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Action of endothelin on the sacral parasympathetic pathway to the colon
October
ABSTRACTS
1990
OF PAPERS
1219
RELEASE OF ENDOGENOUS CATECHOLAMINES DURING VECTIONR.M.Stern, EVOKED GASTRIC DYSRHYTHMIAS IN MAN. K.L.Koch, Depts S.Bingaman, N.Sperry, J.Seaton, T.Harrison. Medicine, Psychology and Surgery, Hershey Medical Center, Penn State University, Hershey , PA 17033. Intravenous infusions of epinephrine in dog an4 man The aim of this stpdy was produce gastric dysrhythmias. to measure endogenous plasma catecholamines.before, during and after vection (illusory self-motion). Vection was produced by rotating a drum lined with ilack and white stripes around seated subjects. Cutaneous electrodes were Blood used to record gastric myoelectrical activity. samples were withdrawn continuously for three five min Results: thirteen healthy periods during vection. subjects were studied; seven developed nausea and 4-9 cpm group) and six remained gastric dysrhythmias (G.D. symptom free and had no dysrhytamias (No G.D. group). drum Gastric dysrhythmias were evoked 2.5 + 1.1 min after Baseline catecholamines were similar in rotation began. Catecholamine results both groups (data not shown). (pg/ml) during the three 5 min periods comprising drum rotation are shown below: 11-15 min 1-5 min 6-10 min Norephinephrine(NE) 1188+141 !129+85x 1261+132* G.D. 848+iO9 739581 780+104 No G.D. Epinephrine(E) 216+35*+ 181+39* 167+44+ G.D. 85T17 86+19 102+29 No G.D. *P
CONTROL OF UES TONE BY LUNG INFLATION REFLEXES. Medda BK. Lang IM. Dodds WJ. Dq.~rtments of Radiology. Surgery and Physiology, Mediclli College of Wisconsin, and Surgical Research Service, Zablocki VAMC. Milwaukee, WI.
ACTION OF ENDOTHELIN ON THB SACRAL PARASYMPATHETIC PATHWAY TO THE COLON. T. Niahimura and J. Krier, Department of Physiology, Michigan State University, East Lansing, MI 48824. The effects of endothelin (ET) on synaptic tran#mission in cat sacral parasympathetic colonic ganglia and on proximal and distal colon circular muscle was studied in vitro using intracellular recording techniques and force measurements. PreViOUBl,', we showed that endothelin-1 (ET) produced membrane depolarization due to activation of calcium and chloride currents in rabbit parasympathetic tmr0m (FASEB J. 4:~976, 1990). Bath application of ET (0.1-l #4) produced membrane depolarization associated After with an increase in membrane conductance. ET-washout, depolarization by ET was often followed by and a decrease in membrane membrane hyperpolarization conductance. ET (1 @l for 3-5 min) blocked orthdromic action potentials elicited by stimulation of pelvic nerve unmasking and then reducing the amplitude of fast excitatory postsynaptic potentials (f-epsp) (from 5-12 mV to 2-6 mV). The actions of ET persisted (10 to 20 min) after removal of ET from the perfusate. We conclude that ET modulates synaptic transmission by membrane depolarization, membrane hyperpolarization and by depression of f-epsp of neurons in cat colonic ganglia. ET (0.1-100 nM) produced a cumulative concentration dependent contraction of circular muscle that persisted (1 to 2 hours) after removal of ET from the perfusete. ET-induced contractions wer 5+blocked by nifedipine (1 @@, suggesting that membrane Ca channels may play an important role in the contractions of ET. ET-induced contraction were not altered by atropine (1 PM), propranolol (1 PM) and by phentolamine (1flM). The data show a diversity of actions of ET on the sacrel parasympathetic pathway to the colon (DK-29920).
THE EFFECT OF MYOTOMY ON THE INITIATION AND PROPAGATION OF THE MYOELECTRIC CORRELATES OF VOMITING. I.M.Lang. Departments of Surgery & Physiology, Medical College of Wisconsin & Surgical Research Service, VAMC, Milwaukee, WI 53295
Upper esophageal sphincter IUESl tone often varies in rhythm with respiration, but the mechanism of this respiratory rhythm is unknown. We conducted studies to determine whether the respiration-related changes in UES tone were generated by reflex activity or central respiratory drive. Twenty-one cats were anesthetized using ketamine (20 mgl kg 1 and bipolar electrodes or strain gauges were implanted on the cricopharyngeus I CP) muscle and diaphragm. Respiratoryrelated UES activity was prciduced by 11, increasing respiratory volume (50 to 100 ml) during artificial respiration, 2) lung inflation by prevention of exhalation 12-3 cycles), and 3) hypercapnia-induced hyperventilation. The effects of cervical vagal or phrenic nerve section were determined. In addition the effects of electrical ll-5V. 1 ms. 10Hz) central vagal stimulation ICVS) or peripheral vagal stimulation (PVS) on UES tpne were determined. We found that lung inflation by all methods increased UES tone in a stimulus-dependent manner and that section of the cervical vagus but not the phrenic nerves blocked these effects. In addition, CVS but not PVS significantly increased UES tone in a stimulusdependent manner. We concluded that 1) central respiratory drive does not alter UES tone, but rather 2) lung inflation reflexes increase UES tone. Therefore, lung inflation reflexes may generate the respiratory rhythm of UES tone which is often observed in animals and man. These studies were funded VA grant 5120-02P ( IML).
