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Intravascular lumen area. *p < .05; **p < .01; mean ± SD. VR, vasoconstriction rate.

Mechanism of vasopressinergic vs adrenergic vasoconstriction. Vasopressin (V1) receptor activation by vasopressin produces short-term vasoconstriction that increases vascular resistance and mean arterial pressure (MAP). ¹⁴ V1 receptor agonists are effective in patients with severe hypotension and renin-angiotensin-aldosterone system (RAAS) blockade when conventional adrenergic treatment fails. ¹⁵

Effects of angiotensin-converting enzyme inhibitor (ACEIs) and angiotensin receptor blockers (ARBs) on vasoconstriction. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by ACEIs or ARBs inhibits hormonal regulation of blood pressure (BP), leaving only the vasopressinergic system fully functional during general anesthesia.

Hypothalamic thermoregulation. Temperature inputs to the hypothalamus are integrated and compared with threshold temperatures that trigger appropriate thermoregulatory responses. Normally these responses are initiated at as little as 0.1°C above and below normal body temperature of 37°C (98.6°F). Therefore the difference between temperatures that initiate sweating versus those initiating vasoconstriction is only 0.2°C. This is defined as the interthreshold range and represents the narrow range at which the body does not initiate thermoregulatory efforts. Most general anesthetics depress hypothalamic responses, widening this interthreshold range to as much as 4°C. Therefore patients are less able to adjust to temperature changes that occur during treatment.

Preparation for the study of rats. General anesthesia was induced and maintained by sevoflurane. Infiltration anesthesia of 0.2 mL of 2% lidocaine without epinephrine was injected in the left side, and 0.2 mL of 2% lidocaine with 1:80,000 epinephrine was injected in the right side. Twenty minutes after injection, fixation was performed by 4% paraformaldehyde via a left ventricle.

Planes of the sections made in this study. (a) Sagittal section. (b) Coronal section. (c) Horizontal section.

Measurement of the intravascular lumen area. Dark brown regions denote vascular smooth muscles. Values in red indicate intravascular lumen areas.

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.

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.