Sheng li xue bao : [Acta physiologica Sinica]
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On the isolated perfused heart model of septic rats, the present study showed that: (1) Calcium content and 45Ca-influx of myocardium increased 190%, 208% (P < 0.01) and that of mitochondria elevated 332%, 178% (P < 0.01) respectively with no change of myocardial 45Ca-release during sepsis. (2) 10(-8) mol/L calcitonin gene-related peptide (CGRP) or 10(-7) mol/L atriopeptin (ANP) added into the Krebs-Henseleit solution could effectively reduce 45Ca-influx to myocardium and mitochondria with no effect on myocardial 45Ca-release. (3) The calcium uptake reserve of mitochondria evaluated in vitro showed that the maximal calcium uptake and uptake velocity of mitochondria during sepsis were reduced 34.6%, 33.3% (P < 0.01) respectively. The data suggested that the net increase of myocardial Ca2+ content resulted from increase of 45Ca-influx with no change of 45Ca-efflux and the reduction of mitochondrial Ca2+ buffering capacity during sepsis were key events in the pathogenesis of intracellular Ca(2+)-overload. CGRP and ANP could effectively alleviate Ca(2+)-overload of myocardium and mitochondria. This may have some cellular protection action during sepsis.
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End-tidal CO2 (ET-CO2) provides a continuous and sensitive monitoring of proper pulmonary ventilation in artificially ventilated animals during single unit recordings of the central nervous system. To determine a reliable standard of ET-CO2 in anesthetized and paralyzed animal, the relationship between ET-CO2 and arterial blood pressure (ABP) was observed in cat under different ventilation level. The results showed that ABP changed tremendously with variation in ventilation, but remained constant at a normal level as long as ET-CO2 was maintained within the range between 4.0-5.0%, i.e. optimally at 4.5 +/- 0.5%.
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With electric stimulation of the splanchnic nerve or the skin of the tip of rabbit's ear to measure visceral or somatic pain threshold, we studied the effects of noradrenaline microinjection into the septal nucleus on visceral pain and somatic pain and the relationship between the intraseptal noradrenaline and the intra-PAG opiate peptidergic system. There was no effect on visceral pain threshold after injections of alpha-agonist clonidine (10 micrograms/2 microliters) or alpha-antagonist phentolamine (10 micrograms/2 microliters). In a group injected with beta-agonist isoprenaline (1 micrograms/2 microliters), visceral pain threshold was raised remarkably, while beta-antagonist propranolol (10 micrograms/2 microliters) injected into bilateral septal nuclei decreased visceral pain threshold. ⋯ Microinjection of anti-leu-enkephalin antiserum (1:20,000) into PAG also attenuated the analgesia. When microinjection of isoprenaline into septal nucleus produced analgesia, the release of leu-enkephalin immunoreactive-like-substance in PAG was significantly increased. The results suggest that the analgesic effect of intra-septal noradrenaline on visceral pain is somehow related with the endogenous opiate peptidergic system in PAG, and the leu-enkephalin in PAG plays an important role in this process.
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The Bezold-Jarisch reflex induced by intracoronary injection of nicotine (ICIN) of 5 micrograms/kg was studied in 40 anesthetized rabbits. Heart rate (HR), arterial blood pressure (ABP), left ventricular pressure (IVP), left ventricular dp/dt (LV dp/dt) and cardiac output (CO) were monitored and total peripheral resistance (TPR) was calculated. HR, ABP, LVP and LV dp/dt were decreased following ICIN. ⋯ With the heart paced artificially to prevent bradycardia, the decreases in CO, TPR and ABP were still significant. Bilateral stellate ganglion section plus atropinization which abolished the decreases in HR and CO, did not significantly change the hypotensive response to ICIN. These data suggest that the hypotension evoked by Bezold-Jarisch reflex in rabbit is largely due to the decreases in TPR and partially caused by the decrease in CO.