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Incidence of maxillary central incisor pulpal anesthesia as determined by lack of response to electrical pulp testing at the maximum setting (percentage of 80 readings), at each postinjection time interval, for the 2 anesthetic formulations. There were no significant differences (P < .05) between the solutions.

Incidence of maxillary first molar pulpal anesthesia as determined by lack of response to electrical pulp testing at the maximum setting (percentage of 80 readings), at each postinjection time interval, for the 2 anesthetic formulations. There were no significant differences (P < .05) between the solutions.

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.