Cólico biliar inducido por morfina / Morphine induced biliary pain: case report

Morphine produces contraction of Oddi’s sphincter, which can be severe and of longer duration in some pathological conditions. This exaggerated response can manifest as a colicky biliary pain, frequently accompanied by a dramatic increase in hepatic enzymes. We report a 32 years old female who consulted in the emergency room for severe low abdominal pain of gynecologic origin, which was completely controlled by morphine. However, she presented a sudden epigastric colicky pain irradiating in the back, which persisted for several hours in spite of the repeated administration of analgesics. Transaminases elevated from previously normal value to over 1,000 U/L, and returned to the normal level without further treatment after several days. Magnetic resonance cholangiography showed normal fine bile duct, without stones. This transient increase in hepatic enzymes was considered as a consequence of high biliary pressure secondary to morphine-induced spastic contraction of Oddi’s sphincter and a consecutive hepatocellular necrosis.

Physiology of the sphincter of oddi - the present and the future? - part 1

The mechanisms controlling the sphincter of Oddi [SO] have received considerable attention over the past two decades. Progress towards their elucidation has been slow, perhaps because of the sphincter's relative inaccessibility and the different responses of the human "resistor" as compared to the "pumper" observed in several animal models. The list of agent affecting the sphincter grows alarmingly. In this review, divided into two parts, substances have been classified as neurotransmitters, hormones, local factors and pharmacological agents. The first part considers the roles of neurotransmitters. These include [a] vasoactive intestinal polypeptide [VIP] and nitric oxide [NO]. Both cause relaxation. A recent model of their complex interrelationships in smooth muscle is described.[b] Substance P [SP] and enkephalins. These produce contractions. The former can act directly. An indirect effect via cholinergic neurones may be the result of SP release from vagal afferents.[c] Catecholamines, which cause contraction or relaxation via activation of alpha or beta adrenoreceptors, respectively. In the second part attention is focussed on cholecystokinin [CCK] which normally relaxes the SO via neuronal mechanisms.A CCK- sensitive pathway from sensory duodenal neurones to SO ganglia has been described. Reactive oxygen species are among the local factors discussed. Their description as being "the good, the bad and the ugly"seems merited. Pharmacological agents include No donors, octreotide and botulinum toxin [BTX]. Octreotide induces tachyoddia and may impair biliary flow. BTX has exciting potential in the diagnosis of SO abnormalities and as a therapeutic alternative to sphincterotomy. In both past of the review current concepts of different aspects of smooth muscle control are presented. In several instance data regarding the SO is lacking. We discuss [a] the role of interstitial cell of Cajal in the control of slow waves, [b] different pathways contributing to tonic and phasic contractions, [c] the 4 levels of neural control, [d] interrelationships of immune and nervous systems, and [e] links between emotional states and gut functions

Alteraçöes da motricidade do esfíncter de Oddi secundárias à administraçäo de algumas drogas / Changes in the motility of the Oddi's sphincter following administration of some drug's

A eletromiografia do esfíncter de Oddi foi realizada em 32 opossums após a administraçäo de álcool etílico, analgésicos, drogas autonômicas e nifedipina. Seis ou sete pares de eletrodos foram implantados no esfíncter de Oddi e intestino delgado e um cateter foi inserido no duodeno ou veia jugular, para a administraçäo de drogas. A instilaçäo intraduodenal de álcool causou um aumento significativo na freqüência de potenciais de açäo (7,4 potenciais/min) por 15 a 20 minutos no esfíncter de Oddi, em todos experimentos. A morfina, a meperidina e a pentazocina causaram um aumento na duraçäo do complexo mioelétrico migratório de 85,4 minutos a 167,7, 143,4 e 129,1 minutos, respectivamente. Períodos de atividade mioelétrica intensa de 1-2 minutos foram observados após a administraçäo da morfina em oito experimentos, da meperidina em seis e da pentazocina em 3. O betanecol aumentou e a atropina aboliu os potenciais de açäo no esfíncter de Oddi e duodeno. A fenilefrina aumentou a motricidade do esfíncter de Oddi, mas diminuiu a freqüência de potenciais de açäo no duodeno. A clonidina, a dobutamina e a terbutalina diminuíram a freqüência de potenciais de açäo no esfíncter de Oddi e duodeno. A infusäo de nifedipina, um bloqueador do canal de cálcio, reduziu a freqüência de potenciais de açäo no esfíncter de Oddi e intestino delgado. Esta reduçäo era dependente da dose infundida. A infusäo de nifedipina a doses elevadas aboliu o complexo mioelétrico migratório no trato gastrintestinal