Collateral bronchopulmonary circulation after spontaneous recanalisation of pulmonary thromboemboli in the dog.

STUDY OBJECTIVE: The aim was to study the fate of enlarged bronchial arteries after resolution of experimental pulmonary embolism. DESIGN: Embolisation of the pulmonary arteries of both lungs was performed with intravenous gelfoam. Pulmonary pressure and pulmonary arteriolar resistance were measured 1 h, 40 d and 80 d after embolisation. Pulmonary angiography and aortography were performed at the same time to evaluate the pulmonary emboli and the collateral bronchopulmonary circulation. Aortography and gross pathological and histological examination of the lungs was performed after 80 d. EXPERIMENTAL MATERIAL: 15 adult mongrel dogs of either sex were studied, weight 22-25 kg. Nine dogs were embolised and there were six controls. MEASUREMENTS AND MAIN RESULTS: All animals survived until 80 d. There was a rise (p less than 0.001) in mean pulmonary artery pressure and arteriolar resistance 1 h after embolisation. Pulmonary artery pressures and resistances were still raised 40 d after embolisation but had returned to normal after 80 d. Pulmonary arteriography at 1 h confirmed massive thromboembolism. After 40 d antegrade pulmonary blood flow was almost completely restored, and the thromboemboli had largely disappeared. Pulmonary angiograms were completely normal after 80 d. Aortography after 40 d showed a well developed collateral bronchopulmonary circulation, most pronounced in the lower lobes, which persisted unchanged until 80 d. Aortography and gross pathological and histological examination at necropsy confirmed the presence of hypertrophic well developed bronchial arteries to both lower lobes and to a lesser extent to the middle and upper lobes, with only a few organised and recanalised thrombi in segmental arteries of both lower lobes. CONCLUSIONS: Our data show a temporal dissociation between the resolution of pulmonary thromboemboli in the present model and the eventual regression of developed bronchopulmonary collateral vessels. The mechanism of this dissociation could not be elucidated.

Bronchial arteries in experimental pulmonary infarction: angiographic and morphometric study.

OBJECTIVES: The aim was to investigate (1) whether collateral bronchopulmonary circulation developing due to chronic pulmonary embolism could prevent the evolution of pulmonary infarction after induction of pulmonary venous outflow impairment; and (2) how collateral bronchopulmonary circulation developed after acute embolisation of the lung with impaired pulmonary venous outflow. METHODS: Fifty two mongrel dogs were studied. Thirty six dogs were experimental animals and 16 were in a control group. Unilateral impairment of pulmonary venous outflow was induced by constriction of the left pulmonary veins in two groups of experimental dogs: (1) three months after and (2) one hour before bilateral embolisation of the pulmonary artery. All animals were killed 12 days after constriction. The size of the bronchial arteries was evaluated from angiograms. The diameter and the wall thickness of the arteries were measured during histology. RESULTS: In all experimental dogs, haemorrhagic infarctions developed distally to emboli in the left lung regardless of whether the bronchial arteries were dilated before induction of pulmonary venous constriction or whether collateral circulation started to develop after pulmonary venous constriction. Constriction of the pulmonary veins was an essential factor for pulmonary infarction to develop as no infarction developed in the embolised regions of the right lungs with intact pulmonary venous outflow. Pulmonary venous constriction alone did not cause dilatation or hypertrophy of the bronchial arteries. After pulmonary artery embolisation, the same enlargement and hypertrophy of the bronchial arteries occurred both in the left lung with previously impaired venous outflow and in the right lung with intact pulmonary veins. CONCLUSIONS: Expanded bronchopulmonary circulation did not prevent the development of infarction in the embolised region of the lung with impaired pulmonary venous outflow. Development of collateral bronchopulmonary circulation was not influenced by previously impaired pulmonary venous outflow.

[Multiple carcinomas arising from congenital cysts of the liver and kidneys]. / Mnohocetný karcinoma vycházející z kongenitálních cyst jater a ledvin.

