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Biomedical subjects

I M Lang

Publications and source records attributed to I M Lang.

At least 73 records · Page 4Linked to original sources
PubMed1991

Videoradiographic, manometric, and electromyographic analysis of canine upper esophageal sphincter.

We assessed upper esophageal sphincter (UES) function in dogs by concurrent recording of cricopharyngeal electromyographic (EMG) activity, intraluminal pressure, and dimensional changes of the pharyngoesophageal junction at rest and during swallowing. Radial and axial pressure profiles of the UES were determined by continuous pull-through manometry. EMG activity of the cricopharyngeus and thyropharyngeus muscles were correlated with UES pressure under static conditions. We also quantified the temporal relationships among EMG activity of the cricopharyngeus, UES pressure, and pharyngoesophageal junction dimensional changes during swallowing of 2, 4, and 6 ml of barium. When the dogs were prone, the anterior and posterior UES pressures were about twice the lateral pressures and the axial length of the UES was approximately 4 cm. All radial pressures equalized to approximately 20 mmHg when the dogs lay on their sides. The peak pressure zone of the UES corresponded closely with the level of the cricopharyngeal electrode, and resting UES pressure correlated closely with cricopharyngeal but not thyropharyngeal EMG activity. During swallowing, the cricopharyngeus relaxed approximately 200 ms before UES opening and 100 ms before UES relaxation. Superior movement of the hyoid and the larynx was associated temporally with UES relaxation, while anterior movement was associated with UES opening. Increases in bolus volume significantly increased maximal sagittal UES diameter during UES opening but did not alter temporal changes in UES function.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Biomechanics of cricopharyngeal bars.

Patients with a prominent cricopharyngeal bar visible on radiography are generally considered to have spasm of the cricopharyngeus, which is the major muscle component of the upper esophageal sphincter. This condition has been termed "cricopharyngeal achalasia." The aim of this study was to determine the pathogenesis of cricopharyngeal bars. Concurrent videofluoroscopic and manometric examinations of the pharynx and upper esophageal sphincter were performed in a cohort of six patients with prominent cricopharyngeal bars and in eight control volunteers. In each subject, swallows of 2-30-mL barium boluses were recorded. The patients with cricopharyngeal bars showed (a) normal peristaltic contraction in the pharynx, (b) normal axial upper esophageal sphincter pressure and relaxation, (c) normal flow rate across the upper esophageal sphincter, and (d) normal duration of upper esophageal sphincter opening for different bolus volumes. The major abnormalities in the patients with cricopharyngeal bars were (a) reduced maximal dimensions of the upper esophageal sphincter during the transsphincteric flow of barium and (b) increased intrabolus pressure upstream to the upper esophageal sphincter. Thus, the increase in intrabolus pressure preserved normal transsphincteric flow rates even though the upper esophageal sphincter did not open normally. Overall, the constellation of findings in the patients studied suggests that the underlying pathogenesis of their cricopharyngeal bar was reduced muscle compliance wherein the relaxed cricopharyngeus did not distend normally during swallowing.

Adult↗
PubMed1990

Digestive tract motor correlates of vomiting and nausea.

The digestive tract from the upper esophageal sphincter to the ileum participates in the vomiting process, but the role of the digestive tract in nausea is unclear. In preparation for vomiting, the proximal stomach relaxes and the small intestine is evacuated orad in a single mass movement by a retrograde giant contraction and caudad in a stripping fashion by a series of phasic contractions. Orad evacuation of the small intestine may not only remove offending substances but may also dilute. or buffer gastric contents with intestinal and pancreaticobiliary secretions. In association with retching and vomiting, the striated muscle of the esophagus contracts longitudinally, pulling the relaxed proximal stomach into the thoracic cavity forming a funnel from stomach to esophagus. However, gastric evacuation does not occur until the hiatal fibers of the diaphragm relax during vomitus expulsion. Nausea is a subjective feeling in humans that is difficult to identify in animals. Various changes in digestive tract activity have been associated with nausea, but no evidence suggests that these events cause nausea. The prodromal signs of vomiting (e.g., increased heart rate and respiration) that occur concomitantly with the gastrointestinal motor correlates of vomiting have been considered autonomic indices of nausea in animals, but this has not been proven. Regardless, the gastrointestinal motor correlates of vomiting do not cause the prodromata. The emetic central pattern generator may be organized in parallel with respect to its individual autonomic correlates, but as groups of responses, the autonomic and somatomotor correlates may be organized in series.

