心肌梗死患者择期行PCI治疗对左心室重构和收缩功能的影响

目的:研究心肌梗死患者择期行经皮冠状动脉介入(PCI)治疗对左心室重构和收缩功能的影响。方法:选取2009年12月到2014年12月我院收治的心肌梗死择期行PCI治疗的患者60例(研究组),另选同期单纯心绞痛行PCI治疗的患者60例(对照组)。比较治疗前、后两组左心室舒张末期容积(LVEDV)、收缩末期容积(LVESV)、每搏量(SV)、左室射血分数(LVEF)、左室收缩末期压(LVESP)和左心室舒张末压(LVEDP)。结果:治疗后研究组LVEDV、LVESV、SV、LVEF、LVESP和LVEDP均显著优于治疗前,比较差异均具有统计学意义(P0.05),对照组治疗前、后LVEDV、LVESV、SV、LVEF、LVESP和LVEDP比较差异均无统计学意义(P0.05)。结论:心肌梗死患者行PCI治疗具有较好的效果,能显著改善患者的左心室重构和收缩功能。     

氧化苦参碱对急性心肌梗死家兔心功能和左心室重构的影响

目的:研究氧化苦参碱对急性心肌梗死家兔模型心功能及左心室重构的影响。方法:采用结扎家兔左前降支建立急性心肌梗死模型,随机分为3组(n=9):假手术组、模型组、氧化苦参碱组,假手术组不结扎冠状动脉。假手术组、模型组常规饲养,氧化苦参碱组在正常饲养基础上用灌胃给药氧化苦参碱1 ml/100 g,每日1次,分别在术后1周、4周观察氧化苦参碱对家兔左心室腔内直径(D)、心室重量指数(VWI)、心室重量(VW)、体重(BW)、心输出量(CO)和左心室收缩末期压(LVESP)、左心室舒张末期压(LVEDP)、左室内压变化率峰值(dp/dtmax)的影响。结果:与假手术组比较,模型组心脏游离左室壁梗死范围由粉红色变为深紫色。术后1周模型组与假手术组相比CO减少(P0.05),术后4周进一步减少(P0.01)。术后1周、4周氧化苦参碱组与模型组相比CO明显增加(P0.01),dp/dtmax增加(P0.05),LVESP明显升高(P0.01),LVEDP明显下降(P0.01);术后4周氧化苦参碱组与模型组相比,D明显减小(P0.01),VWI、VW减小(P0.05)。结论:氧化苦参碱能增加急性心肌梗死后心输出量,改善急性心肌梗死家兔左心室重构参数,改善心功能指标。     

心肌带收缩率与急性心肌梗死患者左心室收缩功能关系

目的:急性前壁心肌梗死明显影响室间隔收缩率和左心室射血分数(left ventricular ejection fraction LVEF)。本文旨在探讨心肌带降段及升段收缩率与急性前壁心肌梗死患者LVEF的相关性。方法:收集2015年4月-2017年2月在心内科住院的急性前壁心肌梗死患者36例,正常对照组患者39例。所有患者取左心室长轴M型超声心动图,测量室间隔收缩率、升段收缩率及降段收缩率。心肌梗死左心室射血分数采用双平面Simpson's法计算。结果:与正常对照组相比,心肌梗死组患者舒张末期心肌带升段厚度没有统计学差异(P=0.69),收缩末期升段厚度(P=0.014)更薄、升段收缩率(P0.01)明显降低;心肌梗死组舒张末期降段厚度(P0.01)更薄、收缩末期降段厚度(P0.01)更薄、降段收缩率(P0.01)明显降低;心肌梗死组左心室射血分数与降段收缩率(r~2=0.13,P=0.026)、室间隔增厚率(r~2=0.19,P0.01)呈正相关,与升段收缩率没有相关性(P0.05)。正常对照组左心室射血分数与室间隔增厚率、降段增厚率及升段增厚率无相关性。经过相关分析,筛选出与心肌梗死LVEF的相关因素,进一步经逐步回归分析,得多元线性回归方程为LVEF=48.206+18.914*LVDD(cm)-25.414*LVSD(cm)。结论:急性前壁心肌梗死室间隔降段收缩率明显受损,与左心室射血分数降低有关。多元线性回归方程可估算前壁心肌梗死LVEF。     