by NIH grant
DC00069 (WJD)
and
A retrograde giant contraction (RGC) occurs in association with vomiting and after CCK-8, but the mechanism of its initiation and propagation are unknown. In prior studies we found that myotomy altered both initiation and propagation of the RGC, but the mechanism of these changes was unclear. In order to better understand the results of our prior studies we determined the effect of myotomy on the myoelecuic events associated with RGC: ECA disruption and the RGC potential. Five dogs were chronically implanted with bipolar electrodes on the small intestine from duodenum to ileum. After recording control responses to emetic agents or CCK-8, we performed a seromuscular myotomy of the intestine 60 cm from the pylorus. The myoelectic responses to emetic agents or CCK-8 were re-examined for 2 months after surgery. We found that myotomy blocked the occurrence of RGC potential but not ECA disruption due to emetics (32 ?. 3 cm) or CCK-8 (12 ? 2 cm) in a caudad direction only. This effect partially recovered after 30 days (26 + 6 and 2 f 2 cm). Total intestinal propagation time of the RGC potential did not change (14.8 + .8 s vs 15.8 f .4 s), but propagation velocity below the myotomy slowed significantly (22.6 f 7.5 vs 11.1 + 1.5 cm/s, p < .05). The delay between ECA disruption and RGC potential was not altered. The myoelectric responses to CCK-8 did not propagate through the jejunum and myotomy had no effect on the time of occurrence of these responses. We conclude that 1) the CNS primarily controls the temporal characteristics of the RGC but the ENS controls its spatial characteristics, 2) the ENS conveys a descending influence on the initiation and propagation of the RGC, and 3) ECA disruption may be a prerequisite for the RGC but is not a myoelecnic correlate. These studies were supported
by VA Merit Review Grant 5120-02P.
ABSTRACTS
1990
OF PAPERS
1219
RELEASE OF ENDOGENOUS CATECHOLAMINES DURING VECTIONR.M.Stern, EVOKED GASTRIC DYSRHYTHMIAS IN MAN. K.L.Koch, Depts S.Bingaman, N.Sperry, J.Seaton, T.Harrison. Medicine, Psychology and Surgery, Hershey Medical Center, Penn State University, Hershey , PA 17033. Intravenous infusions of epinephrine in dog an4 man The aim of this stpdy was produce gastric dysrhythmias. to measure endogenous plasma catecholamines.before, during and after vection (illusory self-motion). Vection was produced by rotating a drum lined with ilack and white stripes around seated subjects. Cutaneous electrodes were Blood used to record gastric myoelectrical activity. samples were withdrawn continuously for three five min Results: thirteen healthy periods during vection. subjects were studied; seven developed nausea and 4-9 cpm group) and six remained gastric dysrhythmias (G.D. symptom free and had no dysrhytamias (No G.D. group). drum Gastric dysrhythmias were evoked 2.5 + 1.1 min after Baseline catecholamines were similar in rotation began. Catecholamine results both groups (data not shown). (pg/ml) during the three 5 min periods comprising drum rotation are shown below: 11-15 min 1-5 min 6-10 min Norephinephrine(NE) 1188+141 !129+85x 1261+132* G.D. 848+iO9 739581 780+104 No G.D. Epinephrine(E) 216+35*+ 181+39* 167+44+ G.D. 85T17 86+19 102+29 No G.D. *P
CONTROL OF UES TONE BY LUNG INFLATION REFLEXES. Medda BK. Lang IM. Dodds WJ. Dq.~rtments of Radiology. Surgery and Physiology, Mediclli College of Wisconsin, and Surgical Research Service, Zablocki VAMC. Milwaukee, WI.
