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141.
Fatigability of the External Anal Sphincter in Anal Incontinence   总被引:2,自引:0,他引:2  
INTRODUCTION Anal incontinence commonly results from external anal sphincter dysfunction. The muscle is routinely assessed by anorectal physiology studies. Fatigability is not routinely measured but should be an important factor in the maintenance of continence. The fatigue rate index has been developed to address this. The purpose of this study was to investigate the fatigability of the external anal sphincter in incontinent patients compared with that in controls and to determine its correlation with symptom severity and pudendal nerve terminal motor latency measurement.METHODS Forty-two patients with anal incontinence (33 female, 9 male) and 20 control patients (17 female, 3 male) were studied. As part of anorectal physiology studies, manometry was measured by a station pull-through technique with a closed-system microballoon. After a rest period of one minute, fatigue was measured over a 20-second squeeze at 1.5 cm in the anal canal with two consecutive readings separated by a further one-minute rest period. The fatigue rate index was calculated from the maximum squeeze pressure and fatigue rate. A validated symptom severity scoring system was used to assess symptomatology in patients with anal incontinence.RESULTS No difference was detected in demographic factors between the two groups. The fatigue rate index was significantly different between the control and incontinent groups (1.85 vs. 0.67 minutes, P = 0.001). No other factors were significantly different between the two groups (maximum squeeze pressure, 89.1 vs. 79 cm H2O, P = 0.42; fatigue rate, –85.8 vs. –101.2 cm H2O/min, P = 0.62). The fatigue rate index demonstrated a significant correlation with symptom score (r = –0.44, P = 0.005). The fatigue rate index did not correlate with latency measurement.CONCLUSIONs A significant difference was detected in the fatigue rate index between incontinent and control patients. The Fatigue Rate Index demonstrated a significant correlation with symptom severity score and it may be a useful discriminating measure of external anal sphincter function.Poster presentation at the meeting of The American Society of Colon and Rectal Surgeons, Chicago, Illinois, June 3 to 8, 2002, and at the meeting of the Association of Coloproctology of Great Britain and Ireland, Harrogate, United Kingdom, July 2 to 5, 2002.  相似文献   
142.

Introduction and objectives

This study investigated whether the vasoactive inotropic score (VIS) is independently predictive of mortality in cardiogenic shock (CS).

Methods

This study was retrospective, observational study. Patients who were admitted to the cardiac intensive care unit from January 2012 to December 2015 were screened, and 493 CS patients were finally enrolled. To quantify pharmacologic support, the patients were divided into 5 groups based on a quintile of VIS: 1 to 10, 11 to 20, 21 to 38, 39 to 85, and > 85. The primary outcome was in-hospital mortality.

Results

In-hospital mortalities in the 5 VIS groups in increasing order were 8.2%, 14.1%, 21.1%, 32.0%, and 65.7%, respectively (P < .001). Multivariable analysis indicated that VIS ranges of 39 to 85 (aOR, 3.85; 95%CI, 1.60-9.22; P = .003) and over 85 (aOR, 10.83; 95%CI, 4.43-26.43; P < .001) remained significant prognostic predictors for in-hospital mortality. With multiple logistic regression to remove any confounding effects, we found that the localized regression lines regarding the odds of death intersected each other's (medical therapy alone and combined extracorporeal membrane oxygenation group) path at VIS = 130. In contrast to linear correlation between VIS and mortality for patients treated with medical therapy alone, there was little association between a VIS of 130 or more and the probability of in-hospital mortality for patients who were treated with extracorporeal membrane oxygenation.