急性心肌梗死患者早期血浆脑钠肽水平与左室重构及预后关系的评估

目的:探讨急性心肌梗死(AMI)早期脑钠肽(BNP)水平与左室重构及预后的关系.方法:用放射免疫法测定AMI患者早期血浆BNP水平;用超声心动图检查测量左室收缩末容积(ESV)、左室舒张末容积(EDV)、射血分数(EF)并通过计算得左室质量(LVM).并根据左心室容积指标分组,左心室容积增加率＞20%为左心室重构组,否则为非重构组,比较两组血浆BNP水平.结果:重构组恢复期左心室舒张末期及收缩末期容积指数均高于非重构组(P＜0.01),亦高于急性期左心室容积(P＜0.01).重构组早期血浆BNP浓度明显高于非重构组(P＜0.01),恢复期也较非重构组高(P＜0.01).重构组早期BNP浓度与恢复期左心室容积及容积变化量之间呈正相关.结论:AMI早期BNP升高与急性期左室重构密切相关,血浆BNP浓度可以作为溶栓治疗再通的观察指标及预后判断依据.     

丹参素注射液对急性心肌梗死大鼠的心室重构、心室功能及肢体导联与胸导联心电图参数的影响

摘要 目的：探讨丹参素注射液对急性心肌梗死大鼠的心室重构、心室功能及肢体导联与胸导联心电图参数的影响。方法：选择SD大鼠40只,将其鼠随机模型组、假手术组、硝酸甘油组、丹参注射液组。假手术组大鼠给予只在冠状动脉处穿针,不进行结扎,其余步骤同其余3组,其余3组均进行动物模型构建。假手术组、模型组大鼠均腹腔注射氯化钠注射液,硝酸甘油组腹腔注射硝酸甘油,丹参注射液组腹腔注射丹参注射液。对比4组大鼠的肢体导联与胸导联心电图参数,对比4组大鼠的血液流变学指标、左心室功能及左心室重构。结果：模型组的Ⅰ、Ⅱ、Ⅲ、aVL、aVF、V1、V2、V5、血浆粘度、纤维蛋白原、红细胞聚集指数、舒张末期室间隔厚度、左室舒张末期内径、左室收缩末期内径、左室舒张末期容积、左室收缩末期容积明显较假手术组、硝酸甘油组、丹参注射液组高,硝酸甘油、丹参注射液组以上指标明显较假手术组高,模型组的的左室舒张末期厚度、左室射血分数、左室短轴缩短率明显较假手术组、硝酸甘油组、丹参注射液组低,硝酸甘油、丹参注射液组的左室舒张末期厚度、左室射血分数、左室短轴缩短率明显较假手术组低。模型组的左心室重量指数、左心室截面直径明显较假手术组、硝酸甘油组、丹参注射液组高,硝酸甘油、丹参注射液组的左心室重量指数、左心室截面直径、梗死面积明显较假手术组高（P<0.05）,硝酸甘油组与丹参注射液组以上指标对比无差异（P>0.05）。结论：丹参素注射液可改善急性心肌梗死大鼠的心室重构、左心室功能及肢体导联与胸导联心电图参数,可能与其可降低大鼠的血液流变学指标水平有关。     

