, Vol. 239, No. 5371Habituation of skin conductance responses and flexor withdrawal activity mediated by the functionally transected human spinal cordBrain Research, Vol. 42, No. 2Spinal mediation of vasomotor reflexes in animals with intact brain studied by electrophysiological methodsPfl�gers Archiv European Journal of Physiology, Vol. 321, No. 3Convergence of visceral and somatic input onto spinal neuronsExperimental Neurology, Vol. 26, No. 1The organisation of cardiovascular neurons in the spinal cordInteractions between visceral and cutaneous afferents in the spinal cord: Reciprocal primary afferent fiber depolarizationBrain Research, Vol. 14, No. 2Summation properties of the spinal vasomotor reflex ARCBulletin of Experimental Biology and Medicine, Vol. 67, No. 5Dorsal Root Potentials and Ventral Root Reflexes Evoked by Nonmyelinated FibersScience, Vol. 162, No. 3858 More from this issue > Volume 211Issue 6December 1966Pages 1292-1298 Copyright & PermissionsCopyright © 1966 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1966.211.6.1292PubMed5956538History Published online 1 December 1966 Published in print 1 December 1966 Metrics

Non-respiratory oscillations in systemic arterial pressure of dogs.

In dogs the condition of the cardiovascular control system was investigated quantitatively during haemorrhage, by using a system of transient inputs and by recording arterial blood pressure. The analysis of our results using standard control system techniques demonstrates a probable increase in open loop gain and a reduction of natural frequency. The implications of these findings are discussed.

SYSTEMIC AND PULMONARY VASOMOTOR WAVES.

Rhythmic oscillations in systemic arterial blood pressure (Mayer waves) were produced in the dog by metabolic acidosis; hypoxia generally augmented the amplitude of the Mayer waves. When the Mayer waves exceeded 20 mm Hg in amplitude, they were associated with rhythmic fluctuations in pulmonary arterial pressure. The pulmonary arterial waves resembled the Mayer waves with respect to frequency and independence of the breathing pattern but were generally smaller in amplitude Measurements of instantaneous pulmonary arterial blood flow indicate that the rhythmic fluctuations in pulmonary arterial pressure represent the passive effects of fluctuations in pulmonary blood flow rather than fluctuations in pulmonary vasomotor activity. In turn, the swings in pulmonary arterial blood flow appear to originate in rhythmic variations in systemic vasomotor activity.

TIME COURSE OF FACTORS CAUSING EXAGGERATED RESPIRATORY VARIATION OF ARTERIAL BLOOD PRESSURE.

Abstract In 5 patients with exaggerated respiratory variation in arterial blood pressure or palpable pulsus paradoxus due to various causes, measurements were made of cardiac output and arterial, right heart, and intrapericardial pressures. Respiratory patterns were altered voluntarily to prolong inspiration or produce expiratory pauses. These maneuvers allow examination of the time course of right ventricular and left ventricular output. Intrapericardial (and venous) pressures consistently fell with inspiration. No effect of "pericardial tensing" was apparent. A decrease in arterial pressure early in inspiration was followed by a rise with overshoot independent of subsequent respiratory activity. This is interpreted as an inspiratory rise in right ventricular output and early inspiratory drop in left ventricular output. The net effect of inspiration, however, is to increase cardiac output. The relation between pulmonary vascular compliance and the excess of right ventricular over left ventricular output dictates the time delay in transmission of augmented right ventricular output to the left ventricle. At certain respiratory frequencies, i.e., the total system natural frequency, marked oscillations of arterial pressure may be induced.

Mechanism of arterial pressure oscillations caused by compressing the cerebral artery.

The effect of adding a side pressure of isotonic character upon the carotid artery, a method originally reported by MIYAKAWA to create sustained oscillations in the mean arterial pressure level of rabbits, was reinvestigated with minor technical modifications in dogs. The expected oscillation was brought about successfully in all dogs. By recording the cerebral perfusion pressure (i. e. the pressure at the point distal to the side pressure loading site) and the cerebral blood flow simultaneously with the systemic arterial pressure, the roles of the Starling's resistance used to add side pressure were clearly demonstrated:(1) it operates as a sort of limiter for cerebral perfusion pressure or blood flow, and thus amplifies the changes of the cerebral arterial pressure in a nonlinear fashion 2 to 12 times as large as that in the systemic arterial pressure, and (2) it also biases the mean operating level of the effective cerebral arterial pressure toward zero from the ordinary systemic arterial pressure level. Both roles increase the over-all gain and time lag of the system response and render the system quite unstable. Thus, the present experiment reveals the feedback nature of arterial pressure oscillation elicited by adding the side pressure upon the cerebral arterial pressure.

Work of the heart under the effect of induced arterial pressure oscillations studied in intact anesthetized dogs.

The arterial system of intact anesthetized dogs and a physical model, which consisted of a "heart," an elastic "arterial" reservoir, and a "peripheral resistance," have both been studied in comparison. In both systems, the volume contained in the arterial reservoir was rhythmically altered by means of a slow sinusoidal piston pump which resulted in slow oscillations of the mean arterial pressure with the arterial pressure pulsations superimposed. It was found that in the physical model, the systolic pressure pulse was larger during the phase of rising pressure (increasing volume) than during the phase of falling pressure (decreasing volume), while in the animal the systolic pressure pulses were equal in either phase. The aortic pressure pulse of the animal was a linear function of the presystolic aortic pressure during pressure oscillation and independent of the induced volume alteration. Recordings of the stroke output of the heart revealed that the heart of the animal adjusted its output in such a manner that the induced systolic changes of the arterial contents were quantitatively compensated. The mechanism by which this is accomplished is of particular interest, since it would also enable the heart to compensate instantaneously for physiological alterations of the volume in the arterial system as caused by changes in peripheral runoff. This mechanism of instantaneous adjustment of the stroke output can be explained on the basis of Starling's Law of the Heart if the procedure of the calculation of the external work is modified.

Adaptation of cardiac output to peripheral runoff studied in intact dogs.

A pump with sinusoidal piston movement was connected to the abdominal aorta of intact anesthetized dogs, causing slow oscillations of arterial blood pressure. Evidence was found for the existence of a mechanism which enables the heart to adjust its output immediately to changes of peripheral outflow.