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Biomedical subjects

T M Skeehan

Publications and source records attributed to T M Skeehan.

13 recordsLinked to original sources
PubMed1995

Comparison of the alteration of cardiac function by sevoflurane, isoflurane, and halothane in the isolated working rat heart.

OBJECTIVES: Despite its widespread use, little is known about sevoflurane's physiologic effects. The direct myocardial effects of sevoflurane were compared with both halothane and isoflurane. DESIGN: Administration of minimum alveolar concentration (MAC) fractions of anesthetic (0 to 3.0) was systematically varied to decrease the possibility of time-related effects on measured parameters. SETTING: Isolated rat hearts were perfused using a working heart model where the parameters affecting myocardial work were carefully controlled and monitored. PARTICIPANTS: To avoid confounding effects of prior anesthetic administration, hearts were removed from rats, after decapitation, in the absence of anesthetic. INTERVENTIONS: In the first series, isolated perfused rat hearts were exposed to one of the three anesthetics in doses of 0 to 1.5 times MAC. In the second series, hearts were exposed to either sevoflurane or isoflurane in doses of 0 to 3.0 times MAC. The following variables were measured: the rate of change of left ventricular pressure; aortic flow rate; cardiac output; left ventricular end-diastolic pressure; the time constant of isovolumetric relaxation; and coronary vascular resistance. Oxygen consumption was measured during the first series. MEASUREMENTS AND MAIN RESULTS: In the first series, all systolic variables were reduced in the presence of halothane when compared with either isoflurane or sevoflurane. Halothane affected diastolic function to a greater degree than either sevoflurane or isoflurane, as measured by the rate of relaxation and end-diastolic pressure. In the second series, at a dose of 3.0 times MAC, both sevoflurane and isoflurane decreased systolic and diastolic function, with a greater reduction in cardiac output, and peak aortic flow and higher left ventricular end-diastolic pressures observed with isoflurane. Coronary resistance and oxygen consumption were not affected by any of the anesthetics. CONCLUSIONS: These data suggest that sevoflurane depresses cardiac function less than either halothane in doses of 1.0 and 1.5 x MAC or isoflurane at doses of 3 x MAC.

Anesthetics, Inhalation↗
PubMed1992

Transvalvular left ventricular pressure measurement in the isolated working rat heart.

A method of continuously measuring left ventricular (LV) pressure in an isolated buffer-perfused working rat heart is described. Transvalvular placement of a micromanometer through the aorta is the unique feature of this procedure. Advantages include catheter stability and lack of myocardial trauma. Changes in cardiac function were quantified by exposing hearts to either isoproterenol (10(-9) M) or halothane (1.5% vol/vol). To examine if any obstruction to LV outflow was caused by the micromanometer, cardiac performance was assessed during pullback from the ventricle to the aorta. Complications such as aortic insufficiency and ventricular arrhythmias were also studied. The results indicate that the transvalvular placement of a micromanometer can provide continuous, high-fidelity reproduction of LV pressure in this small-organ preparation. The presence of the micromanometer did not significantly alter cardiac performance, and proper catheter placement was achieved easily in a high percentage (> 90%) of cases.

Animals↗
PubMed1991

Erroneous mass spectrometer data caused by a faulty patient sampling tube: case report and laboratory study.

We report an error due to faulty sampling of gas for mass spectrometry by side-stream analysis that occurred during a general anesthetic for a surgical procedure. Two defects in the patient sampling tube were present. First, a crack was discovered in the polyvinylchloride tubing at the connection to the patient circuit. Second, secretions had accumulated in the end of the tubing that caused a partial obstruction to gas sampling. This combination promoted the contamination of respiratory gases sampled from the anesthesia circuit with entrained room air. This entrainment, however, occurred only during exhalation while ventilation was being controlled with a descending (during exhalation) bellows. The particular sampling error was reproduced and characterized in a mock circuit to simulate the sampling tube defects. It was determined that both a leak and a partial obstruction were necessary conditions for the sampling error to exist.