曲美他嗪联合麝香保心丸治疗急性心肌梗死的效果研究

目的:研究曲美他嗪(TMZ)联合麝香保心丸(HMP)治疗急性心肌梗死的效果。方法:采用40只雄性C57BL/6J小鼠构建急性心肌梗死模型,随机分成4组,每组10只:(1)假手术组;(2)心肌梗死组;(3)心肌梗死+TMZ组(TMZ 20 mg/Kg灌胃,3次/天);(4)心肌梗死+TMZ+HMP组(HMP 14 mg/Kg灌胃,3次/天)。2周后行心脏超声检查采集心功能参数左室舒张末内径、左室收缩末内径、室间隔厚度、舒张末期左室后壁厚度及射血分数。同时,对心脏标本行形态学分析。结果:TMZ+HMP组左室舒张末内径、左室收缩末内径、舒张末期左室后壁厚度及射血分数均优于于TMZ组(均为P0.05)。心肌组织HE及PSR染色显示TMZ+HMP组心肌细胞坏死及纤维化程度较其余组低。结论:曲美他嗪联合麝香保心丸治疗急性心肌梗死的效果较单用曲美他嗪更加显著。     

参麦注射液联合阿替普酶治疗急性心肌梗死的临床效果研究

目的:研究参麦注射液联合阿替普酶治疗急性心肌梗死的临床效果。方法:选择2015年1月～2016年12月在我院进行诊治的急性心肌梗死患者98例,随机分为两组,每组各49例。对照组静脉滴注阿替普酶100 mg治疗,于90 min内滴注完毕,先静脉推注15 mg,再于30 min内静脉滴注50 mg阿替普酶,最后于60 min内静脉滴注35 mg,每天1次;观察组联合静脉滴注参麦注射液治疗,每次100 mL,每天1次。比较两组的临床治疗效果,治疗前后左心室射血分数、左心室舒张末期内径、左心室后壁厚度等心功能指标及血清心肌肌钙蛋白I(c TnI)、肌酸激酶同工酶(CK-MB)、超氧化物歧化酶以及(SOD)内皮素1(ET-1)水平的变化。随访半年,观察两组的预后情况(再梗死、梗死后心绞痛、血管再通以及冠脉血栓的发生率)。结果:治疗后,观察组的有效率为91.83%(45/49),明显高于对照组[71.43%(35/49)](P0.05);两组的左心室射血分数、左心室舒张末期内径、左心室后壁厚度均较治疗前明显改善(P0.05),且观察组的改善程度明显优于对照组(P0.05);两组的血清TnI、CK-MB、ET-1水平均较治疗前明显降低(P0.05),血清SOD水平均较治疗前明显升高(P0.05),且观察组以上指标的改善情况较对照组更为明显(P0.05);观察组再梗死、梗死后心绞痛以及冠脉血栓的发生率均明显低于对照组(P0.05),血管再通的发生明显高于对照组(P0.05)。结论:与单独使用阿替普酶对比,参麦注射液联合阿替普酶治疗急性心肌梗死临床疗效和安全性较好。     

瑞舒伐他汀强化治疗对急性ST段抬高型心肌梗死患者PCI手术预后的影响

目的:探讨瑞舒伐他汀强化治疗对急性ST段抬高型心肌梗死(STEMI)患者PCI术预后的影响。方法:选择2013年6月-2015年6月我院收治的STEMI患者90例,随机分为研究组与对照组,每组各45例。研究组患者PCI术前及术后均给予瑞舒伐他汀强化治疗,对照组仅在术后给予瑞舒伐他汀治疗。观察并比较两组患者术中慢血流及无复流的发生率,TNI、CK-MB、NT-pro BNP及hs-CRP水平变化,以及左室舒张末期内径、左心房内径、左室射血分数、室间隔厚度。结果:研究组术中慢血流及无复流的发生率显著低于对照组(P0.05);两组患者治疗后TNI、CK-MB、NT-pro BNP、hs-CRP水平均低于治疗前,且研究组低于对照组,差异具有统计学意义(P0.05);两组治疗后左室舒张末期内径、左心房内径、左室射血分数、室间隔厚度比较,差异无统计学意义(P0.05)。结论:瑞舒伐他汀强化治疗可以有效降低STEMI患者心肌坏死及炎症反应的发生率,改善心室重构,值得临床推广应用。     

