Central cholinergic and alpha-adrenergic mediation of gastric slow wave dysrhythmias evoked during motion sickness

1995 ◽  
Vol 268 (4) ◽  
pp. G539-G547 ◽  
Author(s):  
W. L. Hasler ◽  
M. S. Kim ◽  
W. D. Chey ◽  
V. Stevenson ◽  
B. Stein ◽  
...  
Keyword(s):  
Animal Models ◽  
Motion Sickness ◽  
Slow Wave ◽  
Muscarinic Antagonist ◽  
Circular Vection ◽  
Gastric Slow Wave ◽  
Cholinergic Pathways ◽  
Wave Disturbances ◽  
Gastric Dysrhythmias ◽  
Endogenous Prostaglandins

Motion sickness is associated with gastric slow wave disruption. Animal models of slow wave disturbances show dependence on neural and prostaglandin pathways. Roles of these pathways in circular vection-evoked gastric dysrhythmias and nausea were tested. Eight volunteers with histories of motion sickness underwent vection (60 degrees/s), during which nausea (0 = none to 3 = severe) and electrogastrographic parameters were assessed. Tachygastric activity was expressed as the signal percentage at frequencies of > 4.5 cycles/min. Circular vection induced a maximal nausea score of 2.8 +/- 0 at 513 +/- 66 s. Tachygastric activity increased from 18 +/- 2 to 37 +/- 4% (P < 0.05) and peaked before maximal nausea. Atropine reduced nausea scores to 0 +/- 0 (P < 0.01) with no increase in tachygastric activity (14 +/- 6%). In contrast, the peripheral muscarinic antagonist methscopolamine did not reduce tachygastric activity (46 +/- 4%), nausea (1.8 +/- 0.5), or time to maximal tachygastric activity (504 +/- 80 s) with vection. Phentolamine reduced nausea (1.5 +/- 0.3, P < 0.01) and tachygastric activity, and delayed their onset, whereas propranolol and naloxone had no effect. Pretreatment with oral indomethacin (50 mg) three times daily for 3 days had no effect on vection-evoked tachygastric activity or nausea. To conclude, circular vection evokes gastric dysrhythmias that correlate temporally with maximal nausea and are suppressed by atropine, but not methscopolamine, and are reduced by phentolamine. In contrast to other models of slow wave disruption, endogenous prostaglandins play no role. Thus central cholinergic pathways mediate vection-evoked dysrhythmias with additional modulation by alpha-adrenergic pathways.

Effects of ginger on motion sickness and gastric slow-wave dysrhythmias induced by circular vection

2003 ◽  
Vol 284 (3) ◽  
pp. G481-G489 ◽  
Author(s):  
Han-Chung Lien ◽  
Wei Ming Sun ◽  
Yen-Hsueh Chen ◽  
Hyerang Kim ◽  
William Hasler ◽  
...  
Keyword(s):  
Motion Sickness ◽  
Crossover Design ◽  
Controlled Study ◽  
Double Blind ◽  
Vasopressin Release ◽  
Circular Vection ◽  
Gastric Slow Wave ◽  
Gastric Dysrhythmias ◽  
Plasma Vasopressin ◽  
History Of

Ginger has long been used as an alternative medication to prevent motion sickness. The mechanism of its action, however, is unknown. We hypothesize that ginger ameliorates the nausea associated with motion sickness by preventing the development of gastric dysrhythmias and the elevation of plasma vasopressin. Thirteen volunteers with a history of motion sickness underwent circular vection, during which nausea (scored 0–3, i.e., none to severe), electrogastrographic recordings, and plasma vasopressin levels were assessed with or without ginger pretreatment in a crossover-design, double-blind, randomized placebo-controlled study. Circular vection induced a maximal nausea score of 2.5 ± 0.2 and increased tachygastric activity and plasma vasopressin. Pretreatment with ginger (1,000 and 2,000 mg) reduced the nausea, tachygastria, and plasma vasopressin. Ginger also prolonged the latency before nausea onset and shortened the recovery time after vection cessation. Intravenous vasopressin infusion at 0.1 and 0.2 U/min induced nausea and increased bradygastric activity; ginger pretreatment (2,000 mg) affected neither. Ginger effectively reduces nausea, tachygastric activity, and vasopressin release induced by circular vection. In this manner, ginger may act as a novel agent in the prevention and treatment of motion sickness.