Anesthesia, Inhalation↗
PubMed1991

Hemodynamic effects of muscle relaxant drugs during anesthetic induction in patients with mitral or aortic valvular heart disease.

The hemodynamic effects of three nondepolarizing skeletal muscle relaxant drug regimens were compared during the induction of general anesthesia in 64 patients with valvular heart disease using a double-blind protocol. Patients were first stratified according to primary valvular defect (aortic stenosis, aortic regurgitation, mitral stenosis, or mitral regurgitation). Next, patients were randomly allocated to a drug group, either group A (atracurium), group V (vecuronium), or group MP (metocurine plus pancuronium). Data were collected during three periods: awake, postanesthetic induction, and posttracheal intubation. Four cardiovascular variables were designated a priori as primary variables of interest. These were heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), and systemic vascular resistance index (SVRI). Patients with mitral stenosis showed two significant hemodynamic differences among muscle relaxant drug groups: (1) CI increased in group A but decreased in group MP between the awake and postinduction measurements (P = 0.032); and (2) SVRI decreased in group A but increased in group MP between the awake and postintubation periods (P = 0.034). In contrast, patients with aortic stenosis, aortic regurgitation, or mitral regurgitation demonstrated no statistically significant difference in cardiovascular responses among drug groups. Further analysis was performed using the following data: (1) other hemodynamic variables; (2) incidence of deviations from cardiovascular stability; and (3) the frequency of cardiovascular drug use. This examination showed no important differences among the muscle relaxant drug groups. The small but significant hemodynamic changes observed in mitral stenosis patients in drug groups A and MP were not noted with vecuronium.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed1990

Vascular responses to dopamine and dobutamine in the awake calf during constant aortic flow or constant aortic pressure.

We investigated vascular effects of dopamine and dobutamine infusions in awake calves implanted with the Penn State total artificial heart (TAH). This preparation uniquely permits independent servo-control of cardiac output (CO) and arterial blood pressure (BP). Thirty-two studies (22 with dopamine and 10 with dobutamine) were performed in four juvenile calves from 1 to 4 months after TAH implantation. Studies were performed in one of two TAH operating conditions: (a) constant aortic flow, in which the CO is fixed and aortic BP varies with systemic vascular resistance (SVR), or (b) constant pressure, in which the CO varies to maintain a constant BP when SVR changes. During both constant flow and constant pressure studies, dopamine caused a dose-dependent increase and dobutamine caused a dose-dependent decrease in SVR. There was no difference in the SVR response between constant flow or constant pressure conditions at any dose of dopamine or dobutamine (p greater than 0.05). The infusion doses of dopamine required to raise the SVR 20 and 50% during constant flow studies were 7.2 and 12.4 micrograms.kg-1.min-1, respectively. In constant pressure studies, these doses were 7.7 and 13.5 micrograms.kg-1.min-1. The infusion dose of dobutamine resulting in a 20% reduction in SVR was 27.2 micrograms.kg-1.min-1 in constant flow studies 26.2 micrograms.kg-1.min-1 in constant pressure studies. These data suggest that baroreflex and other indirect mechanisms are less important than direct vascular drug effects in this system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Direct effects of myocardial depressant drugs on coronary vascular tone: anesthetic vasodilation by halothane and isoflurane.