α- 酮酸片对维持性血液透析患者心脏功能和结构的影响

目的:探讨α-酮酸片(α-KA)对维持性血液透析(MHD)患者心脏功能和结构的影响。方法:观察30例α-酮酸片(商品名:开同)治疗组维持性血液透析患者与30例对照组患者,分别在治疗前及治疗6个月后超声心动图测定心脏结构指标:左房收缩末期内径(LADs)、左室舒张末期内径(LVEDd)、室间隔舒张末期厚度(IVSTd)、左室后壁舒张末期厚度(LVPWTd),左房内径指数(LAI)、左心室心肌重量指数(LVMI)、相对室壁厚度(RWT),心脏功能指标:左室射血分数(LVEF),左室短轴缩短率(FS),二尖瓣口舒张早期和晚期最大血流速度比(E/A)各项指标等检测,比较治疗前后各指标变化。结果:治疗组MHD患者心脏结构指标:左房收缩末期内径(LADs)、左室舒张末期内径(LVEDd)、室间隔舒张末期厚度(IVSTd)、左室后壁舒张末期厚度(LVPWTd),左房内径指数(LAI)、左心室心肌重量指数(LVMI)值均明显低于对照组,二者差异有显著性(P<0.05),两组相对室壁厚度(RWT)相比没有明显的差异(P>0.05)。心脏功能指标:左室射血分数(LVEF),左室短轴缩短率(FS),二尖瓣口舒张早期和晚期最大血流速度比(E/A)值较对照组明显增高(P<0.05),有统计学意义。结论:α-酮酸片可以改善MHD患者的心脏结构和功能,其对MHD患者心血管并发症的预防和治疗有一定临床指导意义。     

经皮冠状动脉介入治疗冠心病合并心力衰竭的效果

目的探计经皮冠状动脉介入治疗冠心病合并心力衰竭的临床效果。方法选择我院2014～2017年冠心病合并心力衰竭病患者100例,随机分为对照组(n=50)和观察组(n=50),观察组给予经皮冠状动脉介入治疗,对照组给予保守治疗,治疗半年后随访,比较两组治疗前后的左心室收缩末期内径(LVESD)、左心室舒张末期内径(LVEDD)、左室短轴缩短率(FS)、射血分数(LVEF)等心脏构型指标变化,并比较两组心脏功能改善情况与半年内发生心血管事件、心脏射血分数(50%)、心室增大的发生率。结果两组治疗后的LVESD、LVEDD、FS、LVEF等心功能指标变化均有改善,观察组治疗后的LVESD、LVEDD、FS、LVEF等心功能指标优于对照组(P0.05)。观察组心脏功能改善情况、半年内发生心血管事件、心脏射血分数(50%)、心室增大的发生显著优于对照组(P0.05)。结论经皮冠状动脉介入治疗冠心病合并心力衰竭可显著提高心功能状态,减低心血管不良事件的发生。     

Insufficient secretion of atrial natriuretic peptide at acute phase of myocardial infarction.

To investigate the secretion of the plasma levels of atrial natriuretic peptide (ANP) in patients with acute myocardial infarction (AMI), we evaluated the relationship between plasma levels of ANP and pulmonary capillary wedge pressure (PCWP) in 45 consecutive patients during the acute phase of AMI ( approximately 12 h after the attack) (group 1) and compared data with those obtained after 1 mo (group 2). In both groups 1 and 2, plasma ANP levels significantly correlated with PCWP. The slope of the linear regression line between the PCWP and ANP in group 1 was significantly lower, by about one-third, than that in group 2. In addition, we examined changes in ANP levels and left ventricular end-diastolic pressure (LVEDP) over 180 min after AMI induced by injection of microspheres into the left coronary arteries of three dogs. The LVEDP and ANP levels 30 min after AMI were significantly higher than those before; however, despite the persistent high LVEDP during the 180 min after AMI, ANP levels decreased gradually and significantly to 63% of the peak level at 150 min. These findings suggest that the secretion of ANP during the acute phase of myocardial infarction may be insufficient relative to the chronic phase.     

