Reflex inhibitory effects of vagal afferents in experimental myocardial infarction

A bstract. While the reflex influence of selective coronary arterial occlusion on the resistance vasculature has been well delineated, the reflex influence of coronary occlusion on the total capacitance vasculature has not been examined. Thus, selective coronary occlusions were performed in 65 anesthetized dogs. Blood was drained from the vena cavae and returned to the right atrium at a constant rate so that changes in total intravascular volume could be recorded as reciprocal changes in extracorporeal reservoir volume. In 10 animals, 2.5 min of left anterior descending occlusion was associated with only an insignificant total volume increase of 6±4 ml (SEM), whereas 2.5 min of left circumflex occlusion was associated with a 27±4 ml (P < 0.001) increase in volume, which was significantly attenuated (P < 0.001) to only a 7±3 ml increase after cervical vagectomy. Epicardial lidocaine in four animals reduced the volume increment associated with circumflex occlusion from 30±3 to 11±4 ml (P < 0.025). The volume increase was attenuated from 45±6 to 24±5 ml with propranolol administration (P < 0.001) (seven animals) and from 26±5 to 17±6 ml with atropine (P < 0.025) (eight animals), but was not attenuated with phenoxybenzamine (28±7 ml before and 25±2 ml after phenoxybenzamine) (five animals). Double blockade with propranolol and atropine reduced the volume increase to 3±2 ml (NS) in four of these animals.In order to compare the influences of selective beta-1 adrenergic blockade and combined beta-1 and beta-2 blockade, volume responses were assessed before and after administration of metoprolol or propranolol in doses that produced the same amount of beta-1 blockade (15 animals). The volume increase associated with circumflex occlusion was not attenuated after beta-1 blockade (20±4 ml before and 18±5 ml after metoprolol) (eight animals) but was attenuated from 30±5 to 14±5 ml after propranolol (P < 0.05) (seven animals). To examine further the efferent limb of the observed reflex, circumflex occlusions were performed before and after either vagectomy at the level ofthe diaphragm or section ofthe sympathetic splanchnic nerves in 12 animals. The volume increment was significantly attenuated after either procedure. In four animals undergoing prior arterial baroreceptor denervation, volume still increased 30±6 ml (P < 0.001) with circumflex occlusion. Thus, inferior myocardial ischemia is associated with an autonomic reflex that acts to increase total intravascular volume. The afferent limb is mediated through the vagi, and the efferent limb, through changes in peripheral beta adrenergic and parasympathetic receptor stimulation.

Section: Discussionsupporting

confidence: 87%

Reflex influence of selective coronary artery occlusion on the total capacitance vasculature in the dog.

Rutlen¹,

Underwood²

1984

“…In contrast, when hypotension accompanies acute myocardial infarction, increased stimulation of cardiac vagal afferents may inhibit the arterial baroreflex (45)(46)(47)(48)(49)(50)(51)(52)(53). Impaired vasoconstriction during cardiogenic shock could provide an important mechanism for preventing deleterious elevations in left ventricular afterload.…”

Section: Resultsmentioning

confidence: 99%

Interaction of cardiopulmonary and carotid baroreflex control of vascular resistance in humans.

Victor¹,

Mark²

1985

IntroductionPrevious studies in experimental animals indicate an important inhibitory interaction between cardiopulmonary and arterial baroreflexes. In the dog, for example, cardiopulmonary vagal afferents modulate carotid baroreflex control of vascular resistance. On the other hand, previous studies in human subjects have not produced convincing evidence of a specific interaction between these baroreceptor reflexes. The purpose of this study was to determine whether unloading of cardiopulmonary baroreceptors in humans with nonhypotensive lower body negative pressure selectively augments the reflex vasoconstrictor responses to simulated carotid hypotension produced by neck pressure. In nine healthy subjects, we measured forearm vascular responses with plethysmography during lower body negative pressure alone (cardiopulmonary baroreflex), during neck pressure alone (carotid baroreflex), and during concomitant lower body negative pressure and neck pressure (baroreflex interaction). Lower body negative pressure produced a greater than twofold augmentation of the forearm vasoconstrictor response to neck pressure. This increase in resistance was significantly greater (P < 0.05) than the algebraic sum of the increase in resistance from lower body negative pressure alone plus that from neck pressure alone. In contrast, lower body negative pressure did not potentiate the forearm vasoconstrictor responses either to intra-arterial norepinephrine or to the cold pressor test. Thus, the potentiation of the vasoconstrictor response to neck pressure by lower body negative pressure cannot be explained by augmented reactivity to the neurotransmitter or to a nonspecific augmentation of responses to all reflex vasoconstrictor stimuli.In Hypotension and hypovolemia often occur together in the clinical setting, so the arterial and cardiopulmonary baroreceptors are affected simultaneously (1). In most experimental studies of arterial and cardiopulmonary baroreflexes in humans, however, the reflexes have been activated individually, and the possibility of reflex interaction has received little attention (2). In contrast, an important interaction between high and low pressure baroreceptor reflexes has been demonstrated repeatedly in experimental animals (3-12). In the dog, for example, interruption of cardiopulmonary vagal afferents augments vasoconstrictor responses to carotid hypotension ( 12).Baroreflex interactions are obviously more difficult to study in human subjects than in experimental animals. In previous human studies ofthis reflex interaction, cardiopulmonary baroreflexes have been perturbed with lower body negative pressure (LBNP)' and carotid baroreflexes with neck suction. Using these methods, earlier experiments in this laboratory demonstrated that physiologic variations in central venous pressure do not alter carotid baroreflex control of heart rate in humans (13). Previous studies have also examined vascular responses during combined application of LBNP at -40 mmHg and neck suction (14-16). Because LBNP at -4...

“…They showed that 3 h after the injection of metallic mercury into the Cx of closed chest anesthetized dogs there was still a modest tonic inhibitory influence on the sympathetic outflow to the kidney, as indicated by the increases in renal nerve activity that followed vagotomy. It is likely that this inhibition observed 3 h after coronary occlusion by Kezdi et al (25) was mediated primarily via cardiopulmonary receptors outside the ventricle (e.g., left atrium, pulmonary artery, etc.) because left atrial pressure has been shown to be markedly elevated 3 h after Cx occlusion (22).…”

Section: Ilymentioning

confidence: 97%

Reflex Inhibition of Renal Sympathetic Nerve Activity during Myocardial Ischemia Mediated by Left Ventricular Receptors with Vagal Afferents in Dogs

Thames¹,

Abboud²

1979

A B S T R A C T The major goal ofthis investigation was to determine if activation of cardiac receptors during coronary artery occlusion could inhibit efferent renal sympathetic nerve activity. In nine chloralose anesthetized dogs with only carotid (n = 3) or with sinoaortic (n = 6) baroreceptors operative, anterior descending coronary artery (LAD) occlusion resulted in a small decrease in mean arterial pressure (-9.8+±5.1 mm Hg, NS) and in a significant (P < 0.05) increase in renal nerve activity (24.0±4.1%). In these dogs, circumflex coronary artery (Cx) occlusion resulted in greater hypotension (-18