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Biomedical subjects

William L Hasler

Publications and source records attributed to William L Hasler.

27 records · Page 2Linked to original sources
PubMed2002

The irritable bowel syndrome.

Symptoms of IBS are very prevalent. One quarter of symptomatic individuals present for medical care because of symptom severity and psychologic factors. The pathogenesis of IBS is multifactorial, involving abnormalities in the gut, immune system, enteric sensory and motor nerves, and the CNS. IBS is diagnosed by symptomatology according to the Rome criteria and the absence of alarm findings suggestive of organic disease. Minimal testing is advocated to confirm the diagnosis in patients presenting with typical symptoms. Therapy is based on the dominant symptom (IBS subtype). Therapeutic options include dietary modifications, counseling, medications, and psychologic treatments. Novel therapies are being investigated to correct potentially pathogenetic peripheral and CNS abnormalities in IBS.

Central Nervous System↗
PubMed2002

Impaired gastrocolonic response and peristaltic reflex in slow-transit constipation: role of 5-HT(3) pathways.

Colonic motility is modulated by the 5-hydroxytryptamine (5-HT)(3)-dependent gastrocolonic response and 5-HT(3)-independent peristaltic reflex. We compared descending colon tone responses to antral distension, duodenal lipid perfusion, and colonic distension after double-blind placebo or granisetron in 13 healthy volunteers and nine slow-transit constipated patients. Antral distension (100-300 ml) and duodenal lipids (3 kcal/min) evoked increases in colon tone in volunteers, which were blunted in constipated patients (P < 0.05). Granisetron (10 microg/kg) reduced responses to antral distension and lipids in volunteers and to lipids in constipated patients (P < 0.05). The ascending contraction of the peristaltic reflex was blunted in constipated patients (P < 0.05), whereas descending responses were similar. Granisetron did not modify the peristaltic reflex. Colonic responses to bethanechol were similar in patients and volunteers. In conclusion, antral distension- and duodenal lipid-activated gastrocolonic responses and ascending contractions of the peristaltic reflex are impaired with slow-transit constipation with loss of both 5-HT(3)-dependent and -independent function. Thus abnormalities of neural reflex modulation of colonic motor function may play pathophysiological roles in slow-transit constipation.

Adult↗
PubMed2002

Physiology and pathophysiology of the interstitial cells of Cajal: from bench to bedside. VI. Pathogenesis and therapeutic approaches to human gastric dysrhythmias.

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.

Animals↗
PubMedDate not supplied

Nausea, gastroparesis, and aerophagia.

Nausea, gastroparesis, and aerophagia are gastrointestinal phenomena that have variable impact on affected patients. The causes of nausea are varied; treatment of these conditions relates to the underlying etiology. Antiemetic agents acting on several distinct receptor subtypes produce benefits in distinct patient subsets. Gastroparesis is characterized by delays in gastric emptying, usually defined scintigraphically. Standard care of gastroparesis relies on dietary modification, antiemetic drug therapy, and initiation of medications that stimulate gastric motor activity. Recent advances include pyloric injection of botulinum toxin and surgical implantation of an electrical neurostimulator. Other surgical therapies are reserved for refractory cases. Aerophagia presents in individuals of normal and impaired cognitive function, most commonly with symptoms of overdistension or eructation. There are no pharmaceutical remedies for this condition; thus, therapy relies on behavioral treatments.

Aerophagy↗