Vagal control of coronary blood flow in dogs

Tiedt, N; Religa, A

doi:10.1007/bf01907744

Cited by 17 publications

(6 citation statements)

References 23 publications

(16 reference statements)

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“…Prolonged diastoles permitted to determine the zero flow pressure and the instantaneous relationship between the coronary inflow and the driving pressure. This method to induce temporary cardiac arrest is opened to criticism because of the direct vasodilatator effect of vagus nerve stimulation (27), Nevertheless, as this effect was probably the same during control state and vasopressin perfusion, this method has been used successfully in the present study. During prolonged diastoles, the pressure-flow relationship was linear in both control and AVP conditions.…”

Section: Discussionmentioning

confidence: 96%

Effect of vasopressin on phasic coronary blood flow

et al. 1985

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The effects of vasopressin on the coronary circulation have been studied with regard to its general hemodynamic effects. Aortic blood pressure (BP), left ventricular pressure (LVP), aortic blood flow (AoBF), and circumflex blood flow (CBF), were measured in 12 open-chest dogs, under control conditions and during vasopressin infusion (25 mU/kg/min). During vasopressin infusion, the mean aortic blood pressure (MBP) was increased from 104 +/- 23 mm Hg to 161 +/- 23 mm diastolic blood pressure (DBP) was more increased (+55%) than the systolic blood pressure (SBP) (+40%). AoBF was decreased from 2.169 +/- 0.408 l/min to 1.118 +/- 0.303 l/min; and the heart rate was decreased by 18%. The total combined left ventricular power did not change significantly. The increase in total peripheral resistance (TPR) (+200%) was the main change in impedance spectrum. The mean circumflex coronary blood flow (MCBF) was decreased from 48 +/- 8.6 ml/min to 33.4 +/- 9.7 ml/min. This decrease was more important in the diastolic circumflex blood flow (DCBF) (-33%) than in the systolic one (-0.8%). The diastolic pressure time index (DPTI) was more increased than the systolic pressure time index (SPTI). The DPTI/SPTI ratio was increased from 0.91 to 1.3. Long diastoles, induced by vagus nerve stimulation, have permitted to characterise the relationship between pressure and coronary blood flow during diastole. This relationship was linear under basal condition, and during vasopressin perfusion. This made it possible to determine the critical closing pressure (Pf0), and the coronary conductance (the slope of the regression curve). Vasopressin induced an increase in Pf0, from 33.7 +/- 95 to 77.4 +/- 16.07 mm Hg (p less than 0.001), and a decrease in coronary conductance, from 0.8 +/- 0.32 to 0.5 +/- 0.1 ml/min/mm Hg. The effect of an acute change in perfusion pressure on the coronary flow, under control conditions and during vasopressin infusion was studied by opening a large arteriovenous fistula. Unclamping of the fistula, under control conditions, allowed to realize an acute fall in DBP from 82.5 +/- 6.36 to 35.5 +/- 9.19 mm Hg, and in DCBF, from 58.5 +/- 9.2 to 20 +/- 9.8 ml/min. During vasopressin infusion, a similar fall in perfusion pressure lead to a zero diastolic circumflex blood flow, for a diastolic aortic blood pressure of 56 +/- 12 mm Hg. However, vasopressin did not affect the delayed active coronary vasodilatation.

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Section: Discussionmentioning

confidence: 96%

Effect of vasopressin on phasic coronary blood flow

et al. 1985

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“…In animals, invasive VNS attenuated mean arterial blood pressure and reduced the number of arrhythmia episodes in hypertensive rats (Annoni et al, 2015), whereas it increased coronary flow in dogs (Tiedt and Religa, 1979). aVNS elicited cardiovascular responses in rats, characterized by a lowered blood pressure (Mahadi et al, 2019) and heart rate (Gao et al, 2007).…”

