Management of quinidine syncope in twenty cases.
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Adolescent↗
Biomedical subjects
S Pu
Publications and source records attributed to S Pu.
An interactive physiological role of neuropeptide Y and galanin in pulsatile pituitary luteinizing hormone secretion.
Both neuropeptide Y (NPY) and galanin (GAL) systems have been implicated in the excitatory regulation of pulsatile LH secretion in the ovariectomized rat. The present studies were designed to examine the possible interaction of these two neuropeptides in controlling episodic LH release by testing the effects of central infusion of antibodies (Ab) to NPY and GAL, alone or in combination; additional studies tested the effects of central administration of an antisense oligodeoxynucleotide (ODN) to NPY and GAL messenger RNA. Rats were ovariectomized, implanted with a cannula in the third ventricle, and used in experiments 2 weeks later. Central infusion, via Alzet osmotic minipumps, of IgG purified from an NPY Ab produced a dose-related suppression of pulsatile LH secretion. Although an Ab dilution of 1:10 was ineffective, a maximal inhibitory effect was obtained using an NPY Ab dilution of 1:1, which decreased the mean levels, pulse frequency, and pulse amplitude of LH. These parameters of episodic LH secretion were also significantly reduced by central injection of antisense NPY ODN compared to those in vehicle- or missense ODN-treated controls. Similar dose-related inhibitory effects on the parameters of LH secretion were seen after central infusion of GAL Ab. Furthermore, infusion of a combination of NPY Ab and GAL Ab, each at the ineffective dilution of 1:10, resulted in a profound inhibition of LH secretion equivalent to the pattern seen with the maximally effective 1:1 Ab dilution. These results strengthen the idea of a physiological role for both NPY and GAL systems in the mechanism underlying the LHRH pulse generator activity and further suggest that these two excitatory neuropeptides act in concert to generate pulsatile LHRH release.
Animals↗
Evidence that gonadal steroids modulate nitric oxide efflux in the medial preoptic area: effects of N-methyl-D-aspartate and correlation with luteinizing hormone secretion.
Several lines of evidence suggest that nitric oxide (NO) is involved in the neuroendocrine control of reproductive function. This study was undertaken to determine 1) NO activity in the medial preoptic area (MPOA) where LHRH- and NO synthase-containing neurons are coextensive; 2) whether N-methyl-D-aspartate (NMDA) receptor activation, which stimulates LHRH release, augments NO activity in the MPOA; and 3) whether NO activation in the MPOA underlies the steroid dependency of NMDA-induced pituitary LH release. As extracellular levels of cGMP in discrete brain sites are a reliable index of basal and stimulated activity of NO, extracellular cGMP levels in the MPOA of freely moving, awake rats were measured by microdialysis in the current study. In the first experiment, the MPOA of intact and castrated male rats were microdialyzed with artificial cerebrospinal fluid at a rate of 5 microliters/min. The basal level of cGMP efflux was determined from the initial seven samples collected at 20-min intervals. The NO response to a single i.v. injection of NMDA (10 mg/kg) or saline was assessed in the next five samples. In the second experiment, the basal and NMDA-evoked NO effluxes in the MPOA of ovariectomized (ovx) and estrogen-treated ovx rats were examined. Results showed that in both sexes, the absence of gonadal steroids resulted in significantly lower basal cGMP levels. Additionally, the cGMP response to NMDA was steroid dependent. Whereas in castrated rats it failed to affect cGMP efflux, NMDA in intact male rats promptly raised cGMP levels at 20 min, and these elevated levels were maintained through the duration of the experiment. This NMDA-induced cGMP response, observed selectively in intact rats, was also associated with stimulation of plasma LH levels. In female rats, NMDA similarly enhanced MPOA cGMP efflux and pituitary LH secretion in estradiol benzoate-treated, but not in oil-treated, ovx rats. The NMDA receptor antagonist D,L-amino-5-phosphoropentanoic acid and the NO synthase inhibitor, N omega-nitro-L-arginine, completely blocked the NMDA-induced cGMP and LH responses, thereby demonstrating the specificity of the NMDA receptor --> NO line of communication probably operating in the MPOA in the control of pituitary LH release. Therefore, these results show that gonadal steroids augment basal as well as NMDA-induced MPOA cGMP efflux in male and female rats. It is likely that facilitation of NO/cGMP activity in the MPOA may underlie the steroid dependency of NMDA-evoked LH hypersecretion in the rat.
2-Amino-5-phosphonovalerate↗
[The clinical features and long-term follow-up of atrial fibrillation or atrial flutter complicating Wolff-Parkinson-White syndrome].
Twenty six patients (20 male, 6 female, aged 50 +/- 14) with recurrent episodes of atrial fibrillation or atrial flutter (Af/AF) associated with WPW syndrome were retrospectively studied and followed. During Af/AF, 17 patients showed ventricular preexcitation. Of them, 15 patients had hypotention, 8 syncope, 4 precipitating acute heart failure and 4 spontanous degenerated into ventricular fibrillation. Hypotention was found only in 2 of the 9 patients without pre-excited ventricular beats. The mean shortest prexcited R-R intervals of the former were shorter (247 +/- 47 ms) and the average ventricular rates (198 +/- 43 beat/min) were faster than those of the latter (393 +/- 80 ms & 144 +/- 22 beat/min) respectively (P < 0.01). When pre-excited Af/AF occurred, both cardioversion and antiarrhythmic agents of class I and II had marked effect in terminating the Af/AF or slowing pre-exicted ventricular responses. Digitalis and verapamil caused deterioration in the clinical condition of 6 patients (4 with hypotention, one syncope, and one ventricular fibrillation). Management of patients for WPW complicating Af/AF without pre-excited QRS was the same as for the ordinary Af/AF. Over a period of 53 +/- 44 months of follow-up, 5 died (3 of sudden death, one of heart failure, and one of noncardiac cause) in the group with preexcited Af/AF, but all of the patients without preexcited QRS during Af/AF were alive. Conclusion, clinical severity, response to the treatment, and long-term prognosis of patients of WPW with preexcited Af/AF are different from those without.
