Influence of cardiac innervation on intrinsic heart rate in dogs.

Intrinsic heart rate is defined as the rate at which the heart beats when all cardiac neural and hormonal inputs are removed. We determined the effect of prevailing autonomic innervation of the heart on the intrinsic heart rate in chronically maintained, sedated, normally innervated dogs (n = 14), and in 14 other dogs that had previously (greater than 12 day) undergone complete surgical cardiac denervation. Intrinsic rate was determined in both groups using the following two procedures: 1) pharmacological effector blockade; and 2) pharmacological ganglionic blockade. The intrinsic rate determined by effector blockade was 142.9 +/- 7.2 (SE) beats/min in the dogs with intact cardiac innervation. When the same treatment was given after total surgical cardiac denervation, intrinsic rate was 97.9 +/- 4.8 beats/min. Intrinsic heart rate was significantly (P less than 0.05) lower in surgically denervated dogs. Ganglionic blockade in surgically denervated animals yielded an intrinsic rate of 90.0 +/- 8.5 beats/min, which was again significantly lower than the corresponding value of 128.4 +/- 5.5 beats/min in normal dogs. There was no difference in the intrinsic heart rate as determined by effector vs. ganglionic blockade in either group of dogs. An additional six dogs were subjected to selective surgical sinoatrial nodal parasympathectomy; their intrinsic rate (effector blockade) in the conscious state was 115.8 +/- 4.3 beats/min; this was significantly lower than the corresponding value for normal dogs and significantly greater than in dogs subject to total surgical cardiac denervation. The lower rate observed in the totally denervated and selectively denervated dogs after effector and/or ganglionic blockades implies that intrinsic heart rate depends on the level or nature of prevailing autonomic activity.

Endurance training in dogs increases vascular responsiveness to an alpha 1-agonist.

The effects of endurance training on vascular responsiveness to an alpha 1-agonist and the associated changes in baroreflex modulation of heart rate and vascular resistance were studied. Graded dosages of phenylephrine were given to eight treadmill-trained dogs and to eight untrained dogs; both groups were chronically instrumented and were sedated and resting when tested. These dosages were repeated after ganglionic blockade. Aortic pressure, cardiac output, central venous pressure, peripheral resistance, and heart rate were each averaged over 30 s before injection and 90 s after injection. The slope of the peripheral resistance-dose relationship was significantly increased in trained compared with untrained dogs in both the unblocked and blocked cases [unblocked: trained 0.89, untrained 0.47; blocked: trained 4.30, untrained 2.05 (mmHg.l-1.min)/(microgram.kg-1)]. The unblocked resistance slopes were reduced with respect to the blocked slopes by 77 (untrained) and 79% (trained). The slope of the heart rate-aortic pressure response was reduced, but not significantly, by endurance training. We conclude that 6 wk of endurance training in dogs resulted in a doubling of the vascular responsiveness to an alpha 1-agonist, with no significant change in the baroreflex regulation of resistance or heart rate.