Cardiac response to submaximal exercise in dogs susceptible to sudden cardiac death

The hemodynamic response to submaximal exercise was investigated in 38 mongrel dogs with healed anterior wall myocardial infarctions. The dogs were chronically instrumented to measure heart rate (HR), left ventricular pressure (LVP), LVP rate of change, and coronary blood flow. A 2 min coronary occlusion was initiated during the last minute of an exercise stress test and continued for 1 min after cessation of exercise. Nineteen dogs had ventricular fibrillation (susceptible) while 19 animals did not (resistant) during this test. The cardiac response to submaximal exercise was markedly different between the two groups. The susceptible dogs exhibited a significantly higher HR and left ventricular end-diastolic pressure (LVEDP) but a significantly lower left ventricular systolic pressure (LVSP) in response to exercise than did the resistant animals. (For example, response to 6.4 kph at 8% grade; HR, susceptible 201.4 +/- 5.1 beats/min vs. resistant 176.2 +/- 5.6 beats/min; LVEDP, susceptible 19.4 +/- 1.1 mmHg vs. resistant 12.3 +/- 1.7 mmHg; LVSP, susceptible 136.9 +/- 7.9 mmHg vs. resistant 154.6 +/- 9.8 mmHg.) beta-Adrenergic receptor blockade with propranolol reduced the difference noted in the HR response but exacerbated the LVP differences (response to 6.4 kph at 8% grade; HR, susceptible 163.4 +/- 4.7 mmHg vs. resistant 150.3 +/- 6.4 mmHg; LVEDP susceptible 28.4 +/- 2.1 mmHg vs. resistant 19.6 +/- 3.0 mmHg; LVSP, susceptible 122.2 +/- 8.1 mmHg vs. resistant 142.8 +/- 10.7 mmHg). These data indicate that the animals particularly vulnerable to ventricular fibrillation also exhibit a greater degree of left ventricular dysfunction and an increased sympathetic efferent activity.     

Poor Agreement between Pulmonary Capillary Wedge Pressure and Left Ventricular End-Diastolic Pressure in a Veteran Population

Background

Accurate determination of left ventricular filling pressure is essential for differentiation of pre-capillary pulmonary hypertension (PH) from pulmonary venous hypertension (PVH). Previous data suggest only a poor correlation between left ventricular end-diastolic pressure (LVEDP) and its commonly used surrogate, the pulmonary capillary wedge pressure (PCWP). However, no data exist on the diagnostic accuracy of PCWP in veterans. Furthermore, the effects of age and comorbidities on the PCWP-LVEDP relationship remain unknown.

Methods

We investigated the PCWP-LVEDP relationship in 101 patients undergoing simultaneous right and left heart catherization at a large VA hospital. PCWP performance was evaluated using correlation and Bland-Altman analyses. Area under Receiver Operating Characteristics curves (AUROC) for PCWP were determined.

Results

PCWP-LVEDP correlation was moderate (r = 0.57). PCWP-LVEDP calibration was poor (Bland-Altman limits of agreement −17.2 to 11.4 mmHg; mean bias −2.87 mmHg). 59 patients (58.4%) had pulmonary hypertension; 15 (25.4%) of those met pre-capillary PH criteria based on PCWP. However, if LVEDP was used instead of PCWP, 7/15 patients (46.6%) met criteria for PVH rather than pre-capillary PH. When restricting analysis to patients with a mean pulmonary artery pressure of ≥25 mmHg and pulmonary vascular resistance of >3 Wood units (n = 22), 10 patients (45.4%) were classified as pre-capillary PH based on PCWP ≤15 mmHg. However, if LVEDP was used, 4/10 patients (40%) were reclassified as PVH. Among patients with any type of pulmonary hypertension, PCWP discriminated moderately between high and normal LVEDP (AUROC, 0.81; 95%CI 0.69–0.94). PCWP-LVEDP correlation was particularly poor in patients with COPD or obesity.

Conclusion

Reliance on PCWP rather than LVEDP results in misclassification of veterans as having pre-capillary PH rather than PVH in almost 50% of cases. This is clinically relevant, as misclassification may lead to inappropriate therapies and adverse events.     

