The sympathomimetic substance oxedrine (Sympatol) influences, by means of its affinity to alpha- and beta-receptors, cardiac performance and peripheral vascular tone. We studied in 12 healthy male volunteers the influence of intravenous oxedrine on left ventricular contractility parameters as estimated by TM-echocardiography, on cardiac index as well as on arterial blood pressure and peripheral vascular resistance. Under continuous intravenous infusion of 4 mg/min oxedrine the systolic and mean arterial blood pressure increased significantly (p less than 0.005) while the diastolic pressure and heart rate remained unchanged. The cardiac index increased (p less than 0.001) and the peripheral vascular resistance decreased significantly (p less than 0.01). The echocardiographically determined left ventricular contractility parameters, i.e. systolic shortening fraction (SF) as well as maximal velocity of shortening of the left ventricular diameter (VCFmin) also increased significantly (p less than 0.001 and 0.005, resp.). An increase in left ventricular contractility and cardiac index with concomitant decrease of peripheral vascular resistance and without increase in heart rate implies an economical increase in cardiac performance under intravenous infusion of oxedrine.
"Alpha and beta-adrenergic drugs have well-documented effects on the cardiovascular system, indicating synephrine would have similar hemodynamic effects . Similar to our findings, Hofstetter and colleagues  reported that synephrine intake in healthy subjects caused significant elevations in systolic and mean arterial pressures, while diastolic BP and heart rate were unchanged. "
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study was to examine the acute metabolic effects of a high-energy drink in healthy, physically-active women.
Ten women (20.4 +/- 0.70 y; 166.9 +/- 7.2 cm; 67.0 +/- 7.0 kg; 29.6 +/- 6.5% body fat) underwent two testing sessions administered in a randomized and double-blind fashion. Subjects reported to the laboratory in a 3-hr post-absorptive state and were provided either 140 ml of the high-energy drink (SUP; commercially marketed as Meltdown RTD) or placebo (P). Subjects consumed two 70 ml doses of SUP or P, separated by 30 min and rested in a semi-recumbent position for 3 hours. Resting oxygen consumption (VO2) and heart rate (HR) were determined every 5 min during the first 30 min and every 10 min during the next 150 min. Blood pressure (BP) was determined every 15 min during the first 30 min and every 30 min thereafter. Area under the curve (AUC) analysis was computed for VO2, whereas a 3-hour average and hourly averages were calculated for respiratory quotient (RQ), total kcal, HR, BP, and profile of mood states (POMS).
AUC analysis revealed a 10.8% difference (p = 0.03) in VO2 between SUP and P. No difference in VO2 was seen between the groups in the first hour, but VO2 in SUP was significantly greater than P in the second (13.9%, p = 0.01) and third hours (11.9%, p = 0.03). A difference (p = 0.03) in energy expenditure was seen between SUP (1.09 +/- 0.10 kcal x min-1) and P (0.99 +/- 0.09 kcal x min-1) for the 3-hour period. Although no difference in energy expenditure was seen in the first hour, significant differences between SUP and P were observed in the second (1.10 +/- 0.11 kcal x min-1 and 0.99 +/- 0.09 kcal x min-1, respectively; p = 0.02) and third hour (1.08 +/- 0.11 kcal x min-1 and 0.99 +/- 0.09 kcal x min-1, respectively; p = 0.05). Average systolic BP was significantly higher (p = 0.007) for SUP (110.0 +/- 3.9 mmHg) compared to P (107.3 +/- 4.4 mmHg). No differences were seen in HR, diastolic BP, or POMS at any time point.
Results showed a significant increase in energy expenditure in young, healthy women following an acute ingestion of a high-energy drink.
Lipids in Health and Disease 12/2009; 8(1):57. DOI:10.1186/1476-511X-8-57 · 2.22 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study was to investigate the effects of Fructus Aurantii (the unripe fruits of Citrus aurantium L.) on portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague-Dawley rats. Sham-operated (Sham) rats served as controls. Hemodynamic and in vitro contractile studies were performed at 14 days after surgery. Both the aqueous extract of Fructus Aurantii and synephrine, one of its purified principles with pressor activity, were infused into the conscious PVL and Sham rats via a syringe pump. Fructus Aurantii (1.25, 2.5, & 5.0 mg/kg/min) dose-dependently reduced portal pressure in PVL and Sham rats, with the percentage change in portal pressure more pronounced in PVL rats. Mean arterial pressure was dose-dependently elevated by Fructus Aurantii. Synephrine (0.095, 0.19, & 0.38 mg/kg/min) also dose-dependently reduced portal pressure and elevated mean arterial pressure in PVL and Sham rats. Fructus Aurantii (2.8-280 micrograms/ml) induced dose-dependent contractile responses mainly in aorta and mesenteric artery, but little response in portal vein. The results showed that Fructus Aurantii infusion reduced portal pressure, possibly by way of arterial vasoconstriction.
Life Sciences 10/1995; 57(22):2011-20. DOI:10.1016/0024-3205(95)02195-O · 2.70 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We studied the effects of p-synephrine on the immobility behaviors and on the spontaneous motor activity in mice. p-Synephrine at oral doses from 1 to 10 mg/kg significantly decreased the duration of immobility in the tail suspension test and the forced swimming test in mice. At 30 mg/kg, the duration of immobility was returned to control values in both tests. Subcutaneous administration of prazosin hydrochloride (62.5 micrograms/kg), an alpha 1 adrenoceptor antagonist, blocked the p-synephrine (3 mg/kg)-induced decrease in immobility in the tail suspension test. p-Synephrine did not change the spontaneous motor activity at oral doses from 0.3 to 10 mg/kg. These results suggest that p-synephrine elicits an antidepressant-like activity in mouse models of immobility tests, through the stimulation of alpha 1 adrenoceptors.
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