Lecture 8_Neural regulation of cardiac activity and cardiac reflexes.ppsx

Editor's Notes

• #2: reticular substance of the pons, mesencephalon, and diencephalon . In general, the neurons in the more lateral and superior portions of the reticular substance cause excitation, whereas the more medial and inferior portions cause inhibition The posterolateral portions of the hypothalamus cause mainly excitation, whereas the anterior portion can cause either mild excitation or inhibition, depending on the precise part of the anterior hypothalamus Many parts of the cerebral cortex can also excite or inhibit the vasomotor center. Stimulation of the motor cortex, for instance, excites the vasomotor center because of impulses transmitted downward into the hypothalamus and then to the vasomotor center. Also, stimulation of the anterior temporal lobe, the orbital areas of the frontal cortex, the anterior part of the cingulate gyrus, the amygdala, the septum, and the hippocampus can all either excite or inhibit the vasomotor center, depending on the precise portions of these areas that are stimulated and the intensity of the stimulus anterior temporal lobe, the orbital areas of the frontal cortex, the anterior part of the cingulate gyrus, the amygdala, the septum, and the hippocampus
• #5: BSRF brain stem reticular formation Dorsal root ganglion Nts nucleus tractus solitarius
• #7: Mechanorecetors inhibited by vagal afferents
• #9: The sino-atrial node is under the control of right vagus while the atrio-ventricular node is under the control of both vagi with the left being more effective. On stimulation of the sympathetic nerves, the increase in heart rate (decrease in RR interval) begins to manifest in 2.5 to 8 seconds and reaches maximum in 7 – 12 seconds. On stoppage of stimulation the heart rate returns to baseline value in about 15-63 seconds. The increase in vagal activity or stimulation decreases the heart rate (increase in the RR interval) within the next beat i.e. next beat is delayed. On stoppage of vagal stimulation, the heart rate returns to baseline value in 1-3 second
• #10: Sympathetic innervation can be imaged by: MIBG (iodine-123-metaiodobenzylguanidine), SPECT HED (C 11 Hydroxyephedrine) PET
• #12: Total Circulation time is ~ 1min
• #14: Gain= Correction/ Error
• #18: Carotid sinus nerve activity The threshold ~50 mm Hg Maximal activity ~ 200 Hg aortic baroreceptors are similar to those of the carotid receptors except that they operate, in general, at arterial pressure levels about 30 mm Hg higher.
• #19: In addition, mechanisms to maintain and restore the blood volume are also activated as part of baroreflex. These mechanisms occur in concurrence with other mechanism initiated by low blood volume and changes in the osmolality and include: Increase in the renal sympathetic nerve activity (retention of salt and water leading to maintenance of blood volume) (64) Release of vasopressin from Supra-optic nucleus and paraventricular nucleus of hypothalamus (65) Stimulation of the adrenal to release epinephrine and aldosterone Release of adrenocorticotropic hormone via release of corticotropin releasing hormone from paraventricular nucleus of the hypothalamus. Activation of thirst and salt appetite.
• #22: A physiological situation in which arterial blood pressure is decreased for a prolonged period of time is pregnancy. In pregnant animals, the baroreflex function curve shifts to operate at a lower arterial pressure range. Baroreflex responses to immediate increases in pressure are maintained or even potentiated, whereas
• #25: “reverse” Bainbridge reflex has been proposed to explain decreases in heart rate observed under conditions in which venous return is reduced, High-pressure sensitive receptors in the LV and low-pressure responsive elements in the atria and RV consist of stretch-induced mechanoreceptors that respond to pressure or volume changes. These receptors activate myelinated vagal afferent fibers that project to the nucleus solitarius and increase sympathetic nerve activity to the SA node but not to the ventricles, thereby increasing heart rate but not contractility.  Distention of these mechanoreceptors also increases renal excretion of free water by inhibition of antidiuretic hormone secretion from the posterior lobe of the pituitary gland.  It appears highly likely that the Bainbridge reflex may be mediated by distention of these mechanoreceptors. Second, a diffuse receptor network is distributed throughout the cardiac chambers that projects via unmyelinated vagal afferent neurons to the nucleus tractus solitarius.  These receptors behave like the carotid and aortic mechanoreceptors and produce a vasodepressor response consisting of vagus activation concomitant with a simultaneous increase in venous capacitance
• #26: Activation of cardiopulmonary reflexes may help reduce the amount of inspired pollutants that gets absorbed into the blood, protecting vital organs from potential toxicity of these pollutants, and facilitating their elimination.
• #29: A rise in arterial PCO2 stimulates the RVLM, but the direct peripheral effect of hypercapnia is vasodilation. Therefore, the peripheral and central actions tend to cancel each other out. Moderate hyperventilation, which significantly lowers the CO2 tension of the blood, causes cutaneous and cerebral vasoconstriction in humans, but there is little change in blood pressure. Exposure to high concentrations of CO2 is associated with marked cutaneous and cerebral vasodilation, but vasoconstriction occurs elsewhere and usually there is a slow rise in blood pressure.
• #32: neurons from the Pre-Botzinger projects facilitates GABAergic inhibition of the NA, thereby leading to vagal withdrawal during inspiration. The baroreceptive neurons of the NTS send a stimulatory projection to the NA The inspiration results in increase in venous return due to decrease in intra-thoracic pressure. The stretching of the heart by balloon or increase blood volume results increase in heart rate.
• #36: Sympathetic stimulation of the heart results in an increase in cytosolic cyclic adenosine monophosphate (cAMP) hence phosphorylation of several proteins by protein kinase A (PKA). An A kinase anchor protein (AKAP) adjacent to the L-type calcium channel facilitates phosphorylation of this channel and possibly nearby sarcoplasmic reticulum calcium channels. Other proteins phosphorylated by PKA include phospholamban (PLN) and troponin I. Muscarinic agonists (e.g., acetylcholine [ACh]), on the other hand, inhibit this sympathetic cascade by inhibiting the production of cAMP by adenylate cyclase (AC). β-AR, β-adrenergic receptor; ATP, adenosine triphosphate; Gi, inhibitory G protein; M2Rec, muscarinic acetylcholine M2 receptor; Reg, regenerating gene receptor. (Redrawn from Bers DM. Cardiac excitation-contraction coupling. Nature 2002;415:198.)