体外循环中急性肺水肿分析

目的：强调重视和加强体外循环中对肺功能的保护。方法：分析16例在体外循环中发生肺水肿患者术前的肺动脉高压,血红蛋白,肾功能和心功能情况,经PEEP＋利尿药＋激素和超滤器为主,辅以强心,扩血管药的协同治疗。结果：所有患者经治疗后气道阻力下降,均减小至术前水平,无酸中毒,尿量＞100ml/min。平均2．5天拔管停呼吸机,11例患者术后第一天均顺利脱离呼吸机。15例患者出院,1例死于MOF。结论：中度肺动脉高压、贫血和心肾功能功能不全可能是体外循环中急性肺水肿的诱发因素,体外循环时应采取措施预防预防和减轻肺功能损伤。     

Ligation of the bronchial artery in sheep attenuates early pulmonary changes following exposure to smoke.

Smoke inhalation can produce acute pulmonary edema. Previous studies have shown that the bronchial arteries are important in acute pulmonary edema occurring after inhalation of a synthetic smoke containing acrolein, a common smoke toxin. We hypothesized that inhalation of smoke from burning cotton, known to contain acrolein, would produce in sheep acute pulmonary edema that was mediated by the bronchial circulation. We reasoned that occluding the bronchial arteries would eliminate smoke-induced pulmonary edema, whereas occlusion of the pulmonary artery would not. Smoke inhalation increased lung lymph flow from baseline from 2.4 +/- 0.7 to 5.6 +/- 1.2 ml/0.5 h at 30 min (P < 0.05) to 9.1 +/- 1 ml/0.5 h at 4 h (P < 0.05). Bronchial artery ligation diminished and delayed the rise in lymph flow with baseline at 2.8 +/- 0.7 ml/0.5 h rising to 3.1 +/- 0. 8 ml/0.5 h at 30 min to 6.5 +/- 1.5 ml/0.5 h at 240 min (P < 0.05). Wet-to-dry ratio was 4.1 +/- 0.2 in control, 5.1 +/- 0.3 in smoke inhalation (P < 0.05), and 4.4 +/- 0.4 in bronchial artery ligation plus smoke-inhalation group. Smoke inhalation after occlusion of the right pulmonary artery resulted in a wet-to-dry ratio after 4 h in the right lung of 5.5 +/- 0.8 (P < 0.05 vs. control) and in the left nonoccluded lung of 5.01 +/- 0.7 (P < 0.05). Thus the bronchial arteries may be major contributors to acute pulmonary and airway edema following smoke inhalation because the edema occurs in the lung with the pulmonary artery occluded but not in the lungs with bronchial arteries ligated.     

Bilateral coronary fistulae to pulmonic valve in presence of severe three-vessel coronary artery disease

A 62-year-old man was admitted to the coronary care unit due to anginal pain and palpitations--coronary angiography revealed three-vessel coronary artery disease. The unexpected finding was the presence of coronary to pulmonary artery fistulae bilaterally, from both the proximal RCA and the proximal LAD. Right heart catheterization revealed normal right ventricular and pulmonary artery pressure and absence of hemodynamically significant left to right shunt. The patient underwent a triple coronary bypass including the closure of bilateral fistulae, which were draining into the left sinus of the pulmonary valve. One month after the operation he was in good health and had no complaints. Bilateral coronary artery fistulae is a rare anomaly diagnosed in 0.002-0.0013% of adult coronary angiograms. (Int J Cardiovasc Intervent 1999; 2: 249-251).     

Effect of prostaglandin A1 infusion in hypertensive patients with renal artery stenosis

Clinical data, arteriographic findings, peripheral and renal vein plasma renin activity (PRA) studies and responses to prostaglandin A1 infusion are presented from observations in seven hypertensive patients with renal artery stenosis. PGA1 infusion caused an increase in PRA and urine sodium excretion but no significant change in blood pressure. Exaggerated increases in PRA were observed in five patients. With cessation of PGA1 infusion PRA returned toward pre-infusion levels. In two patients bilateral renal and peripheral vein PRA's were determined before and during PGA1 infusion. PGA1 caused a greater increase in renal vein PRA than in peripheral vein PRA indicating a direct enhancement of renin secretion. These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis.     

Bilateral traumatic renal artery thrombosis

A case of bilateral traumatic renal artery thrombosis involving three renal arteries is presented. Four other cases of this entity are summarized for comparison. The recommended course of investigation is outlined, and the urgency of immediate surgical intervention is emphasized.     

