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Myocardial hemodynamics during induced hypotension: A comparison between sodium nitroprusside and adenosine triphosphate
ABSTRACTS
hypotension and bradycardia were observed during any maneuver after the blockade. Since the vagus nerves were kept intact, these results indicate that acute sympathetic denervation of the central organs appears to preserve reflex circulatory responses to physical maneuvers such as producing high intrathoracic pressure, moderate changes in blood pressure or swallowing, though with some suppression of the cardiac aceeleratory response. The results suggest that sympathetic control of heart rate functions as an inhibitor of the vagus rather than an active cardiac accelerator. (Reprinted with permission.)
Myocardial Hemodynamics During Induced Hypotension: A Comparison Between Sodium Nitroprusaide and Adenosine
Triphosphate. Bluet BC, Fukunaga AF, Ma C, et aL Anesthesiology 63:517, 1985. Adenosine triphosphate (ATP) has been reported to be a hypotensive agent similar in effect to sodium nitroprusslde (SNP). The purpose of this study was to examine and compare the effects of both SNP and ATP on general coronary hemodynamics, myocardial O, consumption, and circulating catecholamines. Twelve dogs were anesthetized with 1.0% halothane and given either SNP or ATP by controlled infusion to reduce their systemic blood pressure by 50% for a 2-h period followed by a (blood pressure) recovery period. The ATP-indueed hypotension was rapid, easily controlled, not accompanied by tachyphylaxis over the 120 min studied, and resulted in an increase in coronary sinus blood flow (CSBF), which plateaued at ~60% above control. The increase in CSBF was almost immediate and remained at this elevated level for the duration of the induced hypotension. During the ATP-induced hypotension, there was no change in heart rate or circulating catecholamines. A 60% reduction in myocardial 02 uptake was observed, presumably from the cardiac unloading. In contrast,'SNP-induced hypotension required a marked increase in dose over time, did not significantly increase CSBF, did increase heart rate, and resulted in large increases in circulating plasma eateeholamines. Neither agent affected cardiac output. ATP-induced hypotension resulted in no change in cardiac lactic acid uptake, while SNP caused lactic acid production, indicating possible cardiac ischemia or cyanide toxicity. (Reprinted with permission.)
Inspiratory Work With and Without Continuous Positive Airway Pressure in Patients with Acute Respiratory Failure.
Katz JA, and Marks JD. Anesthesiology 63:598, 1985.
To compare the effects of continuous positive airway pressure (CPAP) with those of ambient end-expiratory pressure (T-tube) on lung mechanics and blood gas exchange, transpulmonary pressure (Pip), tidal volume (Vr), respiratory frequency, and" arterial oxygen and carbon dioxide tensions were measured in 16 spontaneously breathing patients recovering from acute respiratory failure. These variables were measured during breathing through a T-tube; with 18, 12, and 6 cmH20 CPAP; and again during breathing through a T-tube. During all levels of CPAP, mean effective lung compliance (C~r) was higher and mean total pulmonary
193
power during inspiration lower than during breathing through a T-tube before CPAP ( P < 0.05). The data obtained at the level of CPAP producing maximum Cdr (optimum CPAP) were ~?'ouped and compared with values obtained during breathing through a T-tube. Mean total pulmonary power of inspiratory muscles during breathing through a T-tube before CPAP (0.7 ± 0.14 kg • m • rain -z) decreased during optimum CPAP (0.44 ± 0.07 kg • m • min -t) and increased during breathing througti a T-tube after CPAP (0.63 ± 0.12 kg • m . rain-I). Mean VT was higher (557 ± 63 ml vs. 474 ± 47 ml) and frequency lower (17.5 ± 1.6 breaths/rain vs. 22.5 ± 2.5 breaths/rain) during optimum CPAP than during breathing through a T-tube before CPAP, and inspiratory time was significantly longer. Mean minute ventilation was also lower during optimum CPAP (8.7 ~: 0.6 l/rain) than during breathing through a T-tube (9.6 ± 0.8 1/rain); Paces did not change significantly. Mean alveolar-to-arterial oxygen pressure difference decreased significantly during optimum CPAP. The authors conclude that CPAP, when adjusted to the appropriate levels, improves lung mechanics in patients recovering from acute respiratory failure. Continuous positive airway pressure reduces total pulmonary power during inspiration and at the same time improves oxygen and carbon dioxide exchange. In these respects, it is preferable to breathing through a T-tube without CPAP. (Reprinted with permission.)
