Systolic functional response of normal older and younger adult left ventricles to beta-blockade during exercise. Memory impairment induced by intraamygdala beta-endorphin is mediated by noradrenergic influences. The direct vasomotor effect of thyroid hormones on rat skeletal muscle resistance arteries. Rx drugs

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Cardiovasc Drugs Ther. 1995 Apr;9(2):289-94.
Systolic functional response of normal older and younger adult left ventricles to beta-blockade during exercise.

Kyriakides ZS, Papaioannou G, Paraskevaidis IA, Kolettis TM, Kremastinos DT.

Onassis Cardiac Surgery Center, Athens, Greece.

There is controversy over the effects of beta-blockade on the left ventricular systolic response of the heart of the elderly to stress. In this study we compared the effects of acute beta-blockade in normal older and younger adult left ventricles during exercise. The study population consisted of 17 healthy elderly people, 67 +/- 3 years old, while 18 young normal subjects, 31 +/- 4 years old, served as controls. A symptom-limited exercise treadmill test was performed before and 15 minutes after intravenous administration of 0.12 mg propranolol/kg. M-mode echocardiographic studies were performed before and immediately after each test. Intravenous propranolol at rest decreased heart rate by 14 +/- 7 beats/min in the elderly and by 7.5 +/- 8 beats/min in the young (p = 0.02), decreased the double product by 2500 +/- 1200 mmHg/min and 1830 +/- 970 mmHg/min (p = 0.05), respectively; changed the left ventricular end-systolic dimension by +0.21 +/- 0.36 cm and +0.03 +/- 0.24 cm (p = 0.09), respectively; and changed the end-diastolic dimension by +0.22 +/- 0.46 cm in the elderly and by -0.02 +/- 0.32 cm in the young (p = 0.08). The change in fractional shortening was -1.22 +/- 4.17% in the elderly and -0.78 +/- 4.05% in the young (p > 0.05), and the decrease in the systolic blood pressure/end-systolic dimension ratio was 5.9 +/- 7 mmHg/cm and 4.3 +/- 3.8 mmHg/cm, respectively (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Neurobiol Learn Mem. 1995 Mar;63(2):200-5.
Memory impairment induced by intraamygdala beta-endorphin is mediated by noradrenergic influences.

Introini-Collison IB, Ford L, McGaugh JL.

Center for the Neurobiology of Learning and Memory, University of California, Irvine 92717-3800, USA.

These experiments examined the effects on memory in two tasks, inhibitory avoidance and water-maze spatial learning, of intraamygdala injections of drugs affecting noradrenergic and opiate receptors. Male Sprague-Dawley rats (180 g, 50 days old on arrival) were given either a single training trial in an inhibitory avoidance task or eight trials in a water-maze task in which they were trained to swim to a platform submerged 1 cm below the water surface and located in a constant position. Intra-amygdala injections of beta-endorphin (0.03 or 0.1 ng), clenbuterol (10 or 30 ng), or propranolol (0.3 microgram) were given alone or concurrently: beta-endorphin (0.1 ng) + clenbuterol (10 or 30 ng) or beta-endorphin (0.03 ng) + propranolol (0.3 microgram). The injections (0.5 microliter) were administered immediately after inhibitory avoidance training and 5 min before water-maze training. Inhibitory avoidance retention was tested 48 h after training and water-maze retention was tested 24 h after training. In both tasks, clenbuterol attenuated the retention impairing effect of beta-endorphin. Also, in both tasks, low doses of beta-endorphin (0.03 ng) and propranolol (0.3 microgram), which did not affect retention when administered alone, impaired retention when administered concurrently. These results are consistent with extensive previous evidence suggesting that opioid and noradrenergic systems interact in modulating memory storage and provide additional support for the view that the interaction is due to opioid inhibition of noradrenergic activation within the amygdala.

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Anesth Analg. 1997 Oct;85(4):734-8.
The direct vasomotor effect of thyroid hormones on rat skeletal muscle resistance arteries.

Park KW, Dai HB, Ojamaa K, Lowenstein E, Klein I, Sellke FW.

Department of Anesthesia & Critical Care, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.

The present study examines the hypothesis that the hormones have direct vasodilatory effects and attempts to determine whether the effects are endothelium-dependent. Rat skeletal muscle resistance arteries of approximately 100 microns were dissected, and vessel diameter changes were monitored using a videodetection system. After equilibration at 37 degrees C, each vessel was preconstricted with the thromboxane analog U46619 1 microM, and the percentage of dilation was measured after exposure to increasing concentrations of triiodothyronine (T3) or levothyroxine (T4) (10(-10) to 10(-7) M). Dilation in response to T3 was also measured after endothelial denudation and pretreatment with the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NNA) 10 microM, the cyclooxygenase inhibitor indomethacin 10 microM, the adenosine triphosphate-sensitive K+ channel blocker glibenclamide 1 microM, or the beta-adrenergic antagonist propranolol 1 microM. Both T3 and T4 demonstrated concentration-dependent dilation of the U46619-preconstricted vessels (P < 0.001 each), with T3 having a greater effect than T4 (P < 0.05) (36% +/- 9% [mean +/- SD] dilation at 10(-7) M T3 vs 24% +/- 6% dilation at 10(-7) M T4). In comparison, isoproterenol 10(-7) M produced 56% +/- 6% dilation. T3-mediated vasodilation was attenuated but not abolished by endothelial denudation (18% +/- 3% dilation at 10(-7) M T3) (P < 0.01), L-NNA (15% +/- 7% dilation at 10(-7) M T3) (P < 0.01), indomethacin (20% +/- 9% dilation at 10(-7) M T3) (P < 0.05), and glibenclamide (22% +/- 7% dilation at 10(-7) M T3) (P < 0.01), but it was not affected by propranolol (37% +/- 20% dilation at 10(-7) M T3) (P = 0.99). We conclude that thyroid hormones possess direct vasodilatory effects with both endothelium-independent and endothelium-dependent components. Implications: Thyroid hormones may have modest direct vasodilatory effects. This may partially account for the cardiovascular actions of the hormones in hyperthyroidism or when administered pharmacologically in cardiac surgery.

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