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.
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Manometric studies of pharyngeal-upper esophageal sphincter (UES) coordination during swallowing have proven difficult. Asymmetry of the UES makes pressure measurements with a single, unoriented transducer suspect. Perfused systems lack the necessary response rate for measuring peak pharyngeal contraction pressures. ⋯ All timing sequences became progressively longer with increasing bolus size. Residual pressures were unchanged. Timing sequences were also measured for wet (5 ml) and dry swallows in seven volunteers using a Dent sleeve and single perfused orifice in the UES; no differences were seen.
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We investigated in conscious, chronically instrumented dogs whether actions mediated by V1 receptors affect cardiovascular effects elicited by V2-like receptors in response to vasopressin or vasopressin analogues. Infused arginine vasopressin (AVP) (220 pg.kg-1.min-1) did not have any significant effect on arterial pressure, cardiac output (CO), and heart rate (HR) when it was preceded by administration of a V1 receptor antagonist. However, when the same antagonist was administered 1 h after the start of the same infusion of AVP, CO, and HR increased significantly above control pre-AVP values, and total peripheral resistance (TPR) fell significantly below control. ⋯ In another set of experiments, the administration of a selective V1 agonist blunted significantly the CO and HR increase as well as the decrease in TPR normally associated with injection of a selective V2 agonist. However, administration of phenylephrine did not reduce these V2-mediated effects. We conclude that there are significant interactions between V1 and V2-like receptors in the cardiovascular system of conscious dogs, whereby V1 effects appear to 1) immediately antagonize the action of V2 agonists and 2) sensitize the organism to cardiovascular effects mediated by V2-like receptors after a prolonged exposure.(ABSTRACT TRUNCATED AT 250 WORDS)