- Email: [email protected]
Electrical properties and response to noradrenaline of individual heart cells isolated from human ventricular tissue
LITERATURE REVIEW Carol L. Lake, MD, Editor
Dole WP: Autoregulation of the coronary circulation. Prog Cardiovasc Dis 29:293-323, 1987 Coronary blood flow is controlled by autoregulation and metabolic vasodilation. Coronary autoregulation is defined as the intrinsic ability of the heart to maintain constant blood flow after changes in perfusion pressure at constant myocardial oxygen demands. This excellent review discusses the hemodynamic characteristics of autoregulation, including vasodilator reserve and the difficulties involved in research in coronary autoregulation. Autoregulation can be measured using either pressure- or flow-regulated systems, but is not always demonstrable with either method. Autoregulation may be reduced or absent in the right coronary artery circulation due to underestimation of right coronfiry blood flow secondary to collateral flow from the left coronary artery and pressure- and flow-dependent differences in myocardial oxygen consumption. Autoregulation is less in the subendocardium than in the subepicardium. Although autoregulatory vasodilator reserve may be exhausted during maximal coronary vasodilation, administration of intracoronary vasodilators demonstrates the presence of pharmacologic vasodilator reserve. The major methodological problems in the study of coronary autoregulation are the effects of coronary perfusion pressure on myocardial oxygen consumption, collateral coronary flow, and the driving pressure across the coronary bed. Flow measurements using radioactive mierospheres overestimate the degree of autoregulation because they include collateral flow. Use of an upstream flow transducer during alteration of pressure in a selected coronary artery underestimates autoregulation. An additional problem is that alterations of coronary pressure or flow result in directionally similar changes in myocardial oxygen consumption and contractility that also affect autoregulation. A final unresolved issue in the calculation of coronary vascular resistance is whether the "back pressure" opposing flow is coronary venous pressure, tissue pressure, or is actually zero. At present, coronary autoregulation appears to be governed by a metabolic mechanism, as considerable evidence exists against the tissue pressure hypothesis and myogenic theory. Potential metabolic mediators include oxygen (autoregulation is coupled to myocardial PO2), adenosine (does not appear essential for autoregulation), prostaglandins (do not appear to have a major role), and potassium (no major role).
Ducas J, Dural D, Dasilva H, et al: Treatment of canine pulmonary hypertension: Effects of norepinephrine and isoproterenol on pulmonary 366
vascular pressure-flow characteristics. Circulation 75:235-242, 1987 In the standard formula for pulmonary vascular resistance (PVR), left ventricular filling pressure is used as the pulmonary vascular outflow pressure. Using an alternative method in which the slope and extrapolated pressure intercept of the mean pulmonary artery pressure and cardiac output plot are used to define incremental resistance and effective outflow pressure, respectively, the authors noted that isoproterenol decreased pulmonary vascular resistance in experimental animals with acute pulmonary hypertension. N0rcPinephrine at doses that increased blood pressure (low dose) and cardiac output (high dose) also decreased pulmonary vascular resistance. However, isoprotercnol decreased PVR by decreasing incremental resistance, while norepinephrine did not affect pulmonary vascular tone. These studies support the use of isoproterenol in conditions of increased pulmonary vascular resistance.
Mitchell MR, Powell T, Sturridge MF, et al: Electrical properties and response to noradrenaline of individual heart cells isolated from human ventricular tissue. Cardiovasc Res 20:869876, 1986 Isolated human ventricular cells appeared to have sealed intercalated discs, as evidenced by measurements of specific cell membrane resistance and input resistance in these studies. Catecholamines do not freely diffuse in such preparations, but interact with norepinephrine bindi0g sites to enter the cell. Once intracellular, norepinephrine produces pronounced prolongation of the cellular action potential.
