We compared the cardiovascular response to the gastric infusion of distilled water (DI) with that to the gastric infusion of 0.9% saline (SI) and gastric ballooning with 37 degrees C water (BA) through a gastric fistula in splenectomized mongrel dogs (n = 7). DI, and SI amounting to 5% of body wt and the same volume of water were infused in approximately 20 s through the tube and responses in mean arterial pressure (MAP), CVP, heart rate (HR), and intra-esophageal pressure (EP) were monitored continuously. After DI, SI, and BA, the measured variables showed significant increases and attained maximal increases at about 2 min after the treatments. After DI, the maximum elevation in MAP was 21.3 +/- 1.9 mmHg and 2 times higher than in SI and BA. The corresponding value in CVP was 5.0 +/- 0.3 mmHg and 2-3 times higher than with SI and BA, and HR increased by 26.1 +/- 3.0 beats/min showing 3 to 6 times larger increases compared with SI and BA. These gastro-cardiovascular reflexes were abolished after subdiaphragmatic truncal vagotomy. These findings suggest that both the mechanical and osmotic stimuli to the stomach induce cardiovascular reflexes and that the vagus is involved in the reflex.
Analysis of creatoi (CTL, 5-hydroxycreatinine), an oxidative creatinine (Cr) metabolite, in serum and urine of human subjects has indicated that CTL is a useful determinant of renal function. The existence itself of serum CTL (s-CTL) could be a diagnostic sign for chronic renal failure (CRF): in all normal subjects, s-CTL was undetectable, but s-CTL was detectable in sera of all patients with CRF (s-Cr: > 2.0 mg/dl). And the s-CTL values increased in proportion to the severity of CRF in such patients. Furthermore, the molar ratio (CTL/Cr) in both urine and serum increased significantly in proportion to the severity of CRF. Our results indicated not only hyperproduction of CTL but also higher oxygen stress in patients according to the progression of CRF. The diagnostic importance of the CTL value and the CTL/Cr ratio are discussed.
We identified an impact of CYP inducers/inhibitors on the CLB concentration. Our findings demonstrated that clinically relevant interactions occur between CLB and concomitant antiepileptic drugs.
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