Impaired chemoreflex sensitivity during septic shock induced by cecal ligation and perforation.

In this study, we sought to determine the effects produced by cecal ligation and perforation (CLP) on the autonomic responses to the activation of peripheral chemoreflexes in conscious rats. The peripheral chemoreflex was activated with potassium cyanide (KCN; 40 µg·(0.1 mL)(-1); intravenous injection (i.v.)) in male Wistar rats 3, 6, 12, and 24 h after CLP or sham surgery. The mean arterial pressure (MAP), heart rate (HR), and respiratory frequency (fR) were recorded simultaneously. CLP surgery reduced the baseline MAP when compared with the sham animals. In the animals of the sham group, the autonomic responses to KCN produced increases in MAP and fR as well as a decrease in HR. However, 12 and 24 h after CLP surgery, the autonomic responses to KCN were attenuated. The restoration of MAP by i.v. injected l-NAME or phenylephrine did not restore the autonomic response to KCN in rats subjected to CLP. These data show that septic shock induced by CLP compromised the autonomic responses to peripheral chemoreflex activation in conscious rats, suggesting that an important regulatory mechanism is impaired during the course of this condition.

Hypotensive effect of aqueous extract of Averrhoa carambola L. (Oxalidaceae) in rats: an in vivo and in vitro approach.

AIM OF THE STUDY: Averrhoa carambola L. (Oxalidaceae) leaves are used in Brazilian traditional medicine to treat hypertension. This study was conducted to evaluate the hypotensive effect of the aqueous extract of Averrhoa carambola (AEAc) and its underlying mechanisms in the isolated rat aorta. MATERIALS AND METHODS: The effect of AEAc on the mean arterial pressure (MAP) was determined in vivo in anesthetized rats. In vitro, thoracic aortic rings were isolated and suspended in organ baths, and the effects of AEAc were studied by means of isometric tension recording experiments. In HPLC analysis, the fingerprint chromatogram of AEAc was established. RESULTS: In normotensive rats, AEAc (12.5-50.0 mg/kg, i.v.) induced dose-dependent hypotension. In vitro, AEAc caused a depression in the E(max) response to phenylephrine without a change in sensibility. Also, in a depolarized Ca(2+)-free medium, AEAc inhibited CaCl(2)-induced contractions and caused a concentration-dependent rightward shift of the response curves, indicating that AEAc inhibited the contractile mechanisms involving extracellular Ca(2+) influx. CONCLUSIONS: These results demonstrate the hypotensive effects of AEAc, and these effects may, in part, be due to the inhibition of Ca(2+), which supports previous claims of its traditional use.