21毫米人造心脏瓣膜泵的设计及研制

为了研究能够长期置入主动脉瓣环的左心室辅助装置,研制出直径21毫米重27克可植入的主动脉瓣膜泵.装置包括一个转子和一个定子.转子由驱动磁钢和叶轮组成;定子装有带铁心的电机线圈和出口导叶.装置被置於主动脉瓣位置,所以不占用额外的解剖空间.血泵能像自然心脏一样直接将血液由心室输送到主动脉,不需要连接管道和旁路,因此对自然生理循环的干扰可以减到最低.血泵流量由最大到零周期变化.血液动力学测试表明,当血泵转速为17500转/分钟时,可以产生流量5升/分钟、压力增益50毫米汞柱的血流;同一转速下,当流量为零时,血泵能保持主动脉舒张压为80毫米汞柱.     

Systolic pressure gradients between the wall of the left ventricle, the left ventricular chamber, and the aorta during positive inotropic states: implications for left ventricular efficiency

To study systolic pressure gradients developed between the left ventricular wall, its chamber, and the aortic root, in one group of dogs left ventricle ventral wall intramyocardial pressure, left ventricular outflow tract pressure, and aorta pressure were compared with aortic flow as well as left ventricular dimension changes during control conditions as well as during positive intropic states induced by isoproterenol, stellate ganglion stimulation, and noradrenaline. In another group of dogs systolic pressures in the ventral wall of the left ventricle, the main portion of the left ventricular chamber, and the aorta were compared with aortic flow during similar interventions, before and after the administration of phentolamine. Pressure gradients between the wall of the left ventricle and the outflow tract of the left ventricle were minimal during control states, but during the three positive inotropic states were increased significantly. In contrast, pressure gradients between the outflow tract of the left ventricle and the aortic root were insignificant during positive inotropic states; those between the wall and main portion of the chamber were only significantly different during left stellate ganglion stimulation. The data derived from these experiments indicate that useful peak power output of the left ventricle (systolic aortic pressure X flow) is unchanged following isoproterenol infusion, but is increased by stellate ganglion stimulation and noradrenaline. The useful peak power output index (an index of left ventricular efficiency derived by dividing useful peak power output by peak intramyocardial pressure) was reduced more by isoproterenol than the other two interventions.(ABSTRACT TRUNCATED AT 250 WORDS)     

急性心肌梗死患者早期血浆脑钠肽水平与左室重构及预后关系的评估

目的：探讨急性心肌梗死（AMI）早期脑钠肽（BNP）水平与左室重构及预后的关系。方法：用放射免疫法测定AMI患者早期血浆BNP水平;用超声心动图检查测量左室收缩末容积（ESV）、左室舒张末容积（EDV）、射血分数（EF）并通过计算得左室质量（LVM）。并根据左心室容积指标分组,左心室容积增加率〉20%为左心室重构组,否则为非重构组,比较两组血浆BNP水平。结果：重构组恢复期左心室舒张末期及收缩末期容积指数均高于非重构组（P〈0.01）,亦高于急性期左心室容积（P〈0.01）。重构组早期血浆BNP浓度明显高于非重构组（P〈0.01）,恢复期也较非重构组高（P〈0.01）。重构组早期BNP浓度与恢复期左心室容积及容积变化量之间呈正相关。结论：AMI早期BNP升高与急性期左室重构密切相关,血浆BNP浓度可以作为溶栓治疗再通的观察指标及预后判断依据。     

改良大鼠左心室插管术及心衰大鼠左心功能指标的测定

目的完善大鼠左心室插管技术并确定充血性心力衰竭（CHF）大鼠心功能指标参数。方法将80只成年雄性SD大鼠随机分为2组：假手术组（SH）,腹主动脉缩窄模型组（CAA）。采用腹主动脉部分缩窄法制作CHF大鼠模型,BL-420E＋生物信号采集系统测定心功能参数。观察比较2组大鼠第6周后测定的心功能的各项指标。结果（1）经进一步完善大鼠左心室插管技术,成功率明显提高。（2）CAA组大鼠心功能明显减低,左室重量指数（LVMI）、左室舒张末压（LVEDP）升高,左心室内压上升、下降的最大变化速率（±dp/dtmax）下降（P〈0.01）。结论改良大鼠左心室插管术提高成功率,心衰大鼠的心功能指标明显改变。     

Hemodynamic basis for cocaine-induced pulmonary edema in dogs.