冠脉搭桥术后肺水肿患者氧化应激状态的变化观察

目的:研究冠脉搭桥术后肺水肿患者氧化应激状态变化观察,评价氧化应激状态与肺水肿的关联性,为临床减轻冠脉搭桥术后肺部并发症提供依据。方法:将本院2014年1月-2015年6月收治的冠脉搭桥术后肺水肿患者40例作为试验组,另选同期冠脉搭桥术后未发生肺水肿患者40例作为对照组。检测并比较两组患者术后3天、7天及14天的丙二醛(MDA)、总抗氧化能力(TAC)、过氧化氢酶(CAT)、C反应蛋白(CRP)、过氧化脂(LPO)及超氧化物歧化酶(SOD)的水平变化。结果:与对照组患者相比,试验组患者术后3 d、7 d、14 d三个时间点MDA,LPO及CRP表达水平均显著提高,而TAC,SOD及CAT表达水平均显著降低,差异均具有统计学意义(P0.05)。与术后3 d相比,两组患者术后7 d、14 d两个时间点的MDA,LPO和CRP表达水平均显著降低,而TAC,SOD及CAT表达水平均显著提高,差异具有统计学意义(P0.05)。结论:冠脉搭桥术后肺水肿的发生与患者氧化应激状态密切相关,机体自由基增多、抗氧化能力下降是肺水肿发生的重要机制。     

Effect of prostaglandin A1 infusion in hypertensive patients with renal artery stenosis

Clinical data, arteriographic findings, peripheral and renal vein plasma renin activity (PRA) studies and responses to prostaglandin A₁ infusion are presented from observations in seven hypertensive patients with renal artery stenosis. PGA₁ infusion caused an increase in PRA and urine sodium excretion but no significant change in blood pressure. Exaggerated increases in PRA were observed in five patients. With cessation of PGA₁ infusion PRA returned toward pre-infusion levels. In two patients bilateral renal and peripheral vein PRA's were determined before and during PGA₁ infusion. PGA₁ caused a greater increase in renal vein PRA than in peripheral vein PRA indicating a direct enhancement of renin secretion. These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis.     

Pulmonary circulation in experimental pulmonary edema during diverse artificial respiration regimes

In acute experiments on cats with closed chest by ultrasonic method the authors studied the blood flow in low-lobar pulmonary artery and the vein, the blood pressure in pulmonary artery, lung vessels resistance in experimental pulmonary edema caused by intravenous infusion of mixture fatty acids at artificial ventilation of increased frequencies or volumes, at was shown, that artificial ventilation of increased frequencies in pulmonary edema reduces the pressure increase in pulmonary artery, lung vessels resistance and increases the blood flow in pulmonary artery and vein. Artificial ventilation of increased volumes produces more intense pressure increase in pulmonary artery and lung vessels resistance than in initial ventilation but the blood flow was slightly changed. The authors assume that artificial ventilation of increased frequencies or volumes in pulmonary edema due to pulmonary circulation change reduces the pulmonary edema intensity at the beginning.     

Effect of prolonged renal dysfunction on intravascular and extravascular pulmonary fluid volumes during left atrial hypertension

To examine the development of pulmonary edema during experimental renal dysfunction, left atrial pressure was altered in 14 mongrel dogs divided into two groups. Group 1 was composed of seven control animals, and Group 2 was composed of seven animals with surgically induced renal failure (1 week of bilateral ureteral ligation). Data were obtained at two levels of matched transmural pulmonary vascular pressure (defined as mean left atrial pressure less serum protein osmotic pressure). In the animals with renal dysfunction, extravascular lung water (EVLW) (thermal-green dye technique) was higher at moderately (-1 to -2 mm Hg) and severely elevated (11 to 12 mm Hg) vascular driving pressures (11.5 +/- 1.2 cc/kg vs 10.6 +/- 0.8 cc/kg and 14.8 +/- 1.3 cc/kg vs 13.0 +/- 1.9 cc/kg, respectively, both P less than 0.05 vs control). Because protein osmotic pressure was lower in the renal failure group (15.0 +/- 1.8 mm Hg vs 18.4 +/- 1.4 mm Hg, P less than 0.05), greater accumulations of extravascular lung water occurred at lower levels of left atrial pressure (14.2 +/- 1.4 mm Hg vs 17.1 +/- 1.2 mm Hg, P less than 0.05; 26.8 +/- 2.6 mm Hg vs 29.5 +/- 2.3 mm Hg, P less than 0.01). In addition, when the ratio of EVLW/PBV (pulmonary blood volume) was examined in both groups at each stage of the experiment, the ratio was greater in the Group 2 animals at each elevated pressure, suggesting increased permeability with renal dysfunction. In conclusion, pulmonary edema formation occurs at lower left atrial pressures in the setting of sustained renal dysfunction, this phenomenon can be partially explained by lower protein osmotic pressure though altered pulmonary microvascular permeability may contribute to edema formation.     

