The vasodilating effect of a Hintonia latiflora extract with antidiabetic action.

In the present study, it is shown for the first time that an extract of Hintonia latiflora (HLE) which is used as an antidiabetic herbal medicine, is not only able to decrease blood glucose concentration but additionally exerts a vasodilating effect. Accordingly, this extract might have a positive influence on diabetes-associated dysfunction of blood vessels. The vasodilating effect was demonstrated in vitro in aortic rings of guinea pigs as well as in vivo in rabbits. Aortic rings pre-contracted with noradrenaline (NA) could completely be relaxed by HLE (EC50: 51.98 mg/l). In contrast, potassium-induced contractions were not diminished by HLE. Therefore, it can be suggested that the vasodilating effect of HLE is primarily the result of an inhibition of G protein-induced increase in intracellular calcium and not of a blockade of voltage-operated L-type calcium channels. The neoflavonoid coutareagenin (COU), a constituent of HLE which in part is responsible for the blood glucose-lowering effect of HLE, also relaxed NA-induced contractions of aortic rings (EC50: 32.55 mg/l) and only weakly inhibited potassium-induced contractions. Experiments in aortic rat cells revealed that calcium transients evoked by vasopressin were suppressed by 60 mg/l COU supporting the idea of an inhibition of G protein-induced intracellular calcium release by a constituent of HLE. To study the effect of HLE on vascular tone under in vivo conditions, ultrasound measurements were carried out in conscious rabbits which received a single oral dose of HLE. Under the influence of HLE, a vasodilation combined with a lowering of blood flow velocity could be observed in the abdominal aorta and the common carotid artery. Additionally, a decrease in blood glucose concentration in the HLE group occurred. The combination of a blood glucose-lowering with a vasodilating effect may be helpful for reducing angiopathies, typical long-term complications in patients with diabetes mellitus.

Effects of ketamine-xylazine intravenous bolus injection on cardiovascular function in rabbits.

The direct effects of ketamine-xylazine (KET-XYL) on vascular function have not been investigated in rabbits. The short-term cardiovascular effects of intravenous (IV) KET-XYL bolus injection, therefore, should be investigated using vascular ultrasonography.In this prospective experimental study, KET-XYL anesthesia was induced IV in 9 female New Zealand White rabbits before 3 defined test bolus injections of KET-XYL were given IV. Before and for 10 min after each KET-XYL injection vascular and hemodynamic variables were recorded at the left common carotid artery (ACC) after the 1st injection, and at the abdominal aorta (AA) after the 2nd injection. Echocardiography was performed after the 3rd injection to investigate changes in cardiac parameters.Ketamine-xylazine IV caused a significant increase in vessel diameter at the ACC and AA. Average volumetric flow significantly decreased at the ACC and pulsatility index significantly decreased at the AA. Fractional shortening (FS) and heart rate significantly decreased, while mean arterial blood pressure initially increased.Bolus injections of KET-XYL IV produced a transient vasodilatation at the ACC and AA. Despite central vasodilatation, bradycardia, and decrease of FS and average volumetric flow (VFave), mean arterial blood pressure did not significantly decrease indicating well-preserved cardiovascular compensatory mechanism after the ratio and doses of KET-XYL IV bolus injections used in this study.

Effects of medetomidine-midazolam-fentanyl IV bolus injections and its reversal by specific antagonists on cardiovascular function in rabbits.

The objective of this study was to investigate the short-term cardiovascular effects of intravenous (IV) medetomidine-midazolam-fentanyl (MMF) injections in the rabbit using vascular ultrasonography and echocardiography.Anesthesia with MMF was induced intramuscularly (IM) in 8 female New Zealand White rabbits before 3 defined bolus injections of MMF were given IV. Before and for 10 min after each MMF injection the following vascular variables [at the left common carotid artery (ACC) after the first injection and at the abdominal aorta (AA) after the second injection]: vessel diameter (D), peak systolic, minimum diastolic, end-diastolic and average blood flow velocities (psBFV, mdBFV, edBFV, Vave), average volumetric flow (VFave), resistance index (RI) and pulsatility index (PI) and other clinical variables: mean arterial pressure (MAP), heart rate (HR), peripheral arterial oxygen saturation and end-tidal CO2 were recorded. Echocardiography was used after the third injection to investigate changes in cardiac parameters. Additionally, hemodynamic effects were observed at the ACC after complete subcutaneous antagonism of anesthesia by atipamezole-flumazenil-naloxone (AFN) until recovery of the animals.Medetomidine-midazolam-fentanyl IV caused a significant decrease of blood flow velocity in both investigated vessels which was associated with a significant decrease of HR and cardiac performance indicated by the decrease of FS and average volumetric blood flow. Mean arterial pressure significantly increased after each MMF injection; whereas, it significantly decreased after AFN injection. Therefore, MMF and AFN should be carefully used in rabbits and may not be suitable in patients with ventricular dysfunction.

Effects of propofol on ultrasonic indicators of haemodynamic function in rabbits.

OBJECTIVE: To evaluate the cardiovascular effects of intravenous propofol in rabbits. STUDY DESIGN: Randomized, prospective, experimental study. ANIMALS: Thirty-one female New Zealand White rabbits. METHODS: Rabbits were allocated to one of two groups [propofol (P) or conscious (C)]. In C (n = 16) vascular dimensions were measured using ultrasound of the left common carotid artery (ACC) and the abdominal aorta (AA). Group P (n = 15) received propofol 4.0-8.0 mg kg(-1) intravenously (IV). Anaesthesia was maintained with propofol at 1.2-1.3 mg kg(-1) minute(-1). Subsequently, three propofol injections (8 mg kg(-1)) were given. Before and for 10 minutes after each injection the following vascular and haemodynamic variables were recorded (a) at the ACC after the first injection; and (b) at the AA after the second injection: vessel diameter [D, (mm)], peak systolic, minimum diastolic, end-diastolic and average blood flow velocities [psBFV, mdBFV, edBFV, Vave (cm second(-1))], average volumetric flow [VFave (mL s(-1))], resistance index (RI) and pulsatility index (PI) mean arterial pressure (MAP), heart rate (HR), arterial oxygen saturation (SpO(2)) and end-tidal CO(2) (Pe'CO(2)). Echocardiography was performed after the third propofol bolus injection to investigate changes in cardiac parameters [fractional shortening, FS (%)]. RESULTS: Intravenous propofol injections caused a significant decrease in vessel diameter, volumetric flow and edBFV, and significant increases in psBFV, RI and PI. Baseline levels for vessel diameter and psBFV were restored 6-8 minutes after injection. Propofol injection decreased FS significantly by 7 minutes after injection while MAP and HR were significantly reduced for 4 minutes. CONCLUSION AND CLINICAL RELEVANCE: Injections of propofol (8 mg kg(-1)) produced an immediate, transient decrease in vascular diameters, a significant decrease in ventricular performance and an increase in peripheral vascular resistance (ACC and AA). Propofol should probably not be or only carefully used in rabbits with ventricular dysfunction.