Ferguson, David A.

A field study was made of the effect of β-adrenergic receptor blockade (propranolol; Kö 592) on the racing performance of six normal greyhounds and three with chronic extrinsic cardiac denervation. Records were made of the time to race a 5/16-mile course before and after blockade; the heart rate was recorded by telemetry. After the administration of the β-adrenergic receptor-blocking agent to the normal greyhound, racing time was slightly increased, and maximal heart rate was slighdy decreased. After blockade in the cardiac denervated greyhounds, racing time was prolonged, cardiac acceleration was severely limited, and the animals finished running in a state of collapse. The data indicated diat die cardiostimulant action of both sympathetic nerves and circulating catecholamines was necessary for maximal performance. After blockade of one or the other of these mechanisms, racing performance was slightly reduced from normal. Withdrawal of both adjuvants severely limited the performance of maximal exercise.

The possibility of sympathetic vasoconstrictor control of blood flow to active muscles was studied in dogs during graded exercise by comparing the blood flow in the normal with that in the Sympathectomized hind limb. Blood flow was measured by electromagnetic flow transducers around each external iliac artery, or inferred from the oxygen saturation of blood samples from the common iliac veins. The dogs either ran for successive periods of 3 minutes at 5.5 km/hr and grades of 0, 7, 14, 21, and 28% or ran each level of exercise separately. Unilateral lumbar sympathectomy (L-2 through L-7) was performed when the flow transducers were implanted or later by a snare technique. The latter allowed observations during exercise as early as 4 hours after sympathectomy. The magnitude of limb blood flow during exercise and the decline of exercise hyperemia were similar in the normal and the sympathectomized limb, as were the changes in the oxygen saturation of limb venous blood. However, electric stimulation of the lumbar sympathetic chain at the L-5 level in the conscious dog by a chronically implanted electrode reduced limb blood flow at all levels of exercise, the maximal flow of 1,000 ml/min was almost halved.

In anesthetized dogs, the vasoconstrictor nerves to the vessels of the hind limb left the spinal cord in the anterior spinal nerve roots from T-10 through L-4 levels. Maximal vasoconstrictor responses occurred on stimulation of the T-12, T-13, and L-l roots; none occurred on stimulation of roots caudal to L-4. The nerves first entered the lumbar paravertebral chain at or above L-1; the last point of entry was at the L-4, L-5 level. No fibers left the lumbar chain at L-1, L-2, and L-3 levels. The first point of exit was at L-4, and nerves continued to leave as far distal as S-1, The most caudal point examined. The maximal response to stimulation of the lumbar chain was at the L-4, L-5 level. With a single exception, the responses to electric stimulation of the anterior spinal nerve roots, lumbar chain, or sympathetic ganglia were confined to the vessels of the ipsilateral limb. In 22 dogs with unilateral sympathectomy (L-2 through L-7), changes in hind-limb vascular resistance were induced reflexly or by electric stimulation of the anterior spinal roots. The results indicated that sympathetic control of the resistance vessels of the hind limb was still absent 77 days after sympathectomy.