Conclusions

A high level of vasoactive inotropic support during the first 48 hours was significantly associated with increased in-hospital mortality in adult CS patients.  相似文献   
143.
ObjectivesThis study sought to define the 2-dimensional and Doppler echocardiographic hemodynamics associated with each Society for Cardiovascular Angiography and Interventions (SCAI) stage, and to determine their association with mortality.BackgroundThe SCAI shock stages classification stratifies mortality risk in cardiac intensive care unit (CICU) patients, but the echocardiographic and hemodynamic parameters that define these SCAI shock stages are unknown.MethodsUnique CICU patients admitted from 2007 to 2015 who had a transthoracic echocardiogram within 1 day of CICU admission were included. Echocardiographic variables were evaluated as a function of SCAI shock stage. Multivariable logistic regression determined the association between echocardiographic parameters with adjusted hospital mortality.ResultsWe included 5,453 patients with a median age of 69.3 years (interquartile range: 58.2 to 79.0 years) (37% women), and a median left ventricular ejection fraction (LVEF) of 50% (interquartile range: 35% to 61%). Higher SCAI shock stages were associated with lower LVEF and worse systemic hemodynamics. Hospital mortality was higher in patients with LVEF <40%, cardiac index <1.8 l/min/m2, stroke volume index <35 ml/m2, cardiac power output <0.6 W, or medial early mitral valve inflow velocity to early diastolic annular velocity (E/e′) ratio >15 (particularly in SCAI shock Stages A to C). After multivariable adjustment, only stroke volume index <35 ml/m2 (adjusted odds ratio: 2.0; 95% confidence interval: 1.4 to 3.0; p < 0.001) and E/e′ ratio >15 (adjusted odds ratio: 1.52; 95% confidence interval: 1.04 to 2.23; p = 0.03) remained associated with higher hospital mortality.ConclusionsNoninvasive 2-dimensional and Doppler echocardiographic parameters correlate with the SCAI shock stages and improve risk stratification for hospital mortality in CICU patients. Low stroke volume index and high E/e′ ratio demonstrated the strongest association with hospital mortality.  相似文献   
144.
Enlarged hearts secondary to significant pressure overload have a depressed myosin adenosine triphosphatase (ATPase) activity. With mild stress the ATPase activity may be normal or slightly elevated. Enlargement of the heart after exercise or thyroid stress results in an increased ATPase activity. Rapid myothermal techniques, in particular measurements of tension-dependent heat, were used to evaluate: (1) the relation of in vitro measurements of actin-activated ATPase activity to the in vivo behavior of myosin, and (2) the contribution of these changes to the economy of tension development and the time course of crossbridge cycling. Experiments were carried out in animals whose hearts were enlarged secondary to pressure overload (by pulmonary arterial banding) or thyrotoxic stress. In vitro actin-activated ATPase activity levels were 70 and 175 percent of normal for the pressure-overloaded and thyrotoxic hearts, respectively, while the tension-dependent heat per unit tension for the same preparations was, respectively, 78 and 154 percent of normal. Thus there is a reasonable correlation between the in vivo and in vitro measurements of contractile protein ATPase activity, which indicates that the economy of tension development is inversely related to tensiondependent heat per unit tension or actin-activated myosin ATPase activity. Analysis of these data in terms of the kinetics of ATPase activity, crossbridge behavior and tension development leads to the conclusion that in pressure overload hypertrophy the adaptation involves a decrease in the crossbridge cycling rate, an increase in crossbridge off-time and an increase in the on-time of the crossbridge. For thyrotoxic hypertrophy the adaptation involves an increase in the cycling rate, a decrease in the off-time and a decrease in the on-time. The former is adapted for slow, economical tension development and the latter for rapid, less economical tension development.  相似文献   
145.
The effects of intra-arterial infusion of dopamine on superior mesenteric artery blood flow, intestinal flow, intestinal oxygen consumption, and capillary density were studied in anesthetized dogs before and after blockade of dopamine receptors with haloperidol and after beta-adrenergic receptor blockade with propranolol. Mesenteric blood flow to a distal segment of the small intestine was measured with an electromagnetic blood flow-meter and intestinal oxygen consumption was calculated from the measured arteriovenous oxygen difference across the intestine and total blood flow. Intestinal capillary density was estimated from the clearance of 86Rb. In normal animals prior to dopaminergic or beta-adrenergic blockade, dopamine caused a dose-related decrease in mesenteric blood flow, intestinal oxygen consumption, and 86Rb clearance. Only the lowest dose of the drug, 1 mug/Kg.-min., did not significantly change the intestinal capillary density. In dogs pretreated with the dopamine receptor, antogonist, haloperidol, dopamine (20 mug/Kg.-min.) caused a significant increase in blood flow and oxygen consumption and did not significantly alter the number of perfused intestinal capillaries. These increases in haloperidol-blocked animals administered dopamine were reversed by propranolol. Our results indicate that dopamine caused smooth muscle contraction in mesenteric arterioles and precapillary sphincters, thereby producing intestinal ischemia and hypoxia. These findings with haloperidol and propranolol indicate that dopamine stimulates at least two different receptors in the canine mesenteric vascular bed: a constrictor receptor blocked by haloperidol and a dilator receptor blocked by propranolol.  相似文献   