Role of plasma vasopressin as a mediator of nausea and gastric slow wave dysrhythmias in motion sickness

1997 ◽  
Vol 272 (4) ◽  
pp. G853-G862 ◽  
Author(s):  
M. S. Kim ◽  
W. D. Chey ◽  
C. Owyang ◽  
W. L. Hasler
Keyword(s):  
Motion Sickness ◽  
Slow Wave ◽  
Vasopressin Release ◽  
Vasopressin Infusion ◽  
Gastric Slow Wave ◽  
Gastric Dysrhythmias ◽  
Plasma Vasopressin ◽  
Beneficial Action ◽  
Asymptomatic Subjects

The possible role of vasopressin in nausea and gastric dysrhythmias in motion sickness was tested by electrogastrography in 14 subjects during circular vection (60 degrees/s) and vasopressin infusion. Tachygastria was expressed as the signal percent >4.5 cycles/min. Vection evoked nausea scores of 2.6 +/- 0.2 (0 = none to 3 = severe) in 10 subjects with increases in tachygastric activity (15 +/- 2 to 45 +/- 3%) and plasma vasopressin (4.5 +/- 1.5 to 8.4 +/- 2.5 pg/ml) that were blocked by atropine but not indomethacin. Four asymptomatic subjects had no tachygastria or vasopressin release. Vasopressin at 0.2 U/min (plasma level = 322.1 +/- 10.3 pg/ml) evoked nausea (2.6 +/- 0.4) and increases in tachyarrhythmic activity (41 +/- 5%) that were blunted by atropine but not indomethacin. There were no differences in nausea or dysrhythmias with vasopressin infusion in subjects who noted nausea during vection versus those who did not. To conclude, vection evokes nausea, dysrhythmias, and vasopressin release in motion sickness-susceptible humans via cholinergic prostaglandin-independent pathways. Supraphysiological vasopressin infusions evoke nausea and dysrhythmias by similar pathways to equal degrees in motion sickness-susceptible and -resistant subjects. Thus central but not peripheral actions of vasopressin may contribute to nausea and slow wave disruption with vection. Blunting of both the release and action of vasopressin by atropine may explain its beneficial action in motion sickness.

VI. Pathogenesis and therapeutic approaches to human gastric dysrhythmias

2002 ◽  
Vol 283 (1) ◽  
pp. G8-G15 ◽  
Author(s):  
Chung Owyang ◽  
William L. Hasler
Keyword(s):  
Slow Wave ◽  
Animal Studies ◽  
Nausea And Vomiting ◽  
Causative Role ◽  
Therapeutic Approaches ◽  
Receptor Antagonists ◽  
Gastric Slow Wave ◽  
Dopamine Receptor Antagonists ◽  
Gastric Dysrhythmias ◽  
Intestinal Delivery

This review describes recent advances in our knowledge about the pathogenesis and therapeutic approaches to human gastric dysrhythmias. A number of clinical conditions has been found to be associated with gastric slow-wave rhythm disturbances that may relate to the induction of nausea and vomiting. Human and animal studies indicate that multiple neurohumoral factors are involved in the generation of gastric dysrhythmias. Antral distension and increased intestinal delivery of lipids may cause slow-wave disruption and development of nausea. This may be mediated by cholinergic and serotonergic pathways. Similarly, progesterone and estrogen may also disrupt gastric slow-wave rhythm in susceptible individuals. Prostaglandin overproduction in gastric smooth muscle appears to mediate slow-wave disruption in diabetes and with tobacco smoking. On the other hand, central cholinergic pathways play an important role in the genesis of gastric dysrhythmias associated with motion sickness. This may be mediated by vasopressin released from the pituitary. Although it is difficult to ascribe with certainty a causative role of slow-wave rhythm disturbances in the genesis of nausea and vomiting, the search has begun for novel antiemetic therapies based on their abilities to ablate or prevent gastric dysrhythmia formation. This includes the use of prostaglandin synthesis inhibitors, central muscarinic receptor antagonists, and dopamine receptor antagonists. Finally direct gastric electrical stimulation using a surgically implanted neurostimulator has shown promise in reducing emesis in patients with gastroparesis and gastric dysrhythmias.

