Since the first attempts of T. Jonnesco’ to treat angina pectoris by
means of cervico-thoracic sympathectomy, many surgeons have applied
similar techniques with satisfactory results in the majority of instances.2
Nearly without exception, the operations were performed with the de-
clared purpose to sever sensory, pain-conveying, afferent nervous path-
ways, and without realization of the fact that (except in the case of
exclusive section of the posterior roots), the norepinephrine-discharging,
pain-producing efferent sympathetic fibers3 were, likewise, interrupted.
In animal experiments, it has been shown that electrical stimulation
of the cardiac sympathetic nerves is followed by an accumulation of
catecholamines,4.s especially of norepinephrine,’ in the myocardium,
whereas the cardiac catecholamine stores are largely depleted by sym-
pathectomy.7”
The prolongation of the isometric (tension) period (TP) of the left ventricle which
occurred in the majority (72 per cent) of all cases after unilateral or bilateral trans-
thoracic sympathectomy (without or with unilateral or bilateral transthoracic splanch-
nicotomy) indicates a diminution of inotropic cardiac action. It can be assumed to
correspond to the cholinergic (vagal) preponderance which results from a partial or
complete sympathetic denervation of the heart. Reduction of the pulse pressure oc-
curred in 56 per cent of the cases, probably due to the same mechanism. The be-
havior of the heart rate was too irregular to permit any conclusions. Apparently, the
Inotropic mechanisms of the heart are more sensitive to sympathetic denervation than
the chronotropic ones.
The seemingly paradoxical shortening of TP which was persistently maintained,
e.g., in the case of patient 16 over a period of more than five months, is possibly to
be explained as a manifestation of Cannon’s “law of denervation” according to which
the catecholamine sensitivity of sympathetically denervated structures Is greatly aug-
mented, and which has more recently been confirmed also in instances of functional
sympathetic “denervation” (catecholamine deprivation of cardiovascular tissues)
through gangllomc blockade” or rauwolfia drugs.’6 This would mean in the present
cases that their partly or wholly sympathectomized hearts had become oversensitive to
whatever active catecholamines (norepinephrine, eplnephrine) may have reached them
either from remaining sympathetic fibres or through the blood stream. Individual
differences in relative reactivity to two mutually antagonistic factors ([a] absolute
loss of catecholammes, and Eb] exaggerated catecholamine sensitivity, caused by [a 1),
combined with the individual magnitude of absolute cardiac cholinergic activity, may
account for the prevalence of either negative or positive Inotropic cardiac reactions
to sympathectomy.
DOI 10.1378/chest.38.4.423
1960;38;423-428 Chest
W. RAAB, E. KUX and H. MARCHET
