The reflex cardiovascular depression caused by occlusion of the coronary sinus in the dog

Muers, Martin F.; Sleight, Peter

doi:10.1113/jphysiol.1972.sp009751

Cited by 40 publications

(14 citation statements)

References 41 publications

(63 reference statements)

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“…Stimulation of the epi-myocardial nonmedullated endings leads to pronounced depressor responses of the Bezold-Iarisch type (29,126,138,149,162); the dominat ing feature is the vagally mediated bradycardia. There is also a more or less general ized inhibition of sympathetic tone leading to vasodilatation that contributes to the hypotensive response (162).…”

Section: Refl Exes Fr Om Ve Ntricular Receptors With No Nmedullated Vmentioning

confidence: 99%

Overall Cardiovascular Regulation

ÖBerg¹

1976

Annu. Rev. Physiol.

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Section: Refl Exes Fr Om Ve Ntricular Receptors With No Nmedullated Vmentioning

confidence: 99%

Overall Cardiovascular Regulation

ÖBerg¹

1976

Annu. Rev. Physiol.

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“…However, these reflexes have been shown to originate in the left ventricle and not in the sinus wall and to be obliterated by deep anesthesia (Muers and Sleight 1972b); the latter may have occurred in our experiments. A rise in PC, mechanically induces a number of changes within the heart including distention of coronary veins and venules (capillaries are probably affected), and distentlon of lymphatics (the increased turgidity may affect ventricular cardiac muscle fiber contraction).…”

Section: Validation Of the Experzrnental Modelmentioning

confidence: 46%

Effects of coronary sinus pressure elevation on coronary blood flow distribution in dogs with normal preload

Rouleau¹,

White²

1985

Can. J. Physiol. Pharmacol.

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Coronary sinus pressure (Pcs) elevation shifts the diastolic coronary pressure-flow relation (PFR) of the entire left ventricular myocardium to a higher pressure intercept. This finding suggests that Pcs is one determinant of zero-flow pressure (Pzf) and challenges the existence of a vascular waterfall mechanism in the coronary circulation. To determine whether coronary sinus or tissue pressure is the effective coronary back pressure in different layers of the left ventricular myocardium, the effect of increasing Pcs was studied while left ventricular preload was low. PFRs were determined experimentally by graded constriction of the circumflex coronary artery while measuring flow using a flowmeter. Transmural myocardial blood flow distribution was studied (15-micron radioactive spheres) at steady state, during maximal coronary artery vasodilatation at three points on the linear portion of the circumflex PFR both at low and high diastolic Pcs (7 +/- 3 vs. 22 +/- 5 mmHg; p less than 0.0001) (1 mmHg = 133.322 Pa). In the uninstrumented anterior wall the blood flow measurements were obtained in triplicate at the two Pcs levels. From low to high Pcs, mean aortic (98 +/- 23 mmHg) and left atrial (5 +/- 3 mmHg) pressure, percent diastolic time (49 +/- 7%), percent left ventricular wall thickening (32 +/- 4%), and percent myocardial lactate extraction (15 +/- 12%) were not significantly changed. Increasing Pcs did not alter the slope of the PFR; however, the Pzf increased in the subepicardial layer (p less than 0.0001), whereas in the subendocardial layer Pzf did not change significantly. Similar slopes and Pzf were observed for the PFR of both total myocardial mass and subepicardial region at low and high Pcs. Subendocardial:subepicardial blood flow ratios increased for each set of measurements when Pcs was elevated (p less than 0.0001), owing to a reduction of subepicardial blood flow; however, subendocardial blood flow remained unchanged, while starting in the subepicardium toward midmyocardium blood flow decreased at high Pcs. This pattern was similar for the uninstrumented anterior wall as well as in the posterior wall. Thus as Pcs increases it becomes the effective coronary back pressure with decreasing magnitude from the subepicardium toward the subendocardium of the left ventricle. Assuming that elevating Pcs results in transmural elevation in coronary venous pressure, these findings support the hypothesis of a differential intramyocardial waterfall mechanism with greater subendo- than subepi-cardial tissue pressure.

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“…Bezold, were later found to occur after several interventions such as intracoronary and intrapericardial injection of nicotine (20,24,32) obstruction of left ventricular outflow (3,10,17,20) (15,9,11,23) temporary occlusion of a coronary artery (2,8,25,28) or of the coronary sinus (18) and a deliberate increase of coronary perfusion pressure (5). These reflexes are vagally mediated.…”

Section: Discussionmentioning

confidence: 99%

Vagal and sympathetic reflexes of left ventricular origin on the efferent activity of cardiac and renal nerves on anaesthetized cats

Vogt

Thämer

1980

Basic Res Cardiol

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The influence of reflexes of left ventricular origin on the postganglionic sympathetic activity and heart rate was investigated in anaesthetized cats. The experiments were to clarify 1. whether there are regionally different reflex adjustments due to an activation of ventricular receptors, 2. whether an increase of left ventricular diastolic pressure, which is known to activate afferent vagal fibres, causes an inhibition of sympathetic activity, 3. whether a coronary artery occlusion can activate a pressor reflex and a depressor reflex. Left ventricular receptors were stimulated by obstruction of the aortic root, coronary artery occlusion and mechanical stretch of the ventricular wall. In animals with intact CNS, all stimuli led to an inhibition of the activity of the inferior cardiac and renal sympathetic nerves and bradycardia. These reflex effects are initiated by mechanoreceptors and abolished by vagotomy. The inhibition of sympathetic activity was equally pronounced in the cardiac and renal nerves. After coronary artery occlusion and aortic obstruction, inhibition occurred as soon as the ventricular diastolic pressure had risen about 2 mmHg. In spinal animals both stimuli caused a sympathetic activation which was mainly restricted to the cardiac nerve. This activation is not due to mechanical changes, but rather a direct result of myocardial ischaemia. Coronary artery occlusion is able to produce both inhibition and activation of sympathetic fibres, but the activation is normally suppressed and thus seems not to be particularly important for circulatory control.

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The reflex cardiovascular depression caused by occlusion of the coronary sinus in the dog

Cited by 40 publications

References 41 publications

Overall Cardiovascular Regulation

Overall Cardiovascular Regulation

Effects of coronary sinus pressure elevation on coronary blood flow distribution in dogs with normal preload

Vagal and sympathetic reflexes of left ventricular origin on the efferent activity of cardiac and renal nerves on anaesthetized cats

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