A quantitative analysis of peptidergic innervation in sinoatrial node in cases of sudden manhood death syndrome / 法医学杂志

OBJECTIVE@#To study the distribution and proportion of neuropeptide containing nervers in the sinus node in cases of sudden manhood death syndrome (SMDS) and to explore the mechanism of SMDS.@*METHODS@#Immunohistochemical staining and quantitative analysis of neuropeptide Y (NPY) and vasoactive intestinal peptide(VIP) in the sinus node in 6 cases of SMDS and in 12 cases of non-cardiac death(control group) were achieved by LSAB method and computerized image system.@*RESULTS@#As for NPY positive materials, VIP positive materials and the ratio of VIP/NPY in the sinus nodes, there were no significant difference between the control group and SMDS group.@*CONCLUSION@#The mechanism of SMDS and the abnormality of autonomic nervous innervation in the sinoatrial nodes maybe incorrelation.

Heart rate responses to a muscarinic agonist in rats with experimentally induced acute and subacute chagasic myocarditis

We administered arecoline to rats, with experimentally induced chagasic myocarditis, in order to study the sinus node sensitivity to a muscarinic agonist. Sixteen month old rats were inoculated with 200,000 T. cruzi parasites ("Y" strain). Between days 18 and 21 (acute stage), 8 infected rats and 8 age-matched controls received intravenous arecoline as a bolus injection at the following doses: 5.0, 10.0, 20.0, 40.0, and 80.0 mug/kg. Heart rate was recorded before, during and after each dose of arecoline. The remaining 8 infected animals and 8 controls were subjected to the same experimental procedure during the subacute stage, i.e., days 60 to 70 after inoculation. The baseline heart rate, of the animals studied during the acute stage (349 Ý 68 bpm, mean Ý SD), was higher than that of the controls (250 Ý 50 bpm, p < 0.005). The heart rate changes were expressed as percentage changes over baseline values. A dose-response curve was constructed for each group of animals. Log scales were used to plot the systematically doubled doses of arecoline and the induced-heart rate changes. The slope of the regression line for the acutely infected animals (r = - 0.99, b =1.78) was not different from that for the control animals (r = - 0.97, b = 1.61). The infected animals studied during the subacute stage (r = - 0.99, b = 1.81) were also not different from the age-matched controls (r = - 0.99, b = 1.26, NS). Consequently, our results show no pharmacological evidence of postjunctional hypersensitivity to the muscarinic agonist arecoline. Therefore, these results indirectly suggest that the postganglionic parasympathetic innervation, of the sinus node of rats with autopsy proved chagasic myocarditis, is not irreversibly damaged by Trypanosoma cruzi.

Baroreflex control of sympathetic activity in experimental hypertension

The arterial baroreceptor reflex system is one of the most powerful and rapidly acting mechanisms for controlling arterial pressure. The purpose of the present review is to discuss data relating sympathetic activity to the baroreflex control of arterial pressure in two different experimental models: neurogenic hypertension by sinoaortic denervation (SAD) and high-renin hypertension by total aortic ligation between the renal arteries in the rat. SAD depresses baroreflex regulation of renal sympathetic activity in both the acute and chronic phases. However, increased sympathetic activity (100 percent) was found only in the acute phase of sinoaortic denervation. In the chronic phase of SAD average discharge normalized but the pattern of discharges was different from that found in controls. High-renin hypertensive rats showed overactivity of the renin angiotensin system and a great depression of the baroreflexes, comparable to the depression observed in chronic sinoaortic denervated rats. However, there were no differences in the average tonic sympathetic activity or changes in the pattern of discharges in high-renin rats. We suggest that the difference in the pattern of discharges may contribute to the increase in arterial pressure lability observed in chronic sinoaortic denervated rats.

Neural and humoral mechanisms involved in the generation of arterial pressure lability in rats

1. The role of the renin-angiotensin system (RAS) and sympathetic nervous system (SNS) in the generation of the arterial pressure lability (APL) observed after sino-aortic deafferentation (SAD) in rats was evaluated. 2. SAD was performed in normotensive (N = 8), renal hypertensive (2K-1C, N = 8) and spontaneously hypertensive rats (SHR, N = 8) and mean arterial pressure (MAP) recordings were performed 24 h after SAD. 3. MAP was recorded by a computerized technique using a sampling frequency of 30 Hz for 30 min and the data obtained were used to calculate APL. After MAP measurements the activity of the RAS and SNS was pharmacologically evaluated in all groups by the changes in MAP in response to iv injection of captopril and hexamethonium chloride, respectively. 4. SAD produced an increase in MAP (118 +/- 4 vs 99 +/- 2 mmHg) and a large increase in APL (13.4 +/- 1.3 vs 3.8 +/- 0.3 mmHg) in normotensive rats. SAD produced no changes in MAP (161 +/- 7 vs 167 +/- 7 mmHg) in 2K-1C hypertensive rats but induced a large increase in APL (6.7 +/- 0.5 vs 12 +/- 1 mmHg). SAD also produced no changes in MAP (152 +/- 3 vs 152 +/- 4 mmHg) in SHR but induced a marked increase in APL (6.7 +/- 0.3 vs 21 +/- 2.3 mmHg). 5. All SAD rats presented a larger fall in MAP in response to captopril and hexamethonium than the respective control group with intact baroreceptors suggesting an overactivity of both systems after SAD in normotensive, renal hypertensive and spontaneously hypertensive rats. 6. The data also show that SAD produced no additional increase in MAP but promoted a significant increase in APL in renal and spontaneously hypertensive rats. 7. We suggest that APL observed after SAD in different experimental models is dependent on an interaction of RAS and SNS, both of which seem to be overactive after removal of arterial baroreceptors