Animals↗
PubMed1990

Effect of swallowed bolus variables on oral and pharyngeal phases of swallowing.

In this investigation, we studied the effects of bolus volume and viscosity on the quantitative features of the oral and pharyngeal phases of swallowing. Concurrent videofluoroscopic and manometric studies were done in 10 healthy volunteers who were imaged in lateral projection. Videofluorography was done at 30 frames/s while concurrent manometry was done with 5 intraluminal transducers that straddled the pharynx and upper esophageal sphincter (UES). Submental electromyography was recorded also. Swallows of 2-20 ml were recorded for low-viscosity liquid barium and high-viscosity paste barium. Analysis indicated that the major effect of increases in bolus volume was an earlier onset of anterior tongue base movement, superior palatal movement, anterior laryngeal movement, and UES opening. These events provide receptive adaptation for receiving a swallowed bolus. Earlier UES opening was associated with an increase in the duration of sphincter opening and sphincter diameter. The major effects of high bolus viscosity, unrelated to bolus volume, were to delay oral and pharyngeal bolus transit, increase the duration of pharyngeal peristaltic waves, and prolong and increase UES opening. Thus the specific effect of bolus viscosity per se differs substantially from that of bolus volume. We conclude that 1) specific variables of swallowing are affected significantly by the variables of the swallowed bolus, such as volume and viscosity; 2) overall, bolus volume and viscosity affect swallowing in a different manner; and 3) the study findings have implications about the neural control mechanisms that govern swallowing as well as about the diagnosis and treatment of patients with abnormal oral-pharyngeal swallowing.

Adult↗
PubMed1989

Functional localization of specific receptors mediating gastrointestinal motor correlates of vomiting.

The gastrointestinal motor correlates of vomiting consist of two contractile events, 1) a giant retrogradely propagated contraction of the upper small intestine, the retrograde giant contraction (RGC) and 2) a series of post-RGC phasic contractions that occur primarily in the lower small intestine. The effects of cholinergic, dopaminergic, serotonergic, and opioid receptor antagonists and an opioid receptor agonist on vomiting and its gastrointestinal motor correlates initiated by apomorphine (APO), CuSO4, or cholecystokinin octapeptide (CCK-8) were determined in awake dogs. Atropine blocked the retrograde giant contraction only, and hexamethonium blocked all jejunoileal motor responses activated by APO, CuSO4, or CCK-8. Domperidone blocked all effects of APO only, whereas haloperidol, methysergide, 1-(1-naphthyl) piperazine, and fentanyl blocked or inhibited responses to both APO and CuSO4. None of the dopaminergic, serotonergic, or opioid receptor antagonists or the opioid receptor agonist affected the gastrointestinal motor responses to CCK-8. Cinanserin or Sch 23390 had no effect on any of the responses activated by APO, CuSO4, or CCK-8. These results suggested that D2 dopaminergic and 5-HT2 serotonergic receptors of the emetic central pattern generator mediate vomiting and its gastrointestinal motor correlates, whereas opioid receptors may mediate tonic inhibition of these responses. In addition, peripheral muscarinic or nicotinic cholinergic receptors but not peripheral 5-HT2, dopaminergic, or opioid receptors mediate the gastrointestinal motor correlates of vomiting.

Animals↗
PubMed1989

Opening mechanisms of the human upper esophageal sphincter.

