Effect of relaxation training on cardiac parasympathetic tone

To examine the hypothesis that the relaxation response is associated with an increase in cardiac parasympathetic tone, the frequency components of heart rate variability during relaxation training were investigated in 16 college students. Electrocardiograms and pneumograms were recorded during a 5-min baseline period followed by three successive 5-min sessions of the autogenic training (relaxation) or by the same periods of quiet rest (control), while subjects breathed synchronously with a visual pacemaker (0.25 Hz). Although neither the magnitude nor the frequeney of respiration showed a significant difference between relaxation and control, the amplitude of the high-frequency component of heart rate variability increased only during relaxation (p= .008). There was no significant difference in the ratio of the low-frequency (0.04–0.15 Hz) to the high-frequency amplitudes. The increased high-frequency amplitude without changes in the respiratory parameters indicates enhanced cardiac parasympathetic tone. Thus, our results support the initial hypothesis of this study. Enhanced cardiac parasympathetic tone may explain an important mechanism underlying the beneficial effect of the relaxation response.     

Myocardial relaxation. I. Effect of nitroprusside on the tension prolongation phenomenon.

The effects of nitroprusside and cyanide on myocardial relaxation were studied during hypoxia and reoxygenation of isolated rat papillary muscle, and during segmental ischemia and reperfusion in the intact dog heart. Nitroprusside did not affect isolated muscle performance before or during hypoxia. During reoxygenation of hypoxic muscles, the tension prolongation phenomenon (which characterizes abnormal or prolonged relaxation) was only slightly attenuated by the addition of nitroprusside to the muscle bath; in contrast, cyanide (at concentrations that did not prevent the return of tension) abolished tension prolongation during reoxygenation. During reperfusion of ischemic segments in intact hearts, the prolongation of segment tension was not affected by systemic administration of nitroprusside, but was abolished by intracoronary cyanide. Attenuation of the tension prolongation phenomenon by nitroprusside in the isolated muscle may be due to the liberation of cyanide. Inasmuch as nitroprusside did not affect the tension prolongation phenomenon in the intact heart, it is unlikely that the influence of this drug on left ventricular diastolic compliance is mediated through an alteration in the tension prolongation phenomenon.     

心肌核素断层显像中人工左心室长轴选择的校正

论述了作者在心肌核素断层显像图像处理方面的研究工作,采用左心室长轴取向校正算法对明显存在主观性和变异性的左心室长轴人工选择进行校正.在算法上提出应用左心室心肌最大放射性计数值采样及Gauss-Newton最优化方法进行模型参数的拟合.     

Effects on rat parotid amylase and Ca of alpha- and beta-adrenergic sympathetic stimulation.

The roles of alpha- and beta-adrenergic receptors in the regulation of the secretion of amylase and calcium from rat parotid gland were studied by using direct electrical stimulation of the sympathetic innervation to the gland in the presence of selective adrenergic blocking agents. When phenoxybenzamine was administered intraperitoneally 25 min prior to nerve stimulation, the highest [Ca] (12-14 meq/liter) and amylase activity (1,000 mg/microliter) in the evoked saliva were observed. On the other hand, stimulation of the nerve in the presence of propranolol evoked a saliva that contained the lowest [Ca] (5-6 meq/liter) and amylase activity (170 mg/microliter). Furthermore, salivary flow (4.27 +/- 0.42 microliter/min X g) induced by sympathetic nerve stimulation in the presence of phenoxybenzamine was higher than that induced by sympathetic nerve stimulation in the presence of propranolol (2.55 +/- 0.39 microliter/min X g). Therefore, it was concluded that beta-adrenergic receptors play the major role in the regulation of salivary flow and the secretion of amylase and calcium, whereas alpha-adrenergic receptors play a minor role in the regulation of these parameters.     

Effects of selective adrenergic agonists and antagonists on gastric tone in the rat.