Progesterone and estrogen are potential mediators of gastric slow-wave dysrhythmias in nausea of pregnancy

1996 ◽  
Vol 270 (3) ◽  
pp. G506-G514 ◽  
Author(s):  
J. W. Walsh ◽  
W. L. Hasler ◽  
C. E. Nugent ◽  
C. Owyang
Keyword(s):  
Pregnant Women ◽  
Slow Wave ◽  
First Trimester ◽  
Additive Effect ◽  
Signal Power ◽  
Recording Time ◽  
Gastric Slow Wave ◽  
Gastric Dysrhythmias ◽  
First Trimester Of Pregnancy ◽  
In Pregnancy

Women in pregnancy experience nausea, which correlates with gastric slow-wave rhythm disruption. Mediators of these dysrhythmias were explored. To quantitate slow-wave disruption, eight pregnant women with first-trimester nausea underwent electrogastrography after a 250-kcal meal. Results were compared with nonpregnant women with nausea during a prior pregnancy who received estradiol and/or progesterone to levels of the first trimester of pregnancy. Five pregnant women exhibited dysrhythmias, with increases in combined recording time in tachygastria plus bradygastria, as well as decreases in the percentage of electrogastrography signal power in the normal 3 cycle/min range (cpm), compared with nonpregnant women (P<0.05). Estradiol did not evoke dysrhythmias in nonpregnant women; however, progesterone induced increases in recording time in bradygastria plus tachygastria and increases in bradygastric signal power with corresponding decreases in signal power in the 3-cpm range (P<0.05). With estradiol and progesterone coadministration, an additive effect was observed at 3.3 +/- 0.8 h, with increased recording time in bradygastria alone and in bradygastria plus tachygastria with corresponding increases in bradygastric signal power and decreases in power in the 3-cpm range (P<0.05). In conclusion, women with nausea of pregnancy exhibit slow-wave rhythm disruption. Similar dysrhythmias are evoked in nonpregnant women by progesterone alone or in combination with estradiol in doses that reproduce levels in pregnancy. Thus gastric dysrhythmias in pregnancy may be due to a combination of elevated progesterone and estrogen levels.

Mechanisms of burn-induced impairment in gastric slow waves and emptying in rats

2010 ◽  
Vol 299 (1) ◽  
pp. R298-R305 ◽  
Author(s):  
Hanaa S. Sallam ◽  
Hermes M. Oliveira ◽  
Suhuan Liu ◽  
Jiande D. Z. Chen
Keyword(s):  
Gastric Emptying ◽  
Slow Wave ◽  
Delayed Gastric Emptying ◽  
Burn Injury ◽  
Wave Activity ◽  
Cyclooxygenase 2 ◽  
Slow Waves ◽  
Gastric Slow Wave ◽  
Gastric Slow Waves ◽  
Gastric Dysrhythmias

Delayed gastric emptying is common following severe large cutaneous burns; however, the mechanisms of burn-induced delayed gastric emptying remain unknown. The aim of this study was to explore the possible involvement of hyperglycemia and cyclooxygenase-2 receptors in the burn-induced gastric dysrhythmias. Gastric slow waves and gastric emptying were assessed in rats 6 h following sham or burn injury. Animals were randomized to one sham-burn and seven burn groups: untreated; two groups of saline treated (control); insulin treated (5 IU/kg); cyclooxygenase-2 inhibitor treated (10 mg/kg); ghrelin treated (2 nmol/rat); and gastric electrical stimulation treated. It was found that 1) severe burn injury impaired gastric slow waves postprandially and delayed gastric emptying; 2) the impairment in gastric slow waves included a decrease in the slow-wave frequency and in the percentage of normal slow waves, and an increase in the percentage of bradygastria ( P = 0.001, 0.01, and 0.01, respectively vs. preburn values). None of the gastric slow-wave parameters was significantly correlated with gastric emptying; 3) cyclooxygenase-2 inhibitor normalized burn-induced delayed gastric emptying ( P = 0.3 vs. sham-burn), but not gastric dysrhythmias ( P < 0.002 vs. sham), whereas insulin normalized both gastric emptying ( P = 0.4 vs. sham-burn) and gastric dysrhythmias ( P = 0.3 vs. sham-burn); 4) both gastric electrical stimulation and ghrelin accelerated burn-induced delayed gastric emptying ( P = 0.002 and 0.04, respectively, vs. untreated burn). In conclusion, hyperglycemia alters gastric slow-wave activity and delayed gastric emptying, while cyclooxygenase-2 inhibition delays gastric emptying without altering gastric slow-wave activity.