Section: Vagus Nerve Stimulation – From Biophysics To Animal and To Hmentioning

confidence: 99%

Current Directions in the Auricular Vagus Nerve Stimulation I – A Physiological Perspective

et al. 2019

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Electrical stimulation of the auricular vagus nerve (aVNS) is an emerging technology in the field of bioelectronic medicine with applications in therapy. Modulation of the afferent vagus nerve affects a large number of physiological processes and bodily states associated with information transfer between the brain and body. These include disease mitigating effects and sustainable therapeutic applications ranging from chronic pain diseases, neurodegenerative and metabolic ailments to inflammatory and cardiovascular diseases. Given the current evidence from experimental research in animal and clinical studies we discuss basic aVNS mechanisms and their potential clinical effects. Collectively, we provide a focused review on the physiological role of the vagus nerve and formulate a biology-driven rationale for aVNS. For the first time, two international workshops on aVNS have been held in Warsaw and Vienna in 2017 within the framework of EU COST Action “European network for innovative uses of EMFs in biomedical applications (BM1309).” Both workshops focused critically on the driving physiological mechanisms of aVNS, its experimental and clinical studies in animals and humans, in silico aVNS studies, technological advancements, and regulatory barriers. The results of the workshops are covered in two reviews, covering physiological and engineering aspects. The present review summarizes on physiological aspects – a discussion of engineering aspects is provided by our accompanying article ( Kaniusas et al., 2019 ). Both reviews build a reasonable bridge from the rationale of aVNS as a therapeutic tool to current research lines, all of them being highly relevant for the promising aVNS technology to reach the patient.

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“…198 In another study, the maximal effect of vagal stimulation on coronary flow in open-chest dogs occurred within 2 seconds of the onset of stimulation. 199 In still another, vagally mediated increases in transmural coronary flow were reported after ^-receptor blockade, but only one high-stimulation frequency was used (30 Hz), and the response had a sharp onset and decayed rapidly. 156 Thirty seconds into the stimulation, the dilation was a small fraction (20%) of its initial peak value.…”

Section: Glml Added In Perfusion Reservoir) Of Vasoconstrictor Respomentioning

confidence: 99%

Cholinergic constriction in the general circulation and its role in coronary artery spasm.

Kalsner

1989

Circulation Research

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The release of acetylchoUne from autonomic nerves in those tissues that receive a cholinergic innervation is widely believed to dilate blood vessels. Exogenously administered acetylchoUne hi vivo does dilate vascular beds and produce hypotension; however, this latter effect is indirect and probably the result of liberation of endothelium-derived relaxing factor (EDRF) from endothelial cells. Some blood vessels contain a substantial population of medial constrictor receptors for acetylchoUne, and the implications of this presence for vascular control systems has been largely ignored, although it needs to be considered. A survey of the evolution of vasomotor control systems indicates that acetylchoUne serves principally as an excitatory transmitter to blood vessels. NeuraUy mediated cholinergic constriction and not dilation is found in fish, amphibians, reptiles, and birds, with responses initiated by medial muscarinic receptors. AcetylchoUne constricts many vascular preparations from these lower animals, but some vessels relax, reflecting the emergence of an EDRF responsive to acetylchoUne. An examination of cholinergic responses in mammalian vessels reveals that cholinergic (neurogenic) dilation is limited to a very few vascular beds and to only a few species. Both experimental evidence and evolutionary considerations support the likelihood that cholinergic (neural) constriction operates in some vascular regions in mammals and, in particular, in the coronary circulation of some species, including humans. In fact, constriction, and not dilation, may be the dominant vascular response to activation of the cholinergic axis in most mammals, including humans. The complications and contradictions introduced by the simultaneous presence of both EDRF and a cholinergic constrictor innervation involving medial muscarinic receptors are discussed. A variety of evidence is also presented that implicates cholinergic constriction in at least some instances of coronary artery spasm and sudden death. Received March 3, 1988; accepted January 24, 1989. little to say about neurogenic acetylcholine, except to reiterate its traditional functional assignment to a few specialized vascular beds, such as the male genitalia, the nasal mucosa, and the submandibular salivary glands. 3 -s Even such specific attributions of function, however, have generated little research interest in cholinergic mechanisms per se but instead have focused attention on the role of vasoactive peptides in neurogenic dilation. 6In fact, vasodilation by endogenously liberated acetylcholine, in those few beds in which it is postulated to occur, is linked to such ambiguities and uncertainties, with hardly a single exception, as to suggest that even such a restricted and modest assignment may overstate its role. As will be discussed here, the purported cholinergic vasodilator innervation of skeletal muscle, 7 -9 presumed to be activated as part of the defense reaction in the cat and dog, is unverifiable in primates, 10 and its hypothesized role in dilation of thoro...

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Vagal control of coronary blood flow in dogs

Cited by 17 publications

References 23 publications

Effect of vasopressin on phasic coronary blood flow

Effect of vasopressin on phasic coronary blood flow

Current Directions in the Auricular Vagus Nerve Stimulation I – A Physiological Perspective

Cholinergic constriction in the general circulation and its role in coronary artery spasm.

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