The aim of the present in vivo study was to investigate in anaesthetized rats, the effects of selective adrenergic agonists and antagonists on basal gastric tone and phasic contractions by the use of a volumetric method. L-phenylephrine, an alpha-1 agonist, induced hypertension, bradycardia and a significant gastric relaxation. Clonidine, an alpha-2 agonist, caused hypotension, bradycardia and a significant gastric contraction and a reduction of the amplitude of phasic contractions. Salbutamol, a beta-2 agonist, induced a dose-dependent tachycardia and a significant inhibition of gastric tone whereas prenalterol, a beta-1 agonist, induced tachycardia without any significant influence on gastric basal tone. Yohimbine, an alpha-2 blocker, significantly decreased gastric basal tone and reversed the inhibition of phasic contractions induced by clonidine. Prazocine, a selective alpha-1 blocker, and propranolol, a non-selective beta-blocker, had no significant influence on gastric basal tone or phasic contractions. It is concluded that sympathetic inhibition of basal gastric tone in the rat is mediated by alpha-1 and beta-2 adrenergic receptors. Activation of alpha-2 adrenergic receptors significantly increased basal gastric tone and reduced the amplitude of phasic contractions. A blockade of alpha-2 receptors significantly decreased basal gastric tone and restored the amplitude of phasic contractions.     

Effects of beta-adrenergic blockade on lateral hypothalamic lesion-induced thermogenesis

Oxygen consumption is markedly elevated in rats with lesions of the lateral hypothalamus (LH), a response typically associated with hyperactivity. To test for involvement of adrenergic systems in this hypermetabolic state, propranolol was administered before and immediately after LH lesions. Propranolol attenuated both the lesion-induced rise in oxygen consumption and activity in the 12 h after surgery. A second experiment evaluated the contribution of activity to this thermic response by lesioning rats immobilized by a continuous barbiturate infusion. The persistence of lesion-induced increases in oxygen consumption in the absence of activity and the attenuation of this response by propranolol demonstrated that 1) LH lesions directly alter metabolic heat production, and 2) this effect is at least partly mediated by beta-adrenergic systems. The functional significance of increased energy expenditure after LH lesions is discussed in light of the known effects of this lesion on the level of regulated body weight.     

Effects of endotoxin on tone and pressure-responsiveness of Preglomerular juxtamedullary vessels

Endotoxin might affect renal vasoreactivity, but in vivo this is difficult to assess (systemic influences). Therefore, we used the in vitro blood-perfused juxtamedullary nephron preparation to study early changes in preglomerular vascular reactivity induced by exposure to endotoxin. Pressure-evoked vasomotor responses were determined videometrically by measuring steady-state inside vessel diameters at a perfusion pressure of 60 or 120 mmHg. Intraluminal application of endotoxin (primary contact with endothelium) for 120 min elicited an early (within 30 min) and sustained ～25% vasoconstriction from arcuate artery to the distal portions of the afferent arterioles; autoregulatory responses, indicated by pressure-induced vasoconstriction, were unchanged. When topically applied, endotoxin (primary contact with smooth muscle cells) had no vasomotor effects. Significant constrictions, and increases in autoregulatory responses were obtained when the preparation was taken from kidneys from endotoxin-treated rats. Endotoxin had no effect on efferent arteriolar dimensions. Such preferential preglomerular early vasoconstriction is consistent with the early increase in renal resistance and parallel decrease in renal blood flow and glomerular filtration observed during endotoxin shock in vivo. Our results support the concept of local, endothelium-mediated effects of endotoxin on renal vessels.     

Effects of laughter and relaxation on discomfort thresholds

Two experiments were conducted to test the proposal that laughter is a pain antagonist. In Experiment I, thresholds for pressure-induced discomfort of 20 male and 20 female subjects were measured after each subject listened to a 20-min-long laughter-inducing, relaxation-inducing, or dull-narrative audio tape or no tape. Discomfort thresholds were higher for subjects in the laughter- and the relaxation-inducing conditions. In Experiment II, 40 female subjects were matched for pressure-induced discomfort thresholds. Their discomfort thresholds were measured after they listened to a laughter-inducing, interesting narrative, or uninteresting narrative audio tape, completed a multiplication task, or experienced no intervention. Discomfort thresholds increased for subjects in the laughter-inducing condition. Laughter, and not simply distraction, reduces discomfort sensitivity, suggesting that laughter has potential as an intervention strategy for the reduction of clinical discomfort.     

