(1) Changes in systolic and diastolic function occurred concomitantly as mild regional myocardial ischaemia developed and intensified; (2) afterloading significantly worsened regional systolic and diastolic dysfunction during mild ischaemia; and (3) progression of regional ischaemia resulted in loss of load dependent relaxation.
The cardiovascular responses associated with isovolemic hemodilution have been described. However, the stability of these responses over time remains controversial. We hypothesized that the hemodynamic responses to isovolemic hemodilution are stable over time. Nine fentanyl-midazolam-anesthetized dogs were monitored to follow global cardiovascular and regional myocardial function. Isovolemic hemodilution was performed to a moderate (hemoglobin = 7.5 g%) target hemodilutional state that was maintained for 4 h. Data were obtained at each hemodilutional state and each hour during the 4-h period of sustained moderate hemodilution. During acute hemodilution, cardiac output increased from 2.6 +/- 0.5 L/min to 3.0 +/- 0.5 L/min (P < 0.05) and mean coronary flow increased from 20.8 +/- 2.4 mL/min to 31.4 +/- 5.5 mL/min (P < 0.05). Cardiac output and mean coronary flow remained elevated during the extended hemodilutional period. In addition, norepinephrine increased from 586 +/- 152 pg/mL to 1135 +/- 247 pg/mL (P < 0.05) during acute isovolemic hemodilution and remained at this increased level during extended hemodilution. Epinephrine levels did not change with hemodilution. Compensatory mechanisms such as increases in cardiac output and mean coronary flow observed during acute hemodilution persist during extended periods of hemodilution.
We sought to determine the influence of nitrous oxide on the compromised heart during propofol anesthesia. This study investigated the cardiovascular effects of the combination propofol and nitrous oxide (N2O). Seven beagles were monitored to measure global and regional left ventricular function. Recordings both before and after critical constriction (CC) of the left anterior descending coronary artery (LAD) were performed after propofol, 300 micrograms.kg-1.min-1, and 10 min after exposure to and discontinuation of 67% N2O. Data were analyzed with ANOVA for repeated measures at 95% confidence level. In the absence of CC, N2O caused moderate, reversible hemodynamic depression (LVdP/dtmax, -13.8%; cardiac output, -17.2%; LAD coronary blood flow, -10.9%) and no regional dysfunction. After CC global hemodynamic depression was of similar magnitude (LVdP/dtmax, -19.9%; cardiac output, -9.2%; stroke volume, -9.2%) but did not recover completely. Systolic shortening in the compromised area decreased (-30.3%) and postsystolic shortening developed to represent 20.3% of total shortening. Despite only moderate hemodynamic depression, 67% N2O causes substantial regional dysfunction in compromised myocardium when added to propofol.
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