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Cardiovascular Alterations After Injection of 2% Lidocaine With Norepinephrine 1:50,000 (Xylestesin) in Rats
Fatima Neves Faraco PhD,
 Paschoal Laercio Armonia PhD, and
 Stanley F. Malamed PhD
Article Category: Research Article
Volume/Issue: Volume 54: Issue 2
Online Publication Date: Jan 01, 2007
DOI: 10.2344/0003-3006(2007)54[45:CAAIOL]2.0.CO;2
Page Range: 45 – 49

, since each peak represents a cardiac cycle in a previously determined time interval. After the animal was adequately prepared and the Dynograph was calibrated, the equipment was set to record systolic, diastolic, and mean arterial pressures, as well as heart rate. A period of 15 minutes was used to stabilize the experiment (control period). We then administered the test drug intravenously, through the trocar into the surgically exposed jugular vein, in dosages of 0.51 mg/kg lidocaine hydrochloride and 0.51 μg/kg norepinephrine hydrochloride. These doses were

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Figure 1.; Averages for the systolic arterial pressure in mm Hg, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated to norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.
Fatima Neves Faraco,
 Paschoal Laercio Armonia, and
 Stanley F. Malamed
Figure 1.
Figure 1.

Averages for the systolic arterial pressure in mm Hg, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated to norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.

Figure 2.; Averages of the diastolic arterial pressure in mm Hg, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated with norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.
Fatima Neves Faraco,
 Paschoal Laercio Armonia, and
 Stanley F. Malamed
Figure 2.
Figure 2.

Averages of the diastolic arterial pressure in mm Hg, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated with norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.

Figure 3.; Averages of the mean arterial pressure measured in mm Hg, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated with norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.
Fatima Neves Faraco,
 Paschoal Laercio Armonia, and
 Stanley F. Malamed
Figure 3.
Figure 3.

Averages of the mean arterial pressure measured in mm Hg, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated with norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.

Figure 4.; Averages of the mean arterial pressure calculated in mm Hg, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated with norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.
Fatima Neves Faraco,
 Paschoal Laercio Armonia, and
 Stanley F. Malamed
Figure 4.
Figure 4.

Averages of the mean arterial pressure calculated in mm Hg, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated with norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.

Figure 5.; Averages of heart rate, in cycles per minute, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated with norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.
Fatima Neves Faraco,
 Paschoal Laercio Armonia, and
 Stanley F. Malamed
Figure 5.
Figure 5.

Averages of heart rate, in cycles per minute, after intravenous administration of 2% lidocaine hydrochloride (20 mg/mL) associated with norepinephrine hydrochloride (20 μg/mL)—Xylestesin 2%, in a dose proportional to 1.8 mL.

Figure 2.  ; Vasoconstrictor interaction with tricyclic antidepressants and serotonin-norepinephrine reuptake inhibitors.
Mana Saraghi,
 Leonard R. Golden, and
 Elliot V. Hersh
<bold>Figure 2. </bold>
Figure 2. 

Vasoconstrictor interaction with tricyclic antidepressants and serotonin-norepinephrine reuptake inhibitors.

; Figure 3. The adrenergic synapse. The nerve impulse releases norepinephrine (NE), which binds to specific adrenergic receptors on the cell membranes of target tissue. (α1, β1, β2). The neuronal endings contain α2 prejunctional receptors. When activated by NE, further release of the neurotransmitter is inhibited. Adrenergic ligands also arrive at the synapse via the circulatory system. These include epinephrine (E) and norepinephrine (NE) secreted by the adrenal medulla or adrenergic drugs (D). The termination of norepinephrine (NE) is due primarily to reuptake into the nerve ending. Epinephrine (E) from the adrenal medulla and adrenergic drugs (D) are metabolized by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) in local tissues or the liver following absorption. (See text for further explanation.)
Daniel E. Becker

Figure 3. The adrenergic synapse. The nerve impulse releases norepinephrine (NE), which binds to specific adrenergic receptors on the cell membranes of target tissue. (α1, β1, β2). The neuronal endings contain α2 prejunctional receptors. When activated by NE, further release of the neurotransmitter is inhibited. Adrenergic ligands also arrive at the synapse via the circulatory system. These include epinephrine (E) and norepinephrine (NE) secreted by the adrenal medulla or adrenergic drugs (D). The termination of norepinephrine (NE) is due primarily to reuptake into the nerve ending. Epinephrine (E) from the adrenal medulla and adrenergic drugs (D) are metabolized by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) in local tissues or the liver following absorption. (See text for further explanation.)