146.
In characterizing pacemakers of the canine right atrium, cycle lengths after rapid atrial pacing were measured in the alert, conscious dog. Using implanted bipolar electrodes on the atrial appendage, pacing was established at a rate 100 percent above the spontaneous heart rate and was continued for 30, 60, 120 or 180 seconds. The average control cycle length subtracted from the first recovery cycle after cessation of pacing was termed the corrected recovery time. To study comparative responses of the Sinoatrial (S-A) node and subsidiary atrial pacemakers, corrected recovery time was measured before and at intervals after excision of the S-A node. Junctlonal regions frequently (but not invariably) assumed control instantaneously after sinus nodal excision, with subsidiary atrial pacemaker dominance occurring within a few minutes to hours; such control was relatively unstable for a few days. Subsidiary atrial pacemaker dominance gradually stabilized with development of consistent P waves and P-R intervals of 80 to 100 ms. Corrected recovery time after 1 minute of rapid atrial pacing averaged 267 ms before excision of the S-A node, 3,500 to 4,500 ms immediately after and for the 1st week after excision, but progressively decreased toward control levels during the 1st to 20th week thereafter. Thus, corrected recovery time first increased greatly, then regularly decreased with time after excision of the S-A node, but remained high for several weeks in subsidiary atrial pacemakers as compared with control dominance by S-A pacemaker tissues. However, the ultimate assumption of comparable corrected recovery time by the subsidiary pacemakers implies important alterations in electrophysiologic characteristics. One minute of fast pacing elicited longer periods of overdrive suppression than did 30 seconds of pacing, but these periods were not systematically further increased by 2 or 3 minutes of pacing. Although atropine greatly attenuated overdrive suppression in the awake dog model, propranolol altered it little or not at all during quiet rest, with modest exaggeration during alert attention.  相似文献   
147.
This study was designed to determine whether digoxin therapy in the canine heart failing because of mitral regurgitation (MR) provides only hemodynamic benefit and accompanying subjective improvement or if it also reverses the changes in intracellular Ca++ and sarcolemmal Na+-K+-ATPase. The dogs were divided into four groups: control, MR of 3 months' duration, MR of 6 months', and digoxin treatment for 3 months after 3 months of MR. Six months of MR produced a marked decrease in the index of myocardial contractility and function associated with a decrease in intracellular Ca++ and Na+, and an increase in intracellular K+, extracellular space, sarcolemmal Na+-K+-ATPase, and Mg++-ATPase. Digoxin treatment tended to return the changes in the index of myocardial contractility and cardiac function, intracellular Ca++, Na+, K+, extracellular space, and sarcolemmal Na+-K+-ATPase of the failing heart toward control levels. Digoxin treatment did not affect Mg++-ATPase. The right ventricle, which did not fail, also did not show any significant changes in the parameters measured. The results showed that digoxin treatment not only improved the index of myocardial contractility and cardiac function of the failing heart but also tended to return the electrolytes and sarcolemmal Na+-K+-ATPase toward control levels.  相似文献   
148.
Effect of perfusion rate of cholinergic agonist on sinus node automaticity   总被引:1,自引:0,他引:1  
Recent evidence supports a complex relationship between pressure in the sinus node artery and heart rate. In addition, it has been suggested that acetylcholine effects vary depending upon the pressure at which the drug is injected. We examined the cardiac chronotropic responses to acetylcholine, delivered via the sinus node artery using a constant flow perfusion technique. Dogs were anesthetized with chloralose and prepared to record ECG, arterial pressure and bipolar electrograms from the sinus node, sulcus terminalis, right atrium, right ventricle and His bundle. The sinus node artery was catheterized, distribution verified and autologously perfused via the femoral artery. Both vagi and both stellate ganglia were transected. Analog data were processed by computer for each cycle length during perfusion with normal Tyrode solution or Tyrode solution containing acetylcholine. Perfusion of normal Tyrode solution (1-4ml/min) resulted in prolongation in cycle length which was greater at higher flow rates but rapidly dissipated at all flow rates. Beyond mechanically-induced bradycardia, acetylcholine initially prolonged cycle length but cycle length prolongation faded with time. Delivery of acetylcholine at higher flow rates resulted in significantly greater prolongation of cycle length. Cycle length always returned back toward control although perfusion of acetylcholine continued. Thus, responses to acetylcholine are influenced not only by drug concentration but also by the flow rate at which the drug is delivered. This suggests a coupling of mechanical and pharmacologic components of chronotropic influences at the sinus node.  相似文献   
149.
生理学在教学中过于强调学科内容完整性,与临床结合较少。应当通过使用多种教学手段,改进考核方法来增强学生临床思维能力。  相似文献   
150.
教育和教学对个人能力的发展起主导作用,医学生的能力培养成为今后生理学教学的关键。通过认识医学生能力与核心能力的基本范畴,以及能力培养在生理教学中的重要性和必要性,了解医学生理学教学的现状,洞察生理学教学中学生能力培养实现的关键出发点,从而实现生理学教学的有效提升。  相似文献   
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