A case of pheochromocytoma with renal artery stenosis and post-surgical watery diarrhea

A 35-year-old woman was admitted to our hospital with the following complaints, headache, sweating, anxiety, dizziness, nausea, vomiting and severe hypertension. The technical images (abdominal CT, scintigraphic octreotide scan and renal arteriography) revealed the presence of a left adrenal pheochromocytoma and stenosis of the renal artery. Ten days following adrenalectomy, watery diarrhea appeared. The long-acting somatostatin analogue octreotide (LAR, 30 mg/month, i.m.), was started, and after 2 weeks diarrhea decreased and gradually disappeared. In conclusion, we were confronted with an unusual case of pheochromocytoma associated with renal artery stenosis and the appearance of watery diarrhea some days after surgical treatment. Treatment with octreotide brought about the remission of diarrhea in this patient.     

Medical Grand Rounds: refractory hypertension and renal insufficiency in a patient with renal artery stenosis.

Renal artery stenosis has become increasingly common as a cause of refractory hypertension and renal insufficiency. There is a high prevalence of bilateral disease and the lesions tend to progress over time. Newer, less invasive, imaging modalities such as doppler ultrasound, magnetic resonance angiography, and spiral CT scanning are evolving technologies in the diagnosis of renal artery stenosis. Advances in surgical technique, particularly the development of extra-anatomical procedures such as spleno-renal and hepato-renal by pass, have significantly lowered surgical morbidity and mortality and provides revascularization options for patients with complex vascular disease that would previously not have been considered because of their high surgical risk. Improvements in angioplasty technique and the use of stents are broadening the types of lesions that can be successfully approached with these techniques and may be particularly helpful for patients with more severe cardiac or cerebrovascular disease. The benefits of revascularization may be even greater for preservation of renal function than for control of blood pressure in properly selected patients. It is difficult to predict which patients will benefit from surgical revascularization versus medical management of RAS. Knowledge of the progressive nature of RAS, the high prevalence of bilateral disease, and the clinical characteristics that correlate with progression (e.g., decreasing renal size) are helpful in guiding clinical decisions regarding intervention. Additional studies to determine the predictive value of non-invasive tests such as CRS, doppler ultrasound before and after administration of angiotensin converting enzyme inhibitors, and other tests, are needed to assist the clinician in identifying who will benefit most from revascularization both in terms of renal function and blood pressure control.     

Bronchial artery ligation modifies pulmonary edema after exposure to smoke with acrolein

Pulmonary edema can follow smoke inhalation and is believed to be due to the multiple chemical toxins in smoke, not the heat. We have developed a synthetic smoke composed of aerosolized charcoal particles to which one toxin at a time can be added to determine whether it produces pulmonary edema. Acrolein, a common component of smoke, when added to the synthetic smoke, produced a delayed-onset pulmonary edema in dogs in which the extravascular lung water (EVLW) as detected by a double-indicator technique began to rise after 42 +/- 2 (SE) min from 148 +/- 16 to 376 +/- 60 ml at 165 min after smoke exposure. The resulting pulmonary edema was widespread macroscopically but appeared focal microscopically with fibrin deposits in alveoli adjacent to small bronchi and bronchioles. Bronchial vessels were markedly dilated and congested. Monastral blue B when injected intravenously leaked into the walls of the bronchial vessels down to the region of the small bronchioles (less than or equal to 0.5 mm ID) of acrolein-smoke-exposed dogs but not into the pulmonary vessels. Furthermore, ligation of the bronchial arteries delayed the onset of pulmonary edema (87 +/- 3 min, P less than 0.05) and lessened the magnitude (232 +/- 30 ml, P less than 0.05) at 166 +/- 3 min after acrolein-smoke exposure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Local infusion of low-dose streptokinase for renal artery thromboembolism.