ACTION OF ENDOTHELIN ON THB SACRAL PARASYMPATHETIC PATHWAY TO THE COLON. T. Niahimura and J. Krier, Department of Physiology, Michigan State University, East Lansing, MI 48824. The effects of endothelin (ET) on synaptic tran#mission in cat sacral parasympathetic colonic ganglia and on proximal and distal colon circular muscle was studied in vitro using intracellular recording techniques and force measurements. PreViOUBl,', we showed that endothelin-1 (ET) produced membrane depolarization due to activation of calcium and chloride currents in rabbit parasympathetic tmr0m (FASEB J. 4:~976, 1990). Bath application of ET (0.1-l #4) produced membrane depolarization associated After with an increase in membrane conductance. ET-washout, depolarization by ET was often followed by and a decrease in membrane membrane hyperpolarization conductance. ET (1 @l for 3-5 min) blocked orthdromic action potentials elicited by stimulation of pelvic nerve unmasking and then reducing the amplitude of fast excitatory postsynaptic potentials (f-epsp) (from 5-12 mV to 2-6 mV). The actions of ET persisted (10 to 20 min) after removal of ET from the perfusate. We conclude that ET modulates synaptic transmission by membrane depolarization, membrane hyperpolarization and by depression of f-epsp of neurons in cat colonic ganglia. ET (0.1-100 nM) produced a cumulative concentration dependent contraction of circular muscle that persisted (1 to 2 hours) after removal of ET from the perfusete. ET-induced contractions wer 5+blocked by nifedipine (1 @@, suggesting that membrane Ca channels may play an important role in the contractions of ET. ET-induced contraction were not altered by atropine (1 PM), propranolol (1 PM) and by phentolamine (1flM). The data show a diversity of actions of ET on the sacrel parasympathetic pathway to the colon (DK-29920).
THE EFFECT OF MYOTOMY ON THE INITIATION AND PROPAGATION OF THE MYOELECTRIC CORRELATES OF VOMITING. I.M.Lang. Departments of Surgery & Physiology, Medical College of Wisconsin & Surgical Research Service, VAMC, Milwaukee, WI 53295
Upper esophageal sphincter IUESl tone often varies in rhythm with respiration, but the mechanism of this respiratory rhythm is unknown. We conducted studies to determine whether the respiration-related changes in UES tone were generated by reflex activity or central respiratory drive. Twenty-one cats were anesthetized using ketamine (20 mgl kg 1 and bipolar electrodes or strain gauges were implanted on the cricopharyngeus I CP) muscle and diaphragm. Respiratoryrelated UES activity was prciduced by 11, increasing respiratory volume (50 to 100 ml) during artificial respiration, 2) lung inflation by prevention of exhalation 12-3 cycles), and 3) hypercapnia-induced hyperventilation. The effects of cervical vagal or phrenic nerve section were determined. In addition the effects of electrical ll-5V. 1 ms. 10Hz) central vagal stimulation ICVS) or peripheral vagal stimulation (PVS) on UES tpne were determined. We found that lung inflation by all methods increased UES tone in a stimulus-dependent manner and that section of the cervical vagus but not the phrenic nerves blocked these effects. In addition, CVS but not PVS significantly increased UES tone in a stimulusdependent manner. We concluded that 1) central respiratory drive does not alter UES tone, but rather 2) lung inflation reflexes increase UES tone. Therefore, lung inflation reflexes may generate the respiratory rhythm of UES tone which is often observed in animals and man. These studies were funded VA grant 5120-02P ( IML).
by NIH grant
DC00069 (WJD)
and
A retrograde giant contraction (RGC) occurs in association with vomiting and after CCK-8, but the mechanism of its initiation and propagation are unknown. In prior studies we found that myotomy altered both initiation and propagation of the RGC, but the mechanism of these changes was unclear. In order to better understand the results of our prior studies we determined the effect of myotomy on the myoelecuic events associated with RGC: ECA disruption and the RGC potential. Five dogs were chronically implanted with bipolar electrodes on the small intestine from duodenum to ileum. After recording control responses to emetic agents or CCK-8, we performed a seromuscular myotomy of the intestine 60 cm from the pylorus. The myoelectic responses to emetic agents or CCK-8 were re-examined for 2 months after surgery. We found that myotomy blocked the occurrence of RGC potential but not ECA disruption due to emetics (32 ?. 3 cm) or CCK-8 (12 ? 2 cm) in a caudad direction only. This effect partially recovered after 30 days (26 + 6 and 2 f 2 cm). Total intestinal propagation time of the RGC potential did not change (14.8 + .8 s vs 15.8 f .4 s), but propagation velocity below the myotomy slowed significantly (22.6 f 7.5 vs 11.1 + 1.5 cm/s, p < .05). The delay between ECA disruption and RGC potential was not altered. The myoelectric responses to CCK-8 did not propagate through the jejunum and myotomy had no effect on the time of occurrence of these responses. We conclude that 1) the CNS primarily controls the temporal characteristics of the RGC but the ENS controls its spatial characteristics, 2) the ENS conveys a descending influence on the initiation and propagation of the RGC, and 3) ECA disruption may be a prerequisite for the RGC but is not a myoelecnic correlate. These studies were supported
by VA Merit Review Grant 5120-02P.