Because certain vasoactive drugs also possess negative myocardial inotropic properties, it is difficult to determine their direct pharmacological actions on coronary resistance vessels in situ. Thus, a drug's myocardial effects may induce indirect physiological changes in coronary vascular tone that confound measuring its direct action. To separate the direct from indirect drug actions on vascular tone, the authors describe an experimental system utilizing the isolated perfused rat heart arrested with tetrodotoxin. The direct effects of the volatile anesthetics halothane and isoflurane on coronary vascular tone were examined in this preparation, using the concept of minimum alveolar concentration as the measure of potency. Both anesthetics demonstrated a dose-dependent direct coronary vasodilation that was reversible, with the median effective dose being 1.31 +/- 0.08 (mean +/- S.E.) for halothane, and 1.53 +/- 0.12 for isoflurane (P = 0.06; units of measure are the fraction of minimum alveolar concentration for each anesthetic). Further studies indicated that maximal vasodilation by adenosine was diminished after 90 min of perfusion, independent of anesthetic administration. Myocardial oxygen consumption was decreased significantly from the beating state by arrest, but neither anesthetic nor adenosine affected myocardial oxygen consumption further. These data indicate that halothane and isoflurane are equipotent for inducing direct dilation of coronary resistance vessels in the isolated perfused arrested rat heart.

Adenosine↗
PubMed1989

Halothane induces depressor responses to noxious stimuli in the rat.

The effect of halothane on hemodynamic responses to noxious stimuli was investigated in anesthetized male Sprague-Dawley rats. It was found that increasing the end-tidal halothane concentration from sub-MAC to supra-MAC levels was frequently associated with a reversal of the mean arterial pressure response to a noxious stimulus from a pressor response to depressor response. The depressor responses could be produced by noxious stimuli at several sites but were of greatest frequency (100%) and magnitude (up to -80 mmHg) after clamp application at the base of the tail. The depressor responses were often, but not always, accompanied by decreases in heart rate. The correlation coefficient between the changes in heart rate and the changes in mean arterial pressure caused by noxious stimuli was +0.61 (n = 9). The authors further characterized the depressor responses in an additional 18 rats. The depressor responses were not influenced by vagotomy or muscarinic cholinergic blockade and were associated with concurrent decreases in both cardiac output and systemic vascular resistance. The hemodynamic changes associated with the depressor responses were consistent with a centrally mediated withdrawal of sympathetic tone. Knowledge of this effect of halothane on the arterial blood pressure and heart rate responses to noxious stimuli may be important for correctly interpreting animal responses to noxious stimuli in the presence of general anesthetic agents, particularly because animals are frequently used to characterize both the potency and the hemodynamic effects of anesthetic agents. The presence of depressor responses also indicates that mean arterial pressure responses to noxious stimuli cannot be used as a linear index of anesthetic depth in rats anesthetized with halothane.

Anesthesia, General↗
PubMed1988

Mass spectrometry for monitoring respiratory and anesthetic gas waveforms in rats.

A method is presented for real-time monitoring of airway gas concentration waveforms in rats and other small animals. Gas is drawn from the tracheal tube, analyzed by a mass spectrometer, and presented as concentration vs. time waveforms simultaneously for CO2, halothane, and other respiratory gases and anesthetics. By use of a respiratory simulation device, the accuracy of mass spectrometric end-tidal CO2 analysis was compared with both the actual gas composition and infrared spectrophotometry. The effects of various ventilator rates and inspiration-to-expiration ratios on sampling accuracy were also examined. The technique was validated in male Sprague-Dawley rats being ventilated mechanically. The difference between the arterial PCO2 (PaCO2) and the end-tidal PCO2 (PETCO2) was not significantly different from zero, and the correlation between PETCO2 and PaCO2 was strong (r = 0.97, P less than 0.0001). Continuous gas sampling for periods up to 5 min did not affect PaCO2, PETCO2, or airway pressures. By use of this new method for measuring end-tidal halothane concentrations in rats approximately 6.5 mo of age, the minimum alveolar concentration of halothane that prevented reflex movement in response to tail clamping was 0.97 +/- 0.04% atmospheric (n = 14). This mass spectrometric technique can be used in small laboratory animals, such as rats, weighing as little as 250 g. Gas monitoring did not distort either PETCO2 or PaCO2. Under the defined conditions of this study, accurate and simultaneous measurements of phasic respiratory concentrations of anesthetic and respiratory gases can be achieved.

Anesthetics↗