In a 48 year old man suffering from dyspepsia and progressive enlargement of the liver, the clinical suspicion of a malignant cystic disease of the liver was voiced. Six months after the onset of the complaints the disease was diagnosed through a biopsy performed during an operative laporotomy. The patient died in spite of combined antitumorous chemotherapy in some further 7 months in a state of hepatic coma. A detailed pathologico-anatomical examination divulged the picture of a very rare form of carcinoma arising from the membrane covering not only the hepatic cysts but also those in the kidneys. Microscopically it had the structure of a papillary adenocarcinoma. Differential diagnostic variations of this tumour as compared to true neoplastic cysts i. e. cystadenomas or cystadenocarcinomas arising from the lining of hepatic bile ducts, are pointed out in this paper.

[Cardiac tamponade as a complication of acute myocardial infarct. (Clinical and pathologico-anatomic analysis of patients with acute myocardial infarct and cardiac tamponade)]. / Srdecní tamponáda jako komplikace akutního srdecního infarktu. (Klinický a patologicko-anatomický rozbor nemocných s akutním srdecním infarktem a srdecni tamponádou.)

Cardiac tamponade is a frequent cause of death in acute myocardial infarction--in as many 23%. It is encountered in particular in the 7th and 8th decade, in patients with a first infarction which is frequently situated in the anterior wall of the left ventricle. 93% of the patients have obvious ECG manifestations of Q infarction. The diagnosis of cardiac tamponade is easy when during an acute terminal attack slow activity on the ECG tracing is found without a haemodynamic response and the pulse on the great arteries is not palpable even after external cardiac massage. In 80% the onset of cardiac tamponade is very sudden. The presence of shock or cardiac failure makes the diagnosis of cardiac tamponade more difficult. As to investigated indicators, in the development of cardiac tamponade the systemic pressure--systolic as well as diastolic--on admission or during hospitalization, may play a part. The patients have a less marked coronary sclerosis, fibrosis of the cardiac muscle is less frequently present. Previous necroses of the heart muscle may have probably a certain protective effect on the development of cardiac tamponade. Anticoagulants obviously do not influence the development of cardiac tamponade.

[Malignant tumors of the heart from the viewpoint of the surgeon]. / Zhoubné nádory srdce z hlediska chirurga.

The authors present three cases of malignant affections of the heart. In two instances a primary haemangiosarcoma was involved which originated in the right atrium, in the third patient a secondary of a left ovarian carcinoma was involved. They draw attention to the similar symptomatology of the disease and the possibility of echocardiographic visualization of intracardiac formations. The possibilities of radical removal of malignant tumours of the heart are very limited and call for the use of extracorporeal circulation. The incidence of this disease is very rare.

The bronchial arteries of the dog after selective embolization of the pulmonary artery with emboli of various size. A morphological study.

The aim of the study was to investigate whether the development of collateral broncho-pulmonary circulation depends on the size of obliterated branches of the pulmonary artery. Massive embolization of the pulmonary arterial bed was performed with sterile plastic spheres of known size from 0.08 to 1.0 mm in diameter in 25 dogs. Three months after embolization, the bronchial arteries were investigated with the use of post mortem bronchial arteriography and histology. The same investigation of the bronchial arteries was performed in 6 control dogs with intact pulmonary circulation. Bronchial arteriography showed conspicuous dilatation of the bronchial arteries in all dogs in which the emboli of 0.4, 0.6 and 1.0 mm in diameter were used for pulmonary artery embolization. Embolization with spheres of 0.08, 0.175 and 0.3 mm in diameter did not cause any enlargement of the bronchial arteries. They were of the same size as those in control dogs. Histological investigation revealed that the bronchial arteries were enlarged and hypertrophic in all dogs which the elastic branches of the pulmonary artery had been occluded. The bronchial arteries never showed an increase in size in case of embolization of muscular arteries or arteriolae. The results showed that the development of collateral bronchopulmonary circulation in the dog depends on the size of the occluded branch of the pulmonary artery.

Echocardiography of ruptured aortic valvular leaflet.

An echocardiographic finding presenting itself as a ruptured noncoronary aortic cusp is described. The basic finding included a constant diastolic echo separation of the right coronary and noncoronary cusps, noncoronary cusp prolapse in the direction of the posterior aortic wall and its high-frequency diastolic flutter. The diagnosis was confirmed at autopsy. The case study reaffirmed the clinical value of echocardiography which was the only technique, including the invasive ones, permitting to make an accurate morphological diagnosis.