Why the study?
Do intravenous perfusions of angiotensin, norepinephrine, and epinephrine differentially affect aortic elastic behavior in conscious dogs?
Do intravenous perfusions of angiotensin, norepinephrine, and epinephrine differentially affect aortic elastic behavior in conscious dogs?
Different vasoactive substances (epinephrine, norepinephrine, and angiotensin) exhibit distinct potencies for aortic smooth muscle activation, leading to varying degrees of aortic distension and stiffness at the same transmural pressure.
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Differential aortic responses to vasopressors in dogs should not guide human care; extends in vivo observations but remains hypothesis-generating.
The aortic elastic behavior has been studied in conscious dogs chronically instrumented with a pressure microtransducer and two ultrasonic crystals. Pressure and diameter measurements were analyzed in terms of their mean values and systolic-diastolic variations, enabling calculation of Peterson elastic modulus, and were displayed in the x-y form to obtain pressure diameter hysteresis loops. After recovery from surgery and under autonomic blockade, intravenous perfusions of angiotensin, norepinephrine, and epinephrine were made at incremental steps of doses until steady-state pressure-diameter changes were achieved. The slopes of the positive pressure-diameter correlations obtained at each dose of the same vasoactive substance were higher for angiotensin than norepinephrine (p less than 0.01) and epinephrine (p less than 0.001) and were higher for norepinephrine than epinephrine (p less than 0.05). Similarly, the slopes of the elastic modulus to mean pressure relation were significantly lower for angiotensin than for norepinephrine (p less than 0.05) and epinephrine (p less than 0.001) and were significantly lower for norepinephrine than epinephrine (p less than 0.001). Thus, at the same transmural pressure, the distension and stiffness of the aorta were lower and higher with epinephrine than with norepinephrine, respectively, and with norepinephrine than with angiotensin suggesting different potencies of these drugs in terms of smooth muscle activation in the aorta.
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Levenson et al. (1988) studied this question.
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