High-resolution Mapping of Hyperglycemia-induced Gastric Slow Wave Dysrhythmias

BACKGROUND/AIMS: It is now recognised that gastric dysrhythmias are best characterised by their spatial propagation pattern. Hyperglycemia is an important cause of gastric slow wave dysrhythmia, however, the spatiotemporal patterns of dysrhythmias in this context have not been investigated. This study aims to investigate the relationship between hyperglycemia and the patterns of dysrhythmias by employing high-resolution (multi-electrode) mapping simultaneously at the anterior and posterior gastric serosa. METHODS: High-resolution mapping (8 × 16 electrodes per serosal) was performed in 4 anesthetized hounds. Baseline recordings (21 ± 8 minutes) were followed by intravenous injection of glucagon (0.5 mg per dose) and further recordings (59 ± 15 minutes). Blood glucose levels were monitored manually using a glucose sensing kit at regular 5-minute intervals. Slow wave activation maps, amplitudes, velocity, anisotropic ratio, and frequency were calculated. Differences were compared between baseline and post glucagon injection. RESULTS: Baseline slow waves propagated symmetrically and antegrade. The blood glucose levels were increased by an average of 112% compared to the baseline by the end of the recordings. All subjects demonstrated elevated incidence of slow wave dysrhythmias following injection compared to the baseline (48 ± 23% vs 6 ± 4%, P < 0.05). Dysrhythmias arose simultaneously or independently on anterior and posterior serosa. Spatial dysrhythmias occurred before and persisted after the onset and disappearance of temporal dysrhythmias. CONCLUSIONS: Infusion of glucagon induced gastric slow wave dysrhythmias, which occurred across a heterogeneous range of patterns and frequencies. The spatial dysrhythmias of gastric slow waves were shown to be more prevalent and persisted over a longer period of time compared to the temporal dysrhythmias.

Effect of vincristine on the myoelectric activity and motility of the small intestine in rats / 中华消化杂志

Objective To investigate the effects of vincristine on myoelectric activity and motility of the small intestine in conscious rats and its mechanism. Methods Seventy-two SD rats were divided into six groups. The rats in control group were received 0.9% NaCl solution (n=18). The rats in group B were injected with vincristine and subdivided into 0.25 mg/kg(n=6) ,0.5 mg/kg(n=6)and 0.75 mg/kg groups. The group C and D was false operation (n=6)and false operation plus injection with 0.75 mg/kg of vincristine(n=6), respectively. The group E and F was subdiaphragmatic vagotomy plus 0.9% NaCl (n=6) or subdiaphragmatic vagotomy plus 0.75 mg/kg of vincristine (n=6), respectively. The myoelectric activity and motility of the small intestine were recorded. The frequency and area under the curve of slow wave, the periodicity of the migrating myoelectrie complex (MMC) and the duration of MMC Ⅲ were analyzed. The expressions of the myenteric neurons and interstitial cells of Cajal were evaluated by immunofluorescence stain. Results The myoelectric activity in 0.25mg/kg group was not different from the controls, but it changed in 0.5 mg/kg and 0.75 mg/kg groups which correlated with the time of vincristine injection. The irregular spike activity arose and accompanied with disruption of the MMC at (51±14.27) minutes,but recovered at (78.33±13.08) minutes. The periodicity was shorter in 0.5mg/kg [(343.17±142.93)s]and 0.75 mg/kg groups [(302.67±66.67)s] compared with controls [(740.22± 98.92) s, F=31.325, P<0.01]. Three days after vincristine administration, the area under the curve of slow wave decreased to (2.56±0.30) mV·s in 0.5 mg/kg group and (2.57±0.56) mV·s in 0.75 mg/kg group compared with the controls ((4.10±0.80) mV·s , F = 11.442, P<0.01). The intestinal propulsive rate was lower in 0.75 mg/kg group compared with the controls [(33.59±1.43) vs(60.34±2.41)%,t= 23.36, P<0.01]. The expression of the interstitial cells of Cajal was less than those in controls. Three days later, the area under the curve of slow wave in F group was less than that in controls. Conclusions Vincristine provokes alterations of myoelectric activity and motility of the small intestine. The early vincristine-induced escalating in myoelctric activity of the small intestine is through vagus nerve pathway. The decreased motility is contributed to the damage of the interstitial cells of Cajal.

A study on the mechanism of altered gastrointestinal motility in portal hypertensive rats / 中国普通外科杂志

Objective To evaluate the mechanism of altered gastrointestinal motility in portal hypertensive rats. Methods Thirty-two male Sprague-Dawley rats were divided into four groups:sham- operation control (SO, n=8), prehepatic portal hypertension by partial stenosis of the portal vein (PHPH, n=8 ), intrahepatic portal hypertension induced by injection of CCl 4 (IHPH, n=8), and intrahepatic portal hypertension with portacaval shunt (IHPH-PCS, n=8). Gastrointestinal myoelectrical activity and motility were monitored. Gastrointestinal hormones were measured with radioimmunoassay.Results Compared with SO rats, gastrointestinal motor index(MI) were reduced and abnormal myoelectrical activity were recorded (P