Figure 10.; Cardiovascular influences of norepinephrine (and levonordefrin) versus epinephrine.18 A. Both drugs stimulate Beta1 receptors on cardiac muscle, which increase myocardial contractility. This results in an increase in systolic pressure. B. Both drugs stimulate alpha receptors on vessels, which causes them to constrict. Submucosal vessels contain only alpha receptors, so both drugs produce local vasoconstriction when injected submucosally. But submucosal vessels are not illustrated here; they do not influence diastolic pressure. Systemic arteries influence diastolic pressure and contain Beta2 receptors, which vasodilate and are far more numerous than alpha receptors. Norepinephrine has no affinity for Beta2 receptors and constricts systemic arteries by activating the alpha receptors, even though they are less numerous. This increases diastolic pressure. Epinephrine, which has Beta2 as well as alpha receptor activity, produces vasodilation and a reduction in diastolic pressure. C. Both drugs stimulate Beta1 receptors on the Sino-atrial node, which increases heart rate. But this potential effect from norepinephrine is overridden by a reflex explained as follows. Notice that epinephrine has no influence on mean arterial pressure; systolic pressure increases but diastolic decreases and negates any effect on mean arterial pressure. Norepinephrine increases systolic, diastolic, and mean arterial pressures. The increase in mean arterial pressure stimulates baroreceptors in the carotid sinus, which trigger a vagal slowing of heart rate.
Daniel E. Becker and
 Kenneth L. Reed
Figure 10.
Figure 10.

Cardiovascular influences of norepinephrine (and levonordefrin) versus epinephrine.18 A. Both drugs stimulate Beta1 receptors on cardiac muscle, which increase myocardial contractility. This results in an increase in systolic pressure. B. Both drugs stimulate alpha receptors on vessels, which causes them to constrict. Submucosal vessels contain only alpha receptors, so both drugs produce local vasoconstriction when injected submucosally. But submucosal vessels are not illustrated here; they do not influence diastolic pressure. Systemic arteries influence diastolic pressure and contain Beta2 receptors, which vasodilate and are far more numerous than alpha receptors. Norepinephrine has no affinity for Beta2 receptors and constricts systemic arteries by activating the alpha receptors, even though they are less numerous. This increases diastolic pressure. Epinephrine, which has Beta2 as well as alpha receptor activity, produces vasodilation and a reduction in diastolic pressure. C. Both drugs stimulate Beta1 receptors on the Sino-atrial node, which increases heart rate. But this potential effect from norepinephrine is overridden by a reflex explained as follows. Notice that epinephrine has no influence on mean arterial pressure; systolic pressure increases but diastolic decreases and negates any effect on mean arterial pressure. Norepinephrine increases systolic, diastolic, and mean arterial pressures. The increase in mean arterial pressure stimulates baroreceptors in the carotid sinus, which trigger a vagal slowing of heart rate.

; Figure 1. Origin and distribution of somatic and autonomic nerves.1,2 Somatic (voluntary) neurons exit all levels of the brain and spinal cord (CNS). They release acetylcholine (ACh) to activate nicotinic receptors (Nm) on skeletal muscle. Preganglionic parasympathetic neurons exit the brain and sacral spinal cord, where they synapse with ganglia near or within smooth muscle and heart. Here ACh is released and activates nicotinic receptors (Nn) on postganglionic neurons. These neurons also release ACh to activate muscarinic receptors (M) on the target tissues. Preganglionic sympathetic neurons exit the thoracic and lumbar levels (thoracolumbar) of the spinal cord and synapse with ganglia near the cord and, like the preganglionic parasympathetic fibers, release ACh to activate Nn receptors on postganglionic neurons. The most abundant of these distribute to smooth muscle and heart where they release norepinephrine (NE) to activate alpha and beta receptors (α, β). The adrenal medulla is functionally a postganglionic neuron that secrets mostly epinephrine (∼80% epinephrine and 20% norepinephrine), which arrives at the target tissues via the circulation. Also noteworthy is that some postganglionic sympathetic fibers distribute to sweat glands and release ACh where it activates muscarinic receptors (M).
Daniel E. Becker

Figure 1. Origin and distribution of somatic and autonomic nerves. 1,2 Somatic (voluntary) neurons exit all levels of the brain and spinal cord (CNS). They release acetylcholine (ACh) to activate nicotinic receptors (Nm) on skeletal muscle. Preganglionic parasympathetic neurons exit the brain and sacral spinal cord, where they synapse with ganglia near or within smooth muscle and heart. Here ACh is released and activates nicotinic receptors (Nn) on postganglionic neurons. These neurons also release ACh to activate muscarinic receptors (M) on the target tissues. Preganglionic sympathetic neurons exit the thoracic and lumbar levels (thoracolumbar) of the spinal cord and synapse with ganglia near the cord and, like the preganglionic parasympathetic fibers, release ACh to activate Nn receptors on postganglionic neurons. The most abundant of these distribute to smooth muscle and heart where they release norepinephrine (NE) to activate alpha and beta receptors (α, β). The adrenal medulla is functionally a postganglionic neuron that secrets mostly epinephrine (∼80% epinephrine and 20% norepinephrine), which arrives at the target tissues via the circulation. Also noteworthy is that some postganglionic sympathetic fibers distribute to sweat glands and release ACh where it activates muscarinic receptors (M).