Inhalation Anesthetics Augment OxJdont-lnduced Pulmonary Vasoconstriction: Evidence for a Membrane Effect.
Shayevilz JR, Traystrnan R J, Adkinson NF, et aL Anesthesiology 63:624, 1985.
Inhalational anesthetics "fluidize" biologic membranes. Since araehidonate metabolism also occurs in cell membranes, anesthetic agents may modify arachidonie acid mediator production. The authors used the isolated perfused rabbit lung preparation to examine the effects of inhalational anesthetics on the production of arachidonate mediators. The oxidant tert-butyl-hydroperoxide (t-bu-OOH) is known to cause pulmonary vasoconstriction by causing increased production of thromboxane A2 (TxA2). The authors administered three anesthetics (halothane, cyclopropane, and nitrous oxide) of widely different potencies, at different dosages, each to three different groups of preparations and challenged the lungs at each anesthetic dose with t-bu-OOH. They found a dose-related augmentation of the pulmonary vasopressor response to t-bu-OOH. Preparations given t-bu-OOH alone showed nochange in response over time. Lungs perfused with indomethacin (5 tag • mi -I in Krebs-Henseleit buffer), ventilated with cyclopropane (2 MAC), and challenged with t-bu-OOH showed almost complete inhibition of the response to t-bu-OOH, lndomcthaein at this concentration is a specific inhibitor of cyclooxygena~¢. The authors also have demonstrated significantly increased perfusate levels of thromboxane B2 (TxB2), the inactive metabolite of TxA=, after oxidant challenge during exposure to 2% halothane compared with TxB= levels before halothane exposure. The authors believe that the augmented presser response and mediator production occur because of increased substrate (araehidonie acid) availability induced by anesthetic agent. (Reprinted with permission.)
hypotension and bradycardia were observed during any maneuver after the blockade. Since the vagus nerves were kept intact, these results indicate that acute sympathetic denervation of the central organs appears to preserve reflex circulatory responses to physical maneuvers such as producing high intrathoracic pressure, moderate changes in blood pressure or swallowing, though with some suppression of the cardiac aceeleratory response. The results suggest that sympathetic control of heart rate functions as an inhibitor of the vagus rather than an active cardiac accelerator. (Reprinted with permission.)
Myocardial Hemodynamics During Induced Hypotension: A Comparison Between Sodium Nitroprusaide and Adenosine
Triphosphate. Bluet BC, Fukunaga AF, Ma C, et aL Anesthesiology 63:517, 1985. Adenosine triphosphate (ATP) has been reported to be a hypotensive agent similar in effect to sodium nitroprusslde (SNP). The purpose of this study was to examine and compare the effects of both SNP and ATP on general coronary hemodynamics, myocardial O, consumption, and circulating catecholamines. Twelve dogs were anesthetized with 1.0% halothane and given either SNP or ATP by controlled infusion to reduce their systemic blood pressure by 50% for a 2-h period followed by a (blood pressure) recovery period. The ATP-indueed hypotension was rapid, easily controlled, not accompanied by tachyphylaxis over the 120 min studied, and resulted in an increase in coronary sinus blood flow (CSBF), which plateaued at ~60% above control. The increase in CSBF was almost immediate and remained at this elevated level for the duration of the induced hypotension. During the ATP-induced hypotension, there was no change in heart rate or circulating catecholamines. A 60% reduction in myocardial 02 uptake was observed, presumably from the cardiac unloading. In contrast,'SNP-induced hypotension required a marked increase in dose over time, did not significantly increase CSBF, did increase heart rate, and resulted in large increases in circulating plasma eateeholamines. Neither agent affected cardiac output. ATP-induced hypotension resulted in no change in cardiac lactic acid uptake, while SNP caused lactic acid production, indicating possible cardiac ischemia or cyanide toxicity. (Reprinted with permission.)