Our goals in this study were to evaluate the mechanisms operative in swallow-associated opening of the upper esophageal sphincter (UES) and to determine the dynamics of fluid flow across the sphincter. For this purpose, we obtained concurrent videofluorographic and manometric studies of 2- to 30-ml barium swallows in 15 normal subjects. We found that the resting UES high-pressure zone corresponded closely with the location of the cricopharyngeus. The findings indicated that manometric UES relaxation and anterior hyoid traction on the larynx invariably preceded UES opening. With graded increases in bolus volume, progressive increases occurred in UES diameter, cross-sectional area, flow duration, and transsphincteric flow rate. Intrabolus pressure upstream to the UES and within the UES at its opening during transsphincteric flow of barium remained within a narrow physiological range of less than 10 mmHg up to a bolus volume of 10 ml. With increases in bolus volume, anterior hyoid movement, UES relaxation, and UES opening occurred sooner in the swallow sequence to accommodate the early entry of large boluses into the pharynx. We conclude that during swallowing 1) normal UES opening involves sphincter relaxation, anterior laryngeal traction, and intrabolus pressure, 2) volume-dependent adaptive changes in UES dimension accommodate large bolus volumes and flow rates with minimal requirement for increases in upstream, or intrasphincteric, intrabolus pressure or UES opening duration, and 3) volume-dependent changes in UES dimensions as well as timing of UES relaxation and opening indicate a sensory feedback mechanism that modulates some components of the swallow response generated by the brain stem swallow centers.

Adult↗
PubMed1989

Colonic motor response to a meal in dogs.

We investigated the effects of ingestion of a meal on colonic motor activity in six conscious dogs, each instrumented with seven strain-gauge transducers to record circular muscle contractions. A 1,300-kcal meal was given after a 4-h control recording. The post-prandial period of 8 h was subdivided into an early period lasting 2 h and a late period lasting 6 h. The ingestion of the meal did not disrupt the colonic migrating myoelectric complexes (CMMCs) but prolonged their cycle length in the early postprandial period. The cycle length was not different from the control during the late postprandial period. The mean and total duration of contractile activity per hour increased significantly during the early postprandial period in the distal colon but not in the proximal or the middle colon. During the late postprandial period the mean and total duration of contractile activity per hour increased significantly throughout the colon. Giant migrating contractions occurred rarely during the 8-h postprandial period. We conclude that different parts of the colon respond to the ingestion of a meal in different ways. The response also depends on whether the fresh digesta has reached the colon. The late postprandial response is likely to be due to the entry of fresh digesta into the colon.

Animals↗
PubMed1988

Comparison of gastrointestinal responses to CCK-8 and associated with vomiting.

The gastrointestinal motor and myoelectric responses associated with vomiting induced by apomorphine (APO) and activated by cholecystokinin octapeptide (CCK-8) were compared as well as the mechanisms of initiation of these responses. Twelve dogs were surgically implanted with strain-gauge force transducers or bipolar electrodes for chronic recording of contractile or electrical activity. The responses to CCK-8 were determined in the fasted state and compared with the gastrointestinal motor and myoelectric correlates of vomiting activated by APO. After recording control responses, the effects of the following agents on these responses were determined: atropine, domperidone, and proglumide. In addition, the effects of supradiaphragmatic vagotomy or splanchnicectomy were determined. We found that CCK-8 activated contractile and myoelectric responses in the absence of vomiting, which were similar in most respects to those found in association with vomiting. These responses included 1) the retrograde giant contraction (RGC) and 2) the post-RGC phasic contractions. These RGCs were similar with respect to their activation in an all-or-none fashion, magnitude, duration, and position in the small intestine. The myoelectric correlates of these motor responses were similar qualitatively and quantitatively. The responses activated by APO and CCK-8 differed with respect to their coordination at different levels of the gastrointestinal tract. Whether activated by CCK-8 or APO, atropine blocked the RGC but not the post-RGC contractions. Domperidone blocked all responses to APO but not to CCK-8, and splanchnicectomy did not affect responses to either agent. Vagotomy blocked all gastrointestinal responses to APO but not to CCK-8. These results indicated that CCK-8 activates the gastrointestinal motor and myoelectric correlates of vomiting by a peripheral mechanism that does not include dopamine receptors.