We tested the hypothesis that cocaine-induced impairment of left ventricular function results in cardiogenic pulmonary edema. Mongrel dogs, anesthetized with alpha-chloralose, were injected with two doses of cocaine (5 mg/kg iv) 27 min apart. Cocaine produced transient decreases in aortic and left ventricular systolic pressures that were followed by increases exceeding control. As aortic pressure recovered, left ventricular end-diastolic, left atrial (Pla), pulmonary arterial (Ppa), and central venous pressures rose. Cardiac output and stroke volume were reduced when measured 4-5 min after cocaine administration. Peak Ppa and Pla were 31 +/- 5 (SE) mmHg (range 17-51 mmHg) and 26 +/- 5 mmHg (range 12-47 mmHg), respectively. Increases in extravascular lung water content (4.10 to 6.24 g H2O/g dry lung wt) developed in four animals in which Pla exceeded 30 mmHg. Analysis of left ventricular function curves revealed that cocaine depressed the inotropic state of the left ventricle. Cocaine-induced changes in hemodynamics spontaneously recovered and could be elicited again by the second dose of the drug. Our results show that cocaine-induced pulmonary hypertension, associated with decreased left ventricular function, produces pulmonary edema if pulmonary vascular pressures rise sufficiently.     

The effects of changes in inspired oxygen concentration on the experimental production of pulmonary edema in the dog with chronic left ventricular overload.

A twofold increase in left ventricular output was achieved by suturing a Telfon graft between the aorta and left atrium in dogs. Three weeks after surgery the animals were anesthetized and found to have left ventricular end-diastolic pressures averaging 36 mmHg with markedly elevated right ventricular systolic pressures (RVSP). Oxygen breathing resulted in a decrease in left ventricular pressures, RVSP, and arterial pressure in those animals which survived hypoxia. Fifty percent of the shunted dogs subsequently developed fatal pulmonary edema when allowed to breathe 10% oxygen in nitrogen. These animals showed no change in left ventricular function or pulmonary artery pressure (RVSP) in response to pure oxygen administration. It is suggested that there is a gradation of hemodynamic response to pure oxygen depending on the severity of left ventricular overload. In the severest case the 'fixing' of pulmonary hypertension may be due to neurohumoral mechanisms. The subsequent development of pulmonary edema in these animals with hypoxia either involves a change in permeability or a redistribution of hydrostatic pressure within the pulmonary vasculature.     

Effect of increased left atrial pressure on breathing frequency in anesthetized dog

Distension or loading of the isolated canine left heart caused reflex tachypnea in prior studies. The object of the present effort was to explore the possibility that this depended primarily on atrial distension. Cardiopulmonary bypass perfusion and ligation of pulmonary veins were used to isolate the left-heart chambers of anesthetized dogs. Simultaneous distension of the beating left atrium and fibrillating ventricle stimulated breathing frequency (f), whereas isolated ventricular distension did not. At other times, intervals of atrial fibrillation were imposed under two different conditions: 1) while the right heart and lungs were bypassed and systemic perfusion was provided by the left ventricle using blood returned to the left atrium by pump and 2) while the ventricles fibrillated and systemic perfusion was supplied directly by the pump. Atrial fibrillation increased left atrial pressure and stimulated f in condition 1. In condition 2, f increased only if fibrillation was associated with a rise in left atrial pressure. Vagal cooling blocked the effect of fibrillation. I conclude that left atrial distension may initiate reflex tachypnea.