Inspiratory Work With and Without Continuous Positive Airway Pressure in Patients with Acute Respiratory Failure.
Katz JA, and Marks JD. Anesthesiology 63:598, 1985.
To compare the effects of continuous positive airway pressure (CPAP) with those of ambient end-expiratory pressure (T-tube) on lung mechanics and blood gas exchange, transpulmonary pressure (Pip), tidal volume (Vr), respiratory frequency, and" arterial oxygen and carbon dioxide tensions were measured in 16 spontaneously breathing patients recovering from acute respiratory failure. These variables were measured during breathing through a T-tube; with 18, 12, and 6 cmH20 CPAP; and again during breathing through a T-tube. During all levels of CPAP, mean effective lung compliance (C~r) was higher and mean total pulmonary
193
power during inspiration lower than during breathing through a T-tube before CPAP ( P < 0.05). The data obtained at the level of CPAP producing maximum Cdr (optimum CPAP) were ~?'ouped and compared with values obtained during breathing through a T-tube. Mean total pulmonary power of inspiratory muscles during breathing through a T-tube before CPAP (0.7 ± 0.14 kg • m • rain -z) decreased during optimum CPAP (0.44 ± 0.07 kg • m • min -t) and increased during breathing througti a T-tube after CPAP (0.63 ± 0.12 kg • m . rain-I). Mean VT was higher (557 ± 63 ml vs. 474 ± 47 ml) and frequency lower (17.5 ± 1.6 breaths/rain vs. 22.5 ± 2.5 breaths/rain) during optimum CPAP than during breathing through a T-tube before CPAP, and inspiratory time was significantly longer. Mean minute ventilation was also lower during optimum CPAP (8.7 ~: 0.6 l/rain) than during breathing through a T-tube (9.6 ± 0.8 1/rain); Paces did not change significantly. Mean alveolar-to-arterial oxygen pressure difference decreased significantly during optimum CPAP. The authors conclude that CPAP, when adjusted to the appropriate levels, improves lung mechanics in patients recovering from acute respiratory failure. Continuous positive airway pressure reduces total pulmonary power during inspiration and at the same time improves oxygen and carbon dioxide exchange. In these respects, it is preferable to breathing through a T-tube without CPAP. (Reprinted with permission.)
Inhalation Anesthetics Augment OxJdont-lnduced Pulmonary Vasoconstriction: Evidence for a Membrane Effect.
Shayevilz JR, Traystrnan R J, Adkinson NF, et aL Anesthesiology 63:624, 1985.
Inhalational anesthetics "fluidize" biologic membranes. Since araehidonate metabolism also occurs in cell membranes, anesthetic agents may modify arachidonie acid mediator production. The authors used the isolated perfused rabbit lung preparation to examine the effects of inhalational anesthetics on the production of arachidonate mediators. The oxidant tert-butyl-hydroperoxide (t-bu-OOH) is known to cause pulmonary vasoconstriction by causing increased production of thromboxane A2 (TxA2). The authors administered three anesthetics (halothane, cyclopropane, and nitrous oxide) of widely different potencies, at different dosages, each to three different groups of preparations and challenged the lungs at each anesthetic dose with t-bu-OOH. They found a dose-related augmentation of the pulmonary vasopressor response to t-bu-OOH. Preparations given t-bu-OOH alone showed nochange in response over time. Lungs perfused with indomethacin (5 tag • mi -I in Krebs-Henseleit buffer), ventilated with cyclopropane (2 MAC), and challenged with t-bu-OOH showed almost complete inhibition of the response to t-bu-OOH, lndomcthaein at this concentration is a specific inhibitor of cyclooxygena~¢. The authors also have demonstrated significantly increased perfusate levels of thromboxane B2 (TxB2), the inactive metabolite of TxA=, after oxidant challenge during exposure to 2% halothane compared with TxB= levels before halothane exposure. The authors believe that the augmented presser response and mediator production occur because of increased substrate (araehidonie acid) availability induced by anesthetic agent. (Reprinted with permission.)