Animals↗
PubMed1988

Giant migrating contractions of the canine cecum.

We investigated cecal motor activity and its coordination with ileal and colonic motor activities in five conscious dogs instrumented with strain-gauge transducers. Both ileum and colon exhibited the usual migrating motor complexes (MMCs) that were independent of each other. Cecum had no motor complexes, but it periodically generated giant migrating contractions (GMCs) that originated at the apex and migrated to the cecum-colonic junction at a velocity of 13 +/- 1.3 cm/min. The amplitude of cecal GMCs was 1.82 +/- 0.26 and 3.37 +/- 0.39 times larger than that of contractions during ileal and colonic motor complexes, respectively (P less than 0.05). The mean duration and period of cecal GMCs were 45 +/- 4 s and 61.4 +/- 14.2 min, respectively, in the fasted state and 49 +/- 6 s and 68.5 +/- 13.5 min in the fed state, respectively (P less than 0.05). A total of 82 cecal GMCs was recorded in 71 h of fasted recording and 94 in 121 h of fed recording. Cecal GMCs were not coordinated with colonic MMCs. Intravenous motilin, but not morphine, initiated a premature cecal GMC. We concluded that cecum has a unique motor activity that is different from that of the colon and the ileum. The strong caudad GMCs of the cecum may periodically empty cecal contents into the colon.

Animals↗
PubMed1987

An intrinsic neural pathway for long intestino-intestinal inhibitory reflexes.

We studied the mechanisms of initiation and pathways for the propagation of intestino-intestinal inhibitory reflexes induced by close intraarterial injections of neostigmine in conscious dogs. Two or three T-shaped catheters were surgically implanted in the intestinal branches of the superior mesenteric artery to inject pharmacologic agents locally in 10-15-cm-long segments. Migrating myoelectric complexes were recorded by a set of 10 electrodes and strain-gauge transducers. Close intraarterial injection of neostigmine initiated strong contractions of long duration in the perfused segment that terminated phase III activity in progress 90-150 cm distal or proximal to the cannulated sites and stopped its further migration. Atropine or 4-diphenylmethoxy-N-methylpiperidine methiodide injected just before neostigmine administration through the same catheter blocked both the local contractile effects and the reflex inhibition of phase III activity. Pirenzepine or hexamethonium injected in a similar manner did not affect the local response to neostigmine but blocked the reflex inhibition of phase III activity. A transection and reanastomosis in the mid-small intestine blocked the reflex inhibition by close intraarterial injection of neostigmine beyond the transection site. Pirenzepine, atropine, or hexamethonium injected through a middle catheter also blocked the reflex inhibition of phase III activity beyond the site perfused with these cholinergic antagonists. Close intraarterial administration of 4-diphenylmethoxy-N-methylpiperidine methiodide at a middle site had no effect on reflex inhibition. We concluded that strong spasmodic contractions in the small intestine initiate an intestino-intestinal inhibitory reflex in both directions. This reflex is mediated through an intrinsic neural pathway involving nicotinic and M1 muscarinic receptors.

Animals↗
PubMed1987

Differential effects of [Gln4]neurotensin on circular and longitudinal muscle of dog ileum in vitro.