Capabilities and limitations of electrogastrogram in the detection of normal gastric slow wave and gastric dysrhythmias

2000 ◽  
Vol 118 (4) ◽  
pp. A851
Author(s):  
Zhishun Wang ◽  
Liwei Qian ◽  
Tatsuyuki Ueno ◽  
Hui Ouyang ◽  
Jiande Chen
Keyword(s):  
Slow Wave ◽  
Gastric Slow Wave ◽  
Gastric Dysrhythmias

Mediation of hyperglycemia-evoked gastric slow-wave dysrhythmias by endogenous prostaglandins

1995 ◽  
Vol 108 (3) ◽  
pp. 727-736 ◽  
Author(s):  
William L. Hasler ◽  
Hani C. Soudah ◽  
Gareth Dulai ◽  
Chung Owyang
Keyword(s):  
Slow Wave ◽  
Gastric Slow Wave ◽  
Endogenous Prostaglandins

Serosal and cutaneous recordings of gastric myoelectrical activity in patients with gastroparesis

1994 ◽  
Vol 266 (1) ◽  
pp. G90-G98 ◽  
Author(s):  
J. D. Chen ◽  
B. D. Schirmer ◽  
R. W. McCallum
Keyword(s):  
Electrical Stimulation ◽  
Slow Wave ◽  
Test Meal ◽  
Frequency Change ◽  
Fasting State ◽  
Gastric Myoelectrical Activity ◽  
Myoelectrical Activity ◽  
Gastric Slow Wave ◽  
Student’S T ◽  
Student’S T Test

The aims of this study were to 1) investigate gastric myoelectrical activity in patients with gastroparesis, 2) validate the cutaneous electrogastrogram (EGG) in tracking the frequency change of the gastric slow wave, and 3) investigate the effect of electrical stimulation on gastric myoelectrical activity. Gastric myoelectrical activity was recorded in 12 patients with documented gastroparesis using serosal electrodes for > 200 min in each subject. All recordings were made at least 4 days after surgery. Each session consisted of a 30-min recording in the fasting state and a 30-min recording after a test meal. The test meal (liquid or mixed) was selected according to patient's tolerance. Electrical stimulation was performed in three subjects via the serosal electrodes at a frequency of 3 cycles/min. Gastric myoelectrical activity was recorded using serosal electrodes in each session. The serosal recording showed slow waves of 2.5 to 4.0 cycles/min in all 12 subjects. Absence of spikes was noted in 11 of the 12 subjects. The simultaneous serosal and cutaneous recording of gastric myoelectrical activity showed that the frequency of the EGG was exactly the same as that of the serosal recording. Liquid meals resulted in a significant decrease in slow-wave frequency (Student's t test, P = 0.006), and the EGG accurately reflected this change. Electrical stimulation had no effect on the frequency of the gastric slow wave and did not induce spikes.(ABSTRACT TRUNCATED AT 250 WORDS)

Su1561 Neuropathway Involved in the Ameliorating Effect of Electroacupuncture at ST36 on Gastric Slow Wave Dysrhythmia in Rats

2016 ◽  
Vol 150 (4) ◽  
pp. S526
Author(s):  
Nina Zhang ◽  
Shuang Zhang ◽  
Jieyun Yin ◽  
Pankaj J. Pasricha ◽  
Jiande Chen
Keyword(s):  
Slow Wave ◽  
Gastric Slow Wave
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