Anti-Arrhythmia Agents↗
Cholecystokinin gene expression in rat amygdaloid neurons: normal distribution and effect of morphine tolerance.
Previous studies have shown that repeated opioid administration induces a tolerance to opioid, presumably due in part to an opioid-mediated compensatory increase in brain cholecystokinin (CCK) synthesis and/or release. In this study, in situ hybridization histochemistry was used to examine the effect of morphine tolerance on CCK gene expression in the amygdala of rat brains, by using a 35S-labeled synthetic oligonucleotide probe. CCK mRNA-positive neurons in normal rats were seen throughout the amygdaloid complex, with the most heavily labeled neurons in lateral, basal, and cortical nuclei, followed by the medial nucleus. Only a few labeled neurons were found in central and intercalated nuclei. The development of morphine tolerance in the rat was associated with increased hybridization signals for CCK mRNA in each subnucleus of the amygdala. Increases were seen in the numbers of positively labeled neurons and/or the numbers of hybridization grains per positively labeled neuron. Furthermore, differential patterns of increase in CCK mRNA in morphine tolerant rats occurred in different subnuclei of the amygdala, with the highest magnitude of increase in the cortical nucleus, followed in order by the medial, central, basal, intercalated and lateral nuclei. The present study demonstrated that repeated administration of morphine increased CCK gene expression in the amygdaloid complex, and suggested that the development of the tolerance to morphine analgesia is due, in part, to an increase in CCK activity in the amygdaloid complex. These findings substantiate the hypothesis that long-term administration of opioid may induce a compensatory increase in CCK synthesis and/or release, which then results in a progressive antagonism of opioid analgesia.
Amygdala↗
[Effects of air pollution on health of residents in vicinity of an electrometallurgical factory in Chengdu].
Air pollution in an electrometallurgical plant in Chengdu was monitored in 1988. Results showed that atmospheric TSP and Ni concentrations in the vicinity of the plant were higher than those in control area; and TSP content higher than its health standard level. A population of 262 children was physically examined in the same pollution and control areas in May, 1988. Physical examinations were as follows:otorhinolaryngological examination, skin patch test of Ni and Co, immune function test (including PHA skin test, salivary LZM content), Ni levels in human hair and urine etc. We found that body burdens of Ni in population of pollution area increased because of the pollution of Ni compounds in the atmosphere. Hair Ni content in pollution area was significantly higher than that in control area, and the positive rate of Ni skin patch test was also markedly higher than that in control area. Case history indicated that there was a significant difference in Ni content as detected by otorhinolaryngological examinations between the pollution and control areas. Some measures were suggested to improve the air quality based on the study.
Adolescent↗
[Effect of electroacupuncture tolerance by different frequencies on the cardiovascular inhibition of spinal opioid peptides of the rats].
Continuous 6 hour's electroacupuncture (EA) of 2-15Hz or 2Hz applying to both legs of the rats resulted in the electroacupuncture tolerance (ET). Then, we observed: (1) The effect of 2-15Hz ET on the recovery of mean arterial blood pressure (MAP) and heart rate (HR) of rats after hemorrhagic shock; (2) The change in MAP and HR of rats subjected to 2Hz ET after intrathecally (i. t.) administration of DADLE 25 micrograms, a delta opioid agonist. The results showed that, firstly, there was no difference between 2-15Hz ET group and control group in the recovery of MAp and HR after hemorrhagic shock. Secondly, DADLE (25 micrograms) caused almost the same suppression effect both in 2Hz TE group and in control group. These results suggest that unlike the spinal dorsal horn cells (regulating algesia, the spinal lateral horn cells (regulating blood pressure) are insensitive during EA analgesia and can not be made tolerance to continuous EA.
Acupuncture Analgesia↗
[Quantitative analysis of signal-averaged electrocardiograms].
Quantitative analysis of the high frequency components of the terminal portion of the high-resolution surface QRS was performed in 119 normal subjects (N), 62 patients with ventricular tachycardia (VT) including 20 patients with sustained VT or VF (VTs/VF) and in 565 ischemic and nonischemic cardiac patients (NO-VT). High-resolution surface ECG (SAECG) was obtained during sinus rhythm with noise level below 0.4 microV by ART-1200EPX. The vector magnitude of the filtered and signal-averaged standard bipolar orthogonal leads X, Y, Z (V = square root of X2 + Y2 + Z2) were used for analysis. Total duration of the QRS (QRST), the duration of the low amplitude (40 microV) signals in the terminal portion of the QRS (D40) and the amplitude of the signals in the last 40 ms (V40) were measured at filter settings of both 25Hz and 40Hz by the computer. Specific values for each of the indices were identified at both 25Hz and 40Hz filterings, which could separate N as well as NO-VT from VTs/VF. They were greater than or equal to 120 ms for QRST, greater than or equal to 34 ms for D40 and less than or equal to 25 microV for V40 at 25Hz, greater than or equal to 120 ms for QRST, greater than or equal to 39 ms for D40 and less than or equal to 20 microV for V40 at 40 Hz filtering.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Experimental model of fatal arrhythmia after myocardial infarction].
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Animals↗