Although local low-dose therapy with streptokinase has been found to be effective in patients with recent arterial occlusions, there have been few reports of its use in those with renal artery occlusion, perhaps because this condition is difficult to diagnose early. This paper describes a patient with acute renal artery thromboembolism and intermittent tachyarrhythmias in whom treatment with a local low-dose infusion of streptokinase resulted in complete recanalization of the main artery and good recovery of renal function.     

Bronchial circulation in pulmonary artery occlusion and reperfusion

Obstruction of pulmonary arterial blood flow results in minimal biochemical and/or morphological changes in the involved lung. If the lung is reperfused, a syndrome of leukopenia and lung edema occurs. We used the radiolabeled microsphere technique to measure the response of the bronchial circulation in rabbits to acute pulmonary artery occlusion (PAO) and to pulmonary artery reperfusion. We found that the bronchial blood flow (Qbr) decreased from a base line of 0.37 +/- 0.10 to 0.09 +/- 0.04 (SE) ml.min-1.g dry lung-1 (P less than or equal to 0.05) after 4 h of PAO. In a separate group of animals, Qbr 24 h after PAO remained low (0.20 +/- 0.07 ml.min-1.g dry lung-1, P = 0.06). Qbr during PAO was inversely correlated with the wet-to-dry ratio after reperfusion (r = -0.68, P = 0.06). Qbr did not change during 4 h of reperfusion. We speculate that a critical level of Qbr may be necessary during PAO to prevent ischemia/reperfusion injury from occurring.     

Anomalous origin of the left coronary artery from the pulmonary artery treated by palliative Vineberg operation in an infant

Anomalous origin of the left coronary artery from the pulmonary artery was diagnosed in an infant girl who had evidence of transmural myocardial infarction of the free wall of the left ventricle. At age 13 months, she underwent a palliative left Vineberg implant, and remained asymptomatic until she was 8 years of age. At that time, she underwent suturing of the left coronary ostium for obliteration of the left coronary shunt at the pulmonary artery. At age 13, she underwent aortocoronary bypass to the left main coronary artery, with end-to-end anastomosis. The patient remains asymptomatic to date. We believe that this is the first reported case of a Vineberg operation performed in an infant for palliation of an anomalous left coronary artery originating from the pulmonary artery. This method allows time for the development of collateral circulation to the left coronary artery before definitive surgery is performed.     

The ischemic lung: Role of the bronchial arteries in lung function

A patient with a dissecting aortic aneurysm, Type 1, developed acute pulmonary edema unexplained by the usual etiologic factors. Pathologic evidence that bronchial arterial circulation was interrupted led us to hypothesize that pulmonary edema could be due to ischemia of the bronchial circulation. To test this hypothesis, two chronic studies were done in dogs. The first study consisted of selective ligation of the right posterior bronchial artery at its origin at the fifth or sixth intercostal artery. After recovery from surgery, biopsies were taken from the ipsilateral and contralateral lung at time periods from 5 hours to 11 days. Ischemic damage was found in seven of eight dogs (87.5%), and was confined to the right lung. Histological examination revealed initial congestion within 8 hours, followed by pulmonary edema within 72 hours, and finally, disruption of alveolar septa with small emphysematous bullae on the eleventh postoperative day. The left lung remained normal in histological appearance. The second study consisted of transplanting the bronchial artery to the pulmonary artery to create a low pressure system and low O(2) content, and to simulate a regional shock situation. In five of six dogs (83.3%), the anastomosis was occluded within 72 hours, probably due to pressure competition from small collateral bronchial circulation. However, in these five dogs, pulmonary vascular resistance increased by 53%, intrapulmonary shunting increased by 83%, and the alveolar-to-arterial oxygen gradient increased by 150 mm Hg. Pulmonary edema was again confined to the right lung. Bronchial arteriograms demonstrated the extensive and variable distribution of the bronchial circulation in dogs. In the sixth dog, the anastomosis remained patent with a left-to-right shunt, due to a larger bronchial arterial collateral circulation. In this animal, the pulmonary arterial resistance, intrapulmonary shunting, and alveolar-arterial O(2) gradient were normal. Pulmonary edema was absent in lung biopsies. Bronchial circulation is discussed with respect to its clinical implications for lung transplants, shock, thoracic aneurysms, and mediastinal surgery. The results of this study suggest that the systemic bronchial circulation is important for normal lung function.     