Rossi R, Ekroth R, Lincoln C, et ai: Detection of cerebral injury after total circulatory arrest and profound hypothermia by estimation of specific creatine kinase isoenzyme levels using monoclonal antibody techniques. Am J Cardiol 58:1236-1241, 1986 The new monoclonal antibody assay that is specific for the CK-BB homodimer believed to originate from cerebral tissue was performed in 31 children undergoing either closed heart or profound hypothermic circulatory arrest procedures. Although CK-BB represents the fetal form of the enzyme and is replaced in tissues other than the brain by CK-MB and s~ubsequently CK-M M, the authors found that plasma levels of CK-BB were significantly higher in children undergoing circulatory arrest and could be correlated with the duration
Journal of Cardiothoracic Anesthesia, Vol 1, No 4 (August), 1987: pp 366-369
Dole WP: Autoregulation of the coronary circulation. Prog Cardiovasc Dis 29:293-323, 1987 Coronary blood flow is controlled by autoregulation and metabolic vasodilation. Coronary autoregulation is defined as the intrinsic ability of the heart to maintain constant blood flow after changes in perfusion pressure at constant myocardial oxygen demands. This excellent review discusses the hemodynamic characteristics of autoregulation, including vasodilator reserve and the difficulties involved in research in coronary autoregulation. Autoregulation can be measured using either pressure- or flow-regulated systems, but is not always demonstrable with either method. Autoregulation may be reduced or absent in the right coronary artery circulation due to underestimation of right coronfiry blood flow secondary to collateral flow from the left coronary artery and pressure- and flow-dependent differences in myocardial oxygen consumption. Autoregulation is less in the subendocardium than in the subepicardium. Although autoregulatory vasodilator reserve may be exhausted during maximal coronary vasodilation, administration of intracoronary vasodilators demonstrates the presence of pharmacologic vasodilator reserve. The major methodological problems in the study of coronary autoregulation are the effects of coronary perfusion pressure on myocardial oxygen consumption, collateral coronary flow, and the driving pressure across the coronary bed. Flow measurements using radioactive mierospheres overestimate the degree of autoregulation because they include collateral flow. Use of an upstream flow transducer during alteration of pressure in a selected coronary artery underestimates autoregulation. An additional problem is that alterations of coronary pressure or flow result in directionally similar changes in myocardial oxygen consumption and contractility that also affect autoregulation. A final unresolved issue in the calculation of coronary vascular resistance is whether the "back pressure" opposing flow is coronary venous pressure, tissue pressure, or is actually zero. At present, coronary autoregulation appears to be governed by a metabolic mechanism, as considerable evidence exists against the tissue pressure hypothesis and myogenic theory. Potential metabolic mediators include oxygen (autoregulation is coupled to myocardial PO2), adenosine (does not appear essential for autoregulation), prostaglandins (do not appear to have a major role), and potassium (no major role).
Ducas J, Dural D, Dasilva H, et al: Treatment of canine pulmonary hypertension: Effects of norepinephrine and isoproterenol on pulmonary 366
vascular pressure-flow characteristics. Circulation 75:235-242, 1987 In the standard formula for pulmonary vascular resistance (PVR), left ventricular filling pressure is used as the pulmonary vascular outflow pressure. Using an alternative method in which the slope and extrapolated pressure intercept of the mean pulmonary artery pressure and cardiac output plot are used to define incremental resistance and effective outflow pressure, respectively, the authors noted that isoproterenol decreased pulmonary vascular resistance in experimental animals with acute pulmonary hypertension. N0rcPinephrine at doses that increased blood pressure (low dose) and cardiac output (high dose) also decreased pulmonary vascular resistance. However, isoprotercnol decreased PVR by decreasing incremental resistance, while norepinephrine did not affect pulmonary vascular tone. These studies support the use of isoproterenol in conditions of increased pulmonary vascular resistance.
Mitchell MR, Powell T, Sturridge MF, et al: Electrical properties and response to noradrenaline of individual heart cells isolated from human ventricular tissue. Cardiovasc Res 20:869876, 1986 Isolated human ventricular cells appeared to have sealed intercalated discs, as evidenced by measurements of specific cell membrane resistance and input resistance in these studies. Catecholamines do not freely diffuse in such preparations, but interact with norepinephrine bindi0g sites to enter the cell. Once intracellular, norepinephrine produces pronounced prolongation of the cellular action potential.
Rossi R, Ekroth R, Lincoln C, et ai: Detection of cerebral injury after total circulatory arrest and profound hypothermia by estimation of specific creatine kinase isoenzyme levels using monoclonal antibody techniques. Am J Cardiol 58:1236-1241, 1986 The new monoclonal antibody assay that is specific for the CK-BB homodimer believed to originate from cerebral tissue was performed in 31 children undergoing either closed heart or profound hypothermic circulatory arrest procedures. Although CK-BB represents the fetal form of the enzyme and is replaced in tissues other than the brain by CK-MB and s~ubsequently CK-M M, the authors found that plasma levels of CK-BB were significantly higher in children undergoing circulatory arrest and could be correlated with the duration
Journal of Cardiothoracic Anesthesia, Vol 1, No 4 (August), 1987: pp 366-369