We studied the effects of neurotensin analogue [Gln4]-neurotensin on isolated dog ileal longitudinal and circular muscle strips. [Gln4]neurotensin stimulated the spontaneous contractile activity of the circular muscle but inhibited that of the longitudinal muscle in a dose-dependent fashion. Hexamethonium had no effect on the spontaneous longitudinal or circular muscle contractile activity. Atropine and tetrodotoxin (TTX) both inhibited the longitudinal muscle. Atropine had no effect on the circular muscle, but TTX stimulated it. The effects of [Gln4]neurotensin on the circular muscle were reduced but not completely abolished by atropine. The inhibition of the longitudinal muscle by [Gln4]neurotensin was not reduced by any of the above antagonists but was enhanced by atropine. Electrical field stimulation (10 Hz, 100 mA) stimulated the longitudinal muscle and inhibited or stimulated the circular muscle depending on the pulse width of the stimulus. These effects were unaffected by [Gln4]neurotensin. We conclude that [Gln4]neurotensin has differential effects on isolated muscle strips of the two muscle layers in the dog ileum. It stimulates the circular muscle partially through cholinergic nerves at preganglionic sites and partially through a direct myogenic effect. [Gln4]neurotensin inhibits the spontaneous activity of the longitudinal muscle presumably by reducing the excitability of cholinergic nerves at postganglionic sites.

Animals↗
PubMed1986

Myoelectric and contractile effects of motilin on dog small intestine in vivo.

The effects of the close intraarterial administration of motilin on intestinal myoelectric and contractile activities were examined in 37 dogs. After anesthetization or decerebration, a segment of proximal jejunum was instrumented serosally with electrodes and stain gauges. A mesenteric artery supplying a short length of this segment was cannulated for the injection of motilin and other agents. Motilin (0.03-0.3 microgram) caused: a series (1-5 min) of phasic contractions and electrical response activity (ERA) bursts locally; a short (15-60 sec) series of phasic contractions and ERA bursts aborally followed by relaxation; and a series of phasic contractions and ERA bursts whose onset migrated 3.7 +/- 1.0 cm orally. The length of orad response increased to 6.6 +/- 1.9 cm in the decerebrate dogs (P less than 0.01). No other tested agent, including serotonin, bethanechol, morphine, dopamine, substance P, neurotensin, somatostatin, vasoactive intestinal peptide, bombesin, pentagastrin, cholecystokinin octapeptide, prostaglandin F2 alpha or leucine-enkephalin, caused similar responses. All motilin responses were mediated by neural pathways consisting of both nicotinic and muscarinic receptors. The similarity of responses and mechanisms of action of the motilin-activated contractile response with the intrinsic mucosal reflex suggested that motilin may mediate this reflex.

Animals↗
PubMed1986

Gastrointestinal motor correlates of vomiting in the dog: quantification and characterization as an independent phenomenon.

The gastrointestinal motor correlates of vomiting were examined in 8 dogs. Each dog was chronically implanted with extramural strain gage force transducers distributed along the gastrointestinal tract. The following gastrointestinal motor responses accompanied vomiting activated spontaneously or after apomorphine administration (2.5-15 micrograms/kg, i.v.): (a) a retrograde peristaltic contraction (RPC), (b) a peri-RPC inhibitory period, (c) a post-RPC series of phasic contractions, and (d) a post-RPC inhibitory period. These same motor patterns occurred without the somatomotor responses associated with vomiting but sometimes with regurgitation under the following conditions: (a) spontaneously, (b) one-third of the time after low doses of apomorphine (2.5-5.0 micrograms/kg, i.v.), or (c) after the intragastric administration of hypertonic saline or a vinegar solution. We concluded that a set of gastrointestinal motor responses accompany vomiting and that this set of responses represents an independent phenomenon. This phenomenon was vagally mediated but only one phase, the RPC, was cholinergically mediated. Our results suggest that the vomiting center may consist of two functionally distinct parts that are activated sequentially: one controlling the gastrointestinal responses and the other the somatomotor responses.

Animals↗
PubMed1986

Generation of phases I and II of migrating myoelectric complex in the dog.