Effects of dual-action genistein derivatives on relaxation in rat aorta.

Protein tyrosine kinases and nitric oxide (NO) play important roles in several cardiovascular diseases. In this study, we examined the actions of two compounds, each has structure of genistein (a tyrosine kinase inhibitor) and an NO donor, on endothelium-independent relaxation responses in the isolated rat aorta. By rational drug design, genistein was modified to acquire an NO donor, and we synthesized two such compounds (G-II, G-VI). These compounds and genistein induced dose-dependent relaxation responses in endothelium-denuded aortic strips, the rank order of potencies being G-VI > G-II > genistein. Incubation of endothelium-denuded strips with 1H-[1,2,4] oxadiazolo[4,3-a]-quinoxalin-1-one (ODQ, 10 microM), a guanylyl cyclase inhibitor, inhibited both the G-II- and G-VI-induced relaxations, but not the genistein-induced relaxation. The residual relaxations induced by these two compounds were similar to the genistein-induced relaxation. Incubation of endothelium-denuded strips with lysophosphatidylcholine (LPC, 20 microM)-which is a major atherogenic lysophospholipid component of oxidized low-density lipoprotein and is known to activate tyrosine kinase-caused a significant rightward shift in the dose-response curve for genistein. LPC also shifted the G-II- and G-VI-induced relaxation curves to the right; however, these relaxations in the presence of LPC were greater than that induced by genistein. The sodium nitroprusside-induced relaxation in endothelium-denuded strips was similar between in the absence and presence of LPC. These results suggest that each of our newly developed G-II and G-VI compounds has a dual action, as an NO donor and a tyrosine kinase inhibitor. These compounds may be useful against certain cardiovascular diseases.     

Concentration dependence of fluorine impurity spin-lattice relaxation rate in bone mineral.

The concentration dependence of the fluoride ion spin-lattice relaxation rate has been observed by nuclear magnetic resonance experiments on samples of defatted and dried bone. The 19F spin-lattice relaxation rates increased linearly with the bone fluoride concentration. Different results were obtained from trabecular than from cortical bone. For the same macroscopic fluoride content per gram of bone calcium, the relaxation rate is significantly faster in cortical bone. Relaxation rates in cortical bone samples prepared from both rats and dogs were apparently controlled by the same species-independent processes. For samples from beagle dogs, the bulk fluoride concentrations measured by neutron activation analysis were 3.1 +/- 0.3 times greater in trabecular bone than in the corresponding cortical bone. The beagle spin-lattice relaxation data suggest that the microscopic fluoride concentrations in bone mineral were 1.8 +/- 0.4 times greater in trabecular bone than in cortical bone. It is concluded that the accumulation of fluoride impurities in bone mineral is non-uniform.     

Effects of thyroid hormones on cardiac hypertrophy and beta-adrenergic receptors during aging

Administration of thyroxine daily at a dosage of 6.4 mu g/g body weight stimulates cardiac hypertrophy in both 9--13-month-old (mature, n = 34) and 22--24-month-old (senescent, n = 45) Wistar rats. The increase due to thyroxine as well as the time course of the effect do not change with age, although ventricular wet weight to tibial length ratios are higher in senescent animals at 0, 3, and 7 days of treatment (senescent controls = 0.331; senescent hypertrophied = 0.395; mature controls = 0.295; mature hypertrophied = 0.336). Hypertrophy is maximal after 3 days. beta-Adrenergic receptor levels as measured by stereospecific binding of dihydroalprenolol in mature rats are increased about two-fold after 7 days of thyroxine treatment (mature controls = 35 +/- 3 fmol/mg protein, mature treated = 65 +/- 6 fmol/mg protein). Although both stimulated and control values do not differ significantly between mature and senescent groups (senescent controls = 45 +/- 4 fmol/mg protein, senescent treated = 56 +/- 9 fmol/mg protein), the effect of thyroxine on senescent hearts is not statistically significant. In addition, 3-day levels do not increase over 0-day controls at either age. No significant differences in either beta-adrenergic receptor concentrations or affinities between age groups are observed at 0, 3, and 7 days of treatment. However, senescent membrane preparations contain 33% more sialic acid (a rough plasma membrane marker) per unit of protein than mature preparations. Thus, the beta-adrenergic receptor density per unit of sialic acid may be reduced very slightly in the senescent hearts.     