Pulmonary artery pressure and cardiac function in children and adolescents after rapid ascent to 3,450 m

High-altitude destinations are visited by increasing numbers of children and adolescents. High-altitude hypoxia triggers pulmonary hypertension that in turn may have adverse effects on cardiac function and may induce life-threatening high-altitude pulmonary edema (HAPE), but there are limited data in this young population. We, therefore, assessed in 118 nonacclimatized healthy children and adolescents (mean ± SD; age: 11 ± 2 yr) the effects of rapid ascent to high altitude on pulmonary artery pressure and right and left ventricular function by echocardiography. Pulmonary artery pressure was estimated by measuring the systolic right ventricular to right atrial pressure gradient. The echocardiography was performed at low altitude and 40 h after rapid ascent to 3,450 m. Pulmonary artery pressure was more than twofold higher at high than at low altitude (35 ± 11 vs. 16 ± 3 mmHg; P < 0.0001), and there existed a wide variability of pulmonary artery pressure at high altitude with an estimated upper 95% limit of 52 mmHg. Moreover, pulmonary artery pressure and its altitude-induced increase were inversely related to age, resulting in an almost twofold larger increase in the 6- to 9- than in the 14- to 16-yr-old participants (24 ± 12 vs. 13 ± 8 mmHg; P = 0.004). Even in children with the most severe altitude-induced pulmonary hypertension, right ventricular systolic function did not decrease, but increased, and none of the children developed HAPE. HAPE appears to be a rare event in this young population after rapid ascent to this altitude at which major tourist destinations are located.     

Extravascular lung water measurements and hemodynamic monitoring in the critically ill: bedside alternatives to the pulmonary artery catheter

The recently completed Fluid and Catheter Treatment Trial conducted by the National Institutes of Health ARDSNetwork casts doubt on the value of routine pulmonary artery catheterization for hemodynamic management of the critically ill. Several alternatives are available, and, in this review, we evaluate the theoretical, validation, and empirical databases for two of these: transpulmonary thermodilution measurements (yielding estimates of cardiac output, intrathoracic blood volume, and extravascular lung water) that do not require a pulmonary artery catheter, and hemodynamic measurements (including estimates of cardiac output and ejection time, a variable sensitive to intravascular volume) obtained by esophageal Doppler analysis of blood flow through the descending aorta. We conclude that both deserve serious consideration as a means of acquiring useful hemodynamic data for managing shock and fluid resuscitation in the critically ill, especially in those with acute lung injury and pulmonary edema, but that additional study, including carefully performed, prospective clinical trials demonstrating outcome benefit, is needed.     

Carotid artery injury with cerebral infarction following head and neck blunt trauma: report of a case

Blunt injury to the carotid artery is rare but may produce a devastating outcome with longterm morbidity. Initial recognition by clinicians is often difficult because of the diverse clinical manifestations, the delay in presentation of symptoms, and the associated multi-organ system injuries that accompany carotid injury. Early diagnosis and successful management of traumatic carotid artery injury require a high index of clinical suspicion. We report herein a 20-year-old male victim of internal carotid artery injury induced by a motorcycle accident, who initially presented with a clear consciousness and had normal computed tomogram (CT) of brain. Two days after injury, the patient suffered from left hemiplegia and coma. The follow-up brain CT showed acute infarction of right cerebrum and severe cerebral edema. Emergency craniotomy for brain decompression and anticoagulation therapy was carried out. After a three-month treatment, he was discharged and underwent regular follow-up in the outpatient department. Six months later, the patient had intact awareness but remained in a left-sided hemiparetic state.     

Pulmonary fluid balance following pulmocutaneous baroreceptor denervation in the toad

Pulmonary hemodynamics and net transcapillary fluid flux (NTFF) were measured in conscious toads before and following bilateral denervation of the recurrent laryngeal nerves (rLN), which contain afferents from baroreceptors located in the pulmocutaneous arteries. Denervation caused an acute doubling of the arterial-venous pressure gradient across the lung and a threefold increase in pulmonary blood flow. Calculated pulmonary vascular resistance fell and remained below control values through the period of experimentation. NTFF increased by an order of magnitude (0.74-7.77 ml X kg-1 X min-1), as filtration increased in response to the hemodynamic changes caused by rLN denervation. There was a better correlation between NTFF and pulmonary blood flow than between NTFF and pulmonary driving pressure. Our results support the view that tonic neural input from pulmocutaneous baroreceptors protects the anuran lung from edema by restraining pulmonary driving pressure and blood flow and perhaps by reflexly maintaining vascular tone in the extrinsic pulmonary artery, therefore tending to increase the pre-to-postpulmonary capillary resistance ratio and biasing the Starling relationship in the pulmonary capillaries against filtration.