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PubMed2004

Presence of C-type natriuretic peptide (CNP) in guinea pig caecum: role and mechanisms of CNP in circular smooth muscle relaxation.

The distribution and role of C-type natriuretic peptide (CNP) in the gastrointestinal tract are still unclear. This study was designed to investigate the distribution of CNP in guinea pig caecum and the inhibitory mechanisms of CNP in caecal circular smooth muscle cells. CNP immunoreactivity was recognized in smooth muscle cells, myenteric and submucosal neurons of the caecum by immunohistochemistry. CNP mRNA expression was demonstrated in both freshly dispersed and cultured smooth muscle cells by reverse-transcription polymerase chain reaction. CNP inhibited 1 nmol L(-1) cholecystokinin octapeptide (CCK-8)-induced smooth muscle cell contraction in a dose-dependent manner, with an IC(50) value of 0.24 nmol L(-1), and significantly stimulated the production of intracellular cyclic guanosine monophosphate. Furthermore, inhibitors of both soluble and particulate guanylate cyclase (GC) partially but significantly inhibited CNP-induced relaxation. This is the first report demonstrating that CNP localizes in gastrointestinal smooth muscle cells and the enteric nervous system. These results suggest that CNP acts locally through neural and autocrine pathways to modulate colonic motility via both particulate and soluble GC systems. These two pathways appear to be through natriuretic peptide receptor (NPR)-B, which has particulate GC domain, and NPR-C, which activates soluble GC, judging from previous findings that NPR-A is not expressed in these cells.

Animals↗
PubMed1988

Optimization of respiratory muscle relaxation during mechanical ventilation.

The authors calculated the active work of inspiration (Wp) and the inspiratory muscle pressure-time product (integral of Pmus.dt) in seven patients undergoing mechanical ventilation (MV). This was done by comparing the areas under the inflation pressure-volume and inflation pressure-time curves generated when the patient was contributing to the work of ventilation with those following sedation, when inspiratory muscle activity was absent (defined as absence of diaphragmatic EMG activity and of palpable accessory muscle contraction). Inspiratory muscle inactivity could be predicted by the observation of a smooth rise in inflation pressure that was highly reproducible from breath to breath. Relaxation was present without sedation during MV in the control mode with inspiratory flow rates above 65 1/min. In the assist mode (AMV), both Wp and integral of Pmus.dt were significantly (P less than 0.05) greater than in the control (CMV) mode. Reducing trigger sensitivity during AMV further increased Wp and integral of Pmus.dt (P less than 0.05). During AMV and CMV Wp and integral of Pmus.dt decreased with increasing rate of inspiratory flow delivered by the ventilator. With AMV at low trigger sensitivity and low flow rates, Wp approached 65% of the total inspiratory work. The authors conclude that inspiratory muscle activity can be substantial during MV, particularly during AMV at low trigger sensitivity and flow. Monitoring of inflation pressure is a simple means of determining the degree of inspiratory muscle rest during MV.

Humans↗