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The blockade effect of propranolol (Pro) on hemodynamic changes by drug interaction between adrenaline (AD) and chlorpromazine (Ch) on mean blood pressure (MBP) (a) and pulse rate (PR) (b) (Ch + saline: n = 4; Ch + Pro + AD: n = 3). AD induced modest hypertension, but did not significantly influence pulse rate change in Pro + Ch–pretreated rats. P values are for between-agent comparisons (vs the value for Ch + saline) at specified time intervals by using 2-way analysis of variance with Bonferroni's post hoc test. Data represent means ± SD.

A schematic depicting the experimental schedule. Propranolol (10 mg/kg) was injected intraperitoneally 15 minutes prior to the experiments. The systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were measured by placing the sphygmomanometer cuff around the tail of each rat. The baseline values were recorded as control values 5 minutes prior to the experiments. The SBP, DBP, and HR were also monitored immediately after the injection of normal saline, dexmedetomidine (DEX; 0.5, 5, or 50 μg/kg) alone, 100 μg/kg epinephrine alone, or 5 μg/kg DEX combined with 2% lidocaine and every 5 minutes thereafter for 30 minutes.

Cardiovascular effects of treatment with normal saline (NS; n = 10), dexmedetomidine (DEX; 0.5, 5, or 50 μg/kg; n = 10 for each experiment) alone, 100 μg/kg epinephrine (n = 10) alone, or 5 μg/kg DEX combined with 2% lidocaine (n = 10) on propranolol-treated hypertensive rats. White circles represent the NS group; black circles represent the 0.5 μg/kg DEX (0.5D) group; black triangles represent the 5 μg/kg DEX (5D) group; black squares represent the 50 μg/kg DEX (50D) group; black diamonds represent the 100 μg/kg epinephrine (Epi) group; white squares represent the 5 μg/kg DEX combined with 2% lidocaine (5DL) group.

Electrocardiogram with normal sinus rhythm.

Transthoracic echocardiogram results. Normal left ventricular size and function, mild hypokinesis in basal segments. Ejection fraction 55–60%, normal right ventricular size and function, no hemodynamically significant valvular abnormalities.

Epinephrine‐beta blocker interaction. In this illustration the following cardiovascular changes follow the administration of epinephrine in a dosage of 10 µg/min. (A) First, it is essential to understand the precise cardiovascular influences of epinephrine in a normal (control) patient. The cardiotonic effects of epinephrine are most familiar. It activates beta‐1 receptors on the sinoatrial node to increase heart rate (HR) and also activates beta‐1 receptors on myocardial cells increasing their force of contraction. This provides an increase in systolic blood pressure (SBP). In addition to its cardiotonic effects, epinephrine has the ability to activate both alpha and beta‐2 receptors on blood vessels producing constriction or dilation, respectively. Epinephrine is commonly viewed only as a vasoconstrictor by many clinicians because this is the effect it produces when injected subcutaneously or submucosally. This is because the tiny vessels found in these locations contain only alpha receptors and are constricted by epinephrine. In contrast, larger systemic arteries that determine vascular resistance and diastolic blood pressure contain both alpha and beta‐2 receptors, with the latter most prevalent. Following absorption, low doses of epinephrine found in local anesthetic formulations (eg, 20–100 µg) preferentially activate beta‐2 receptors which dilate the arteries, and diastolic blood pressure (DBP) actually declines. (B) In the presence of a nonselective beta blocker (eg, propranolol) the cardiovascular influences of epinephrine are strikingly different. This is primarily due to the blockade of beta‐2 receptors on systemic arteries. Epinephrine will now activate the remaining alpha receptors leading to vasoconstriction and an increase in diastolic blood pressure. To meet this increase in resistance, intrinsic mechanisms within myocardial cells respond with greater force and elevate systolic blood pressure as well. Together this will increase mean arterial pressure (MAP). The sudden elevation in MAP is sensed by baroreceptors within the carotid sinuses triggering a reflex slowing in heart rate, which is further accentuated by the fact that the beta‐1 receptors in the sinoatrial node are blocked.