The mechanisms of generation of most of the phases of the migrating myoelectric complex (MMC) are unclear. Except for phase III activity, this issue has not been investigated directly. We have qualitatively examined the relations between different phases of the MMC cycle in order to provide an objective basis for the formation of theories. Eight dogs of either sex were implanted with 10 bipolar electrodes distributed along the gastrointestinal tract. Myoelectric activity was recorded during the fasted state or after feeding until the return of the MMC cycle. The relations between phase I duration, phase II duration, phase III migration time, and phase III period were examined using simple linear-regression methods. We found that only phase I duration was highly correlated (r = 0.87, P less than 0.01) with phase III migration time and that only phase II duration was highly correlated (r = 0.90, P less than 0.01) with phase III period. In either the fed or fasted state, phase III activity that began in the midjejunum was accompanied concurrently with phase I activity of the duodenum and upper jejunum, where phase III activity had not occurred. Also, the position of phase III activity in the lower small intestine when phase I activity of the upper small intestine ended was 277 +/- 24 cm (83 +/- 5% of the small intestinal length) from the pylorus, and the coefficient of variation of this position was significantly smaller (P less than 0.01) than that of the other cycle variables.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Gastrointestinal myoelectric correlates of vomiting in the dog.

Prior to vomiting, two gastrointestinal contractile events occur in succession: a giant contraction that propagates retrograde from mid-small intestine to the antrum (RGC) and a series of phasic contractions that occur at all levels of the gastrointestinal tract. We quantitatively examined the gastrointestinal myoelectric events associated with vomiting and correlated them with the previously defined contractile events. Twelve dogs of either sex were implanted with electrical or contractile recording devices implanted on the stomach and small intestine. After an overnight fast, gut activity was recorded before and after apomorphine administration (2.5-15 micrograms/kg, iv). We found that the RGC was correlated with two successive electrical events: disruption of electrical control activity (ECA) cycling and a potential change occurring at the upstroke of the RGC. However, the initial myoelectric event associated with vomiting was ECA frequency slowing of the antrum and lower half of the small intestine. The post-RGC phasic contractions were associated with ECA-dependent response activity and occurred during the period of ECA frequency slowing. Atropine (100 micrograms/kg iv) blocked the RGC and its associated electrical events but not the slowing of ECA frequency. Supradiaphragmatic vagotomy eliminated all gastrointestinal contractile and myoelectric events but antral ECA frequency slowing. Spontaneous occurrences of the myoelectric correlates of vomiting were not different from those activated by apomorphine. These results suggest that ECA disruption may be important for retrograde propagation of the RGC. The function of ECA frequency slowing, however, remains unknown.

Animals↗
PubMed1985

Dose- and time-dependent biphasic response to morphine on intestinal migrating myoelectric complex.

We investigated the biphasic response to morphine infusion on migrating myoelectric complex (MMC) cycling in seven conscious dogs. Morphine infusions at the rate of 20, 50, 100, 200, 500 and 1000 micrograms/kg/hr were started at 0 or 40% of MMC cycle and continued for 3 hr in each experiment. All infusion rates starting at 40% of MMC cycle initiated the first postinfusion MMC cycle prematurely (P less than .05). The mean period of the first postinfusion MMC cycle decreased for higher infusion rates. After the first premature MMC cycle, higher infusion rates (500 and 1000 micrograms/kg/hr) inhibited MMC cycling completely whereas the lower infusion rates inhibited MMC cycling in a dose-dependent manner. When infusion was started at 0% of MMC cycle, the first premature MMC cycle occurred consistently only at 20 micrograms/kg/hr. For higher infusion rates, initiation of premature MMC cycle or inhibition of MMC cycling was dose-dependent. Naloxone blocked both the excitatory and the inhibitory effects of morphine on MMC cycling. Morphine infusions also initiated phase III activity in the postprandial state in a dose-dependent manner. Truncal vagotomy and splanchnectomy did not abolish the excitatory or the inhibitory effects of morphine on MMC cycling. We conclude that morphine infusion has a biphasic effect on MMC cycling. The exact nature of the response depends on the dose of morphine and the time in the MMC cycle when infusion is started. Both the excitatory and the inhibitory responses may be mediated through peripheral mu opiate receptors.

Animals↗