The American journal of physiology
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We studied the effects of increased intra-abdominal pressure on the lower esophageal sphincter (LES) pressure in 15 healthy subjects. The role of the diaphragm in the genesis of LES pressure during increased intra-abdominal pressure was determined by measuring diaphragm electromyogram (EMG). The latter was recorded using bipolar intraesophageal platinum electrodes that were placed on the nonpressure sensing surface of the sleeve device. ⋯ The increase in LES pressure during periods of increased intra-abdominal pressure is associated with a tonic contraction of the crural diaphragm as demonstrated by EMG recording. Atropine inhibited the resting LES pressure by 50-70% in each subject but had no effect either on the peak LES pressure attained during increased intra-abdominal pressure or tonic crural diaphragm EMG. We conclude that 1) there is an active contraction at the esophagogastric junction during periods of increased intra-abdominal pressure and 2) tonic contraction of the crural diaphragm is a mechanism for this LES pressure response.
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The ileocecal sphincter in the cat demonstrates a reflex contraction to colonic distension. This study investigates the pathway mediating this reflex in the intact bowel using an in vivo model. The ileocecal sphincter (ICS) and distal ileal intraluminal pressures were recorded in fasted chloralose-anesthetized cats. ⋯ The substance P antagonist, [DArg1,DTrp7,9,Leu11]substance P failed to antagonize substance P and failed to inhibit the ICS contractile response to colonic balloon distension. Spinal anesthesia inhibited this reflex. We have thus demonstrated that the ICS reflex contraction to colonic balloon distension in the intact bowel is mediated by an extrinsic spinal neural pathway involving both tachykinin and catecholamines as neurotransmitters.
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Hypoperfusion states cause lactic acidosis, and the acidemia further reduces the inadequate cardiac output. Conceivably, the adverse effect of lactic acidemia on cardiac output is due to depressed contractility demonstrated in isolated myocardium. Alternatively, factors governing venous return cause a relative hypovolemic state and/or acidemic pulmonary vasoconstriction-induced right ventricular dysfunction. ⋯ Lactic acidemia caused a 40% reduction in stroke volume, which could be attributed to depressed LV contractility, characterized by a decrease in maximum dP/dt as well as a fall in slope (Emax) with no change in volume intercept (Vo) of the left ventricular pressure-volume relationship at end systole. Neither the measured left ventricular end-diastolic pressure nor the estimated left ventricular end-diastolic volume (LVEDV) decreased with acidemia, suggesting that the reduced venous return did not result from relative hypovolemia. However, acidemic pulmonary hypertension may have interfered with the expected response to myocardial depression, which is an increase in LVEDV.