We thank Dr. Prys-Roberts for his interest in our work. We carefully reviewed his 1971 article but found no data concerning the postoperative course of hypertensive patients (see table 5 in the article by Prys-Roberts et al.1
). Our article 2
is a continuation of his earlier work, as shown by references to his 1971 and 1986 work and the title of a previous submission. 3
Although we stated that “cardiac baroreflex sensitivity has not previously been studied after more extensive surgery or in surgical patients with concomitant essential hypertension,” it is more accurate to leave out the “or” because our clear focus was on the postoperative period. Another limitation of the our article 2
is the lack of discussion of previous postoperative results 4
similar to present results.
Dr. Prys-Roberts suggests that the similarities (e.g., in baroreflex slope) between his study and ours may be related to the actions of both methyldopa (his work) and clonidine (our study) at the α2-adrenergic receptor. Methyldopa does have α2-adrenergic actions, although far less so than clonidine. The suggestion is interesting, but difficult to assess without added work.
We add two further observations. From a methodologic point of view, drug-induced sigmoids in healthy supine resting volunteers showed that the slope obtained from the sequence technique 5
is smaller than that obtained from the phenylephrine technique (fig. 6b in the report by Parlow et al.6
). However, the generating of drug-induced sigmoids was difficult, in our hands, in hypertensive patients recovering from major surgery. The sequences technique seemed to be the only viable option to generate robust postoperative data. 2
From a physiologic point of view, hypertensive patients recovering from major surgery generate sympathetic surges, lasting 2–20 s. 7
To compensate, cardiac vagal motoneurons should slow the heart rate, with a brief delay (100 ms to 2 s). 8
Placebo patients (fig. 3B in our article 2
) show a high pressure variability combined with a fixed heart rate. Postoperative hypertension may be explained by vasomotor sympathetic acti-vation reinforcing the slow kinetics of the windkessel, with the cardiac parasympathetic system unable to rapidly buffer these surges. Clonidine patients (fig. 3D in our article 2
) shows little lability in pressure 3
linked to a reduced number or amplitude of bursts of sympathetic activity 9
combined with a large sinus arrhythmia at resting pressures.
L. Quintin M.D., Ph.D.
M. Ghignone M.D., F.R.C.P.C.
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5. Di Rienzo M, Bertinieri G, Mancia G, Pedotti A: A new method for evaluating the baroreflex role by a joint pattern analysis of pulse interval and systolic blood pressure series. Med Biol Eng Comp 1985; 23:313–4
6. Parlow J, Viale JP, Annat G, Hughson RL, Quintin L: Spontaneous cardiac baroreflex in humans: Comparison with drug-induced responses. Hypertension 1995; 25:1058–68
7. Fritsch JM, Eckberg DL, Graves LD, Wallin BG: Arterial pressure ramps provoke linear increases of heart period in humans. Am J Physiol 1986; 251:R1086–90
8. Katona PG, Barnett GO: Central origin of asymmetry in the carotid sinus reflex. Ann N Y Acad Sci 1969; 156:779–86
9. Wallin BG, Frisk-Holmberg M: The antihypertensive mechanism of clonidine in man: Evidence against a generalized reduction of sympathetic activity. Hypertension 1981; 3:340–6
© 2000 American Society of Anesthesiologists, Inc.