Adrenergic control of myocardial contractility in conscious hyperthyroid dogs

L-Thyroxine (0.75 mg x kg^-1 x day^-1) was administered for 7 days to 9 conscious dogs instrumented with miniature left ventricular (LV) pressure gauges to measure pressure and dP/dt, ultrasonic transducers to measure LV diameter and dD/dt, and catheters to measure arterial pressure. Cardiac output was measured using the radioactive microsphere technique. The hyperthyroid state was associated with increases in mean arterial pressure (11.5 ± 4.3% from 95.0 ± 4.0 mmHg), LV systolic pressure (16.2 ± 3.8% from 126.0 ± 5.5 mmHg), LV dP/dt (67.0 ± 12.5% from 3550 ± 230 mmHg/s), LV dD/dt (31.1 ± 6.8% from 75.4 ± 7.3 mm/s), LV end-diastolic diameter (3.0 ± 1.1% from 36.86 ± 1.19 mm), heart rate (77.3 ± 13.0% from 92.0 ± 8.3 beats/min), and cardiac output (78.0 ± 1.7% from 2.96 ± 0.62 l/min), with a decrease in LV stroke shortening (15.8 ± 2.4% from 8.37 ± 1.07 mm). When the effects of tachycardia were eliminated by pacing the dogs at a rapid rate in the euthyroid state, the changes in LV dynamics induced by the hyperthyroid state were similar to those responses observed when heart rate rose, with the exception that LV stroke shortening increased (36.8 ± 7.3% from 4.83 ± 0.40 mm). With the induction of hyperthyroidism, the contractile responses to exogenous norepinephrine and isoproterenol were similar to those observed in the euthyroid state. However, propranolol reduced myocardial contractility more in the hyperthyroid state than in the euthyroid state. Thus, with the induction of hyperthyroidism in the conscious dog, there are substantial increases in LV contractility mediated by both direct effects of thyroid hormone and increased β-adrenergic activity. However, contractile responses to exogenous norepinephrine and isoproterenol were not augmented.