PubMed · 6121640
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J F Huddleston. 1982. Preterm labor.. https://doi.org/10.1097/00003081-198203000-00017
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BACKGROUND: In humans, intracoronary infusion of substance P reduces left ventricular end-systolic pressure and left ventricular peak systolic pressure because of earlier onset of left ventricular relaxation induced by paracrine myocardial action of mediators released from the coronary endothelium. The present study investigated in humans the effects of beta-adrenergic stimulation, which also induces earlier left ventricular relaxation, on the left ventricular myocardial contractile response to intracoronary infusion of substance P. METHODS AND RESULTS: Data were obtained in 13 patients after cardiac transplantation and in 3 patients with dilated nonischemic cardiomyopathy. Microtip left ventricular pressure recordings were obtained during a 5-minute intracoronary infusion of substance P (20 pmol/min) under control conditions and then repeated during concurrent intravenous administration of dobutamine. In the presence of dobutamine, intracoronary substance P caused a greater fall in left ventricular end-systolic pressure (transplantation control, -9 +/- 11 versus transplantation dobutamine, -20 +/- 18 mm Hg [P < .05]; cardiomyopathy control, -4 +/- 1 versus cardiomyopathy dobutamine, -10 +/- 3 mm Hg [P < .05]) and in left ventricular peak systolic pressure (transplantation control, -14 +/- 10 versus transplantation dobutamine, -30 +/- 22 mm Hg [P < .01]; cardiomyopathy control, -9 +/- 7 versus cardiomyopathy dobutamine, -15 +/- 6 mm Hg [P = .1]). CONCLUSIONS: Dobutamine enhances the cardiodepressant effect on myocardial contractile performance of receptor-mediated coronary endothelial stimulation in transplant recipients and in patients with dilated nonischemic cardiomyopathy. This enhancement could result from a potentiating interaction of the relaxation-hastening effect exerted by beta-adrenergic stimulation and by mediators released from the coronary endothelium, such as nitric oxide.
PURPOSE: The use of 10-15 micrograms epinephrine as an epidural test-dose is controversial. Isoproterenol would be a better alternative. However, before 5 micrograms isoproterenol can be incorporated in an epidural test-dose, neurotoxicological studies have to be performed. The present study was designed to assess spinal somatosensory evoked potentials (spinal SSEP) before and after epidural isoproteronol. METHODS: Spinal SSEPs were recorded before, 30 min after, and 72 hr after 50 micrograms isoproterenol were given epidurally (L3-4) to six chronically instrumented awake sheep. The spinal SSEPs after epidural (L3-4) administration of 15 ml lidocaine 2% were used to evaluate the model. The SSEPs were generated by transcutaneous stimulation of the sciatic nerve in the thigh. Spinal SSEPs were recorded directly from the spinal cord at vertebra T12 using a monopolar epidural electrode referenced to a subcutaneous needle electrode in the adjacent paraspinal area. RESULTS: Thirty minutes and 72 hr after epidural injection of 50 micrograms isoproterenol the latency and the amplitude of the SSEP waves were similar to baseline values. After lidocaine, no SSEPs could be generated in three sheep while in three sheep the latency of wave 2 (W2) was prolonged and the amplitude diminished. CONCLUSION: Administration of epidural isoproterenol did not affect spinal SSEPs in this study indicating an absence of neurotoxic side effects.
Ethanol may downregulate G-protein-coupled beta-adrenoreceptors (beta AR). beta AR may also be dysregulated in panic disorder (PD). In clinical samples, many patients have comorbid alcohol dependence (AD) and PD. Therefore, we investigated beta AR coupling in patients with these disorders. We harvested polymorphonuclear leukocytes from 24 healthy volunteers (Vs), and from 22 abstinent AD patients, 7 PD patients, and 9 patients with comorbid AD/PD. beta AR were assayed using saturation and agonist-displacement experiments. Group differences were tested using one-way analysis of variance (ANOVA). All beta AR binding parameters were similar in AD patients and Vs. The ratio of the agonists' dissociation constant from the receptor in the low affinity state (KL) to that in the high affinity state (KH) was significantly higher in PD patients than in AD patients and Vs (930.97 +/- 440.80 vs. 226.2 +/- 94.47 vs. 197.05 +/- 61.03, respectively, p < .01). This finding suggests that beta AR are supercoupled to GS in patients with PD. There was a trend for higher total receptor density (RT) in AD/PD and PD patients (Vs = 39.06 +/- 42.57 vs. AD = 27.93 +/- 23.07 vs. AD/PD = 66.85 +/- 79.02 vs. PD = 68.36 +/- 49.20, p < .08). There were no differences between AD/PD and PD patients, who combined had a significantly higher RT than Vs and AD patients (Vs = 38.95 +/- 8.81 vs. AD = 29.63 +/- 5.07 vs. AD/PD = 67.51 +/- 17.00, fmol/mg protein, p < .04). Finally, AD/PD patients had a significantly higher receptor density in the low-affinity conformational state than Vs and AD patients, but not PD patients (25.96 +/- 11.59 vs. 10.69 +/- 1.53 vs. 7.62 +/- 1.08 vs. 17.07 +/- 5.26 fmol/mg protein, respectively, p < .005). beta AR function in polymorphonuclear leukocytes is normal in abstinent alcoholics. The previously reported abnormal beta AR regulation in alcoholism may be state dependent. The higher RT and KL/KH ratio in AD/PD and PD, but not in AD patients, suggest that increased beta AR function may be important in the pathophysiology of PD.