Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2004
Neither the accuracy nor the precision of thermal dilution cardiac output measurements is altered by acute tricuspid regurgitation in pigs.
Whether measurement of cardiac output using the thermal dilution technique (TDCO) is valid in the presence of tricuspid regurgitation (TR) is controversial. We assessed the accuracy and precision of the technique in pigs by comparison with data from an electromagnetic flowmeter on the aorta (EMCO). TR was created with sutures that immobilized the free-wall leaflets of the tricuspid valve, and cardiac output was adjusted with dobutamine to give values comparable to control measurements. TR reduced forward stroke volume from 17.2 to 12.6 mL/beat and caused the right atrium to dilate and pulse in synchrony with the right ventricle. Acute TR did not affect the linear regression relation between TDCO and EMCO and did not alter the correlation coefficient (r = 0.94 during both control and TR). These data demonstrate that acute TR does not affect the accuracy or precision of TDCO in pigs. ⋯ Cardiac output is a valuable measurement that guides the medical care of patients with heart and lung disease. This study demonstrates that the thermal dilution technique of determining cardiac output is valid when acute tricuspid valve regurgitation is present in pigs.
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Anesthesia and analgesia · Apr 2004
The effects of propofol on hypothalamic paraventricular nucleus neurons in the rat.
The mechanism of hypotension induced by anesthetics is not completely understood. Because no electrophysiologic examination of the effects of propofol on the central nervous system has shown its involvement in the control of sympathetic and cardiovascular functions, we investigated the actions of propofol on rat hypothalamic paraventricular nucleus (PVN) neurons using the whole-cell mode of the patch-clamp technique in rat hypothalamic PVN slice preparations. Propofol induced Cl(-) currents at concentrations of 10(-5) and 10(-4) M, which were sensitive to picrotoxin and, to a lesser extent, to strychnine. Propofol (10(-6) M) enhanced gamma-aminobutyric acid(A) (GABA(A); 10(-6) M)-induced current synergistically. Moreover, propofol (10(-5) and 10(-4) M) significantly increased the decay time of evoked-inhibitory postsynaptic currents, which suggests a postsynaptic modulation of GABA(A) receptors. In addition, propofol (10(-5), 10(-4), and 2 x 10(-4) M) reversibly inhibited voltage-gated Ca(2+) currents. Taken together, these results suggest that propofol enhancement of GABA(A)-receptor mediated currents and inhibition of voltage-gated Ca(2+) currents at the central level, which is involved in the control of cardiovascular and sympathetic functions may be, at least in part, involved in general anesthetic-induced cardiovascular and sympathetic depression. ⋯ We investigated the actions of propofol on the rat hypothalamic paraventricular nucleus neurons, which are involved in the control of cardiovascular and sympathetic functions. The results suggest that propofol enhancement of gamma-aminobutyric acid(A)-receptor mediated currents and inhibition of voltage-gated Ca(2+) currents at the central level may be, at least in part, involved in general anesthetic-induced cardiovascular and sympathetic depression.
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Anesthesia and analgesia · Apr 2004
The effects of alfentanil on cytosolic Ca(2+) and contraction in rat ventricular myocytes.
Previous investigations of the effects of potent opioid analgesics on the heart have concentrated on effects on contraction magnitude and time course, but little is known about their effects on cytosolic Ca(2+) regulation in cardiac tissue. In this study, we sought to assess the effects of alfentanil on contractility and the cytosolic Ca(2+) transient in ventricular myocytes isolated from the rat ventricle by enzymatic dispersion. Cells were loaded with fura-2 and electrically stimulated at 1 Hz, and Ca(2+) transients and contractions were recorded optically at 30 degrees C. Alfentanil 10(-8) and 10(-7) M had no effect on the magnitude or time course of contraction or the cytosolic Ca(2+) transient. In contrast, 10(-6) M alfentanil induced a significant (P < 0.001) positive inotropic effect, increasing the mean (+/-SEM) unloaded shortening from 7.3 +/- 1.3 microm to 8.7 +/- 1.4 microm (an increase of 20%), with no change in the cytosolic Ca(2+) transient. Myofilament Ca(2+) sensitivity was significantly (P = 0.027) increased by 10(-6) M alfentanil but unaffected at 10(-7) M alfentanil. These data show that 10(-6) M alfentanil, a concentration close to the maximum clinical free plasma concentration, induced a positive inotropic effect due to sensitization of the myofilaments to Ca(2+) rather than to modified cytosolic Ca(2+) regulation. ⋯ Alfentanil, at concentrations achieved in clinical practice, increased contraction in ventricular cells by a mechanism involving an increase in the sensitivity of the contractile apparatus to Ca(2+).