The effects of varying clinically relevant patterns of anaesthetic-vasoconstrictor combinations used for periradicular surgery on plasma concentrations of catecholamines and haemodynamic responses was studied in the canine model. Five mongrel dogs were anaesthetized with sodium pentobarbitol. A femoral cannula was inserted to measure central blood pressure and an ECG was used to monitor heart rate and any associated arrhythmias. Femoral venous blood samples were drawn before initial injection and at 3 and 10 min after injections. Plasma catecholamine concentrations were determined using high pressure liquid chromatography (HPLC). Injection protocols used three time periods, 30, 60 and 90 s, with solutions containing 1:100,000 and 1:50,000 adrenaline. No significant changes in heart rates or presence of arrhythmias were noted over the experimental protocol. Catecholamine levels in pico moles mL-1 were within the normal range at the 3-min sample level. At the 10-min sample time there was a more erratic range of concentrations, with most samples within the normal range. This may have been due to endogenous release of catecholamines in specific animals. The data identified trends in both the haemodynamic parameters and plasma catecholamine levels that can legitimately support the careful use of higher levels of a vasoconstrictor when patient profiles and surgical needs dictate.
The acute hemodynamic effects of 20 mg iv amlodipine were evaluated in a placebo-controlled study in 16 normotensive patients 15 +/- 1 days after an acute myocardial infarction by covariance analysis. Atenolol was given orally for at least 1 week before the study to maintain the heart rate between 50 and 60 beats/min. All patients were given two doses of 10 mg of amlodipine, or 10 ml of a placebo twice, in i.v. infusion lasting 2 minutes each. Hemodynamic data were collected during the control period and 15 minutes after each of the two amlodipine or placebo infusions. At the time of the last measurements, 15 minutes after the second amlodipine or placebo infusion, the plasma amlodipine level was 31 +/- 16 micrograms/l and the plasma atenolol level was 773 +/- 564 mu/l in the amlodipine group versus 795 +/- 916 micrograms/l in the placebo group. There were no chronotropic, dromotropic, or inotropic effects. The main hemodynamic effect was a fall in systemic vascular resistance (1548 +/- 591 dynes.sec.cm-5 to 1176 +/- 526 dynes.sec.cm-5, p = 0.045) with decreases in aortic pressure and in the left ventricular stroke work index. The left ventricular ejection fraction was 51 +/- 12% in the placebo group and 56 +/- 15% in the amlodipine group (ns) during the control period, and did not change after infusion of placebo or amlodipine. Left ventricular compliance seemed to be enhanced by amlodipine, because the end-diastolic left ventricular volume index rose from 82 +/- 11 ml/m2 to 87 +/- 11 ml/m2 (p = 0.026) 15 minutes after the beginning of the second infusion of 10 mg of amlodipine, without any change in end-diastolic left ventricular pressure. Intravenous infusion of 20 mg of amlodipine is well tolerated 15 days after acute myocardial infarction in normotensive patients without deeply depressed left ventricular systolic function and chronically treated with atenolol. The main hemodynamic effects observed are potentially useful for such patients.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.