Effects of pH on vascular tone in rabbit basilar arteries

Effects of pH on vascular tone and L-type Ca2+ channels were investigated using Mulvany myograph and voltage-clamp technique in rabbit basilar arteries. In rabbit basilar arteries, high K+ produced tonic contractions by 11+/-0.6 mN (mean+/-S.E.,n=19). When extracellular pH (pHo) was changed from control 7.4 to 7.9 ([alkalosis]o), K+-induced contraction was increased to 128+/-2.1% of the control (n=13). However, K+-induced contraction was decreased to 73+/-1.3% of the control at pHo 6.8 ([acidosis] o, n=4). Histamine (10 microM) also produced tonic contraction by 11+/-0.6 mN (n=17), which was blocked by post-application of nicardipine (1 microM). [alkalosis]o and [acidosis]o increased or decreased histamine-induced contraction to 134+/-5.7% and 27+/-7.6% of the control (n=4, 6). Since high K+- and histamine-induced tonic contractions were affected by nicardipine and pHo, the effect of pHo on voltage-dependent L-type Ca2+ channel (VDCCL) was studied. VDCCL was modulated by pHo: the peak value of Ca2+ channel current (IBa) at a holding of 0 mV decreased in [acidosis]o by 41+/-8.8%, whereas that increased in [alkalosis]o by 35+/-2.1% (n=3). These results suggested that the external pH regulates vascular tone partly via the modulation of VDCC in rabbit basilar arteries.     

Effects of alpha- and beta-adrenergic stimulation on free magnesium concentrations in platelets from healthy and obese individuals.

We performed this study to investigate whether alpha- and beta-adrenergic agonists are able to regulate intracellular free magnesium concentrations [Mg2+]i in platelets from healthy and obese individuals. Twenty-six informed-consent men (14 healthy and 12 obese) were enrolled in the study. We measured fasting plasma glucose, insulin, epinephrine and norepinephrine. Platelet [Mg2+]i at the baseline and after stimulation with clonidine or isoproterenol was measured by fluorescent probe mag-fura-2. In platelets from healthy subjects, alpha-adrenergic stimulation by clonidine led to a dose-dependent decrease in [Mg2+]i (basal: 245 +/- 39 microM; clonidine 5 pg/mL: 109 +/- 27 microM, p < 0.05; clonidine 10 pg/mL: 77 +/- 26 microM, p < 0.01), while no significant change in platelet [Mg 2+]i was detected in obese men. Furthermore, the co-incubation with clonidine (10 pg/mL) and yohimbine (50-100 pg/mL) completely abated the effect of clonidine on [Mg2+]i in platelets from healthy individuals. Analysis of the time course for platelet magnesium showed that the intracellular magnesium loss induced by clonidine (10 pg/mL) was time-dependent. Conversely, the beta-adrenergic agonist isoproterenol was able to produce a significant rise in [Mg2+]i in platelets from healthy individuals (basal: 234 +/- 40 microM; isoproterenol 2.5 pg/mL: 594 +/- 44 microM, p < 0.05: isoproterenol 5 pg/mL: 681 +/- 56 microM, p < 0.01), while no such finding was detectable in platelets from obese patients. When platelets from healthy subjects were co-stimulated with isoproterenol (5 pg/mL) and propranolol (10-20 pg/mL), the ionophoric effect of the beta-adrenergic agonist was completely reverted. The time course of isoproterenol (5 pg/mL) effect on platelet [Mg2+]i showed that the ionophoric effect of isoproterenol was time-dependent. In conclusion, (1) the stimulation of alpha-adrenergic receptor by clonidine is able to induce a significant dose- and time-dependent fall in platelet [Mg2+]i; (2) the stimulation of beta-adrenoceptors by isoproterenol lead to a signifcant time- and dose-dependent rise in platelet [Mg2+]; (3) the ionic effect of alpha- and beta-adrenergic stimulation is not detectable in obese subjects, in whom is probably present a reduced sensitivity to the ionic effect of adrenergic agonists.