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Biomedical subjects

C A Wagenvoort

Publications and source records attributed to C A Wagenvoort.

At least 19 recordsLinked to original sources
PubMed1996

A stable model of respiratory distress by small injections of oleic acid in pigs.

OBJECTIVE: Development of a stable model of respiratory distress in pigs with oleic acid, fulfilling clinical criteria of the adult respiratory distress syndrome (ARDS). DESIGN: Eight pigs (9.1 +/- 0.7 kg) were anesthetized with pentobarbital, paralyzed with tubocurarine and mechanically ventilated with an FIO2 of 0.6, an I:E ratio of 2:3 and a PEEP of 0.2 kPa. Oleic acid (dissolved 1:1 in 96% alcohol) was administered in a series of multiple injections of 0.1 ml until PaO2 was lower than 8 kPa. MEASUREMENTS AND RESULTS: Careful titration of the oleic acid injections on guidance of the PaO2 established a reproducible respiratory distress (PaO2 = 7.3 +/- 0.8 kPa), in which gas exchange and hemodynamic variables were stable for at least 4 h. The number of oleic acid injections (22 +/- 11, mean and SD) varied between the animals. CONCLUSIONS: With the use of multiple injections of oleic acid, a stable model of early respiratory distress in pigs can be achieved, in spite of individual differences in sensitivity. Such a stable model allows for a diversity of studies on early respiratory distress.

Animals↗
PubMed1996

Pulmonary hypertension after transjugular intrahepatic portosystemic shunt (TIPS).

We reported the case of a patient in whom severe, and ultimately fatal, pulmonary hypertension developed 1.5 yrs after transjugular intrahepatic portosystemic shunt (TIPS). Pulmonary artery pressures were not affected by 100% oxygen, prostacyclin or nifedipine. Postmortem examinations showed pulmonary and vascular abnormalities typical of pulmonary hypertension. Pulmonary artery pressures should be measured in each patient with otherwise not readily explained dyspnoea following transjugular intrahepatic portosystemic shunt.

Fatal Outcome↗
PubMed1995

Pathology of pulmonary thromboembolism.

The incidence of pulmonary thromboembolism is hard to assess by the pathologist as a result of seasonal variation of embolism and disappearance of emboli by thrombolysis. However, the great differences in estimates of the incidence in routine hospital autopsies is mainly related to variation in scrutiny of the investigation and in size of area searched microscopically. Obstruction of major pulmonary arteries almost always results from thromboembolism which is most often found in its acute stage. In chronic major vessel embolism, arterial obstruction by an organized mass may produce pulmonary hypertension. Recanalization of such a mass results in so-called bands and webs. There are no reliable criteria to differentiate between emboli and primary thrombi or their sequelae. In peripheral, particularly muscular pulmonary arteries, thrombi are most likely primary, especially when associated with advanced age and with pulmonary hypertension. However, small arteries may be subject to extensive microembolism following fragmentation of large thromboemboli. Thrombotic arteriopathy is the pulmonary arterial disease based upon either primary thrombosis or embolism. It is often associated with pulmonary hypertension, and characterized by irregular, nonlaminar, often obliterative, intimal fibrosis. Recanalization channels, sometimes widening to separate intravascular fibrous septa, are characteristic features. Reversibility of post-thrombotic lesions is very limited.

Chronic Disease↗
PubMed1993

Thrombotic lesions in primary plexogenic arteriopathy. Similar pathogenesis or complication?

In 78 patients with primary plexogenic arteriopathy (PPA), numbers of organized and recanalized thrombi were established in histologic slides of lung tissue and expressed per square centimeter of section. Three control groups of ten individuals each were used: normal, plexogenic arteriopathy secondary to ventricular septal defect, and hypoxic pulmonary hypertension. Thrombotic lesions were scarce in normal individuals but numerous in all three groups with pulmonary hypertension. There is also a positive correlation with age. Thrombotic lesions are absent or scarce in children but more common in adults, even in normal control subjects and particularly in pulmonary hypertension by whatever cause. In PPA there is likely to be a relation with the duration of illness but not with the stage of the disease. The complete pattern of plexogenic arteriopathy may develop in the absence of thrombotic lesions, which clearly are not essential for its pathogenesis. Rather than being part specifically of PPA, as sometimes suggested, thrombotic lesions complicate various types of hypertensive pulmonary vascular disease. Apparently the combination of sustained pulmonary hypertension and age, possibly through endothelial injury, may elicit thrombosis and its sequelae, which in turn may aggravate the pulmonary arterial pressure.

Adolescent↗
PubMed1993

Pulmonary vasoconstriction in oleic acid induced lung injury. A morphometric study.

Distribution and severity of active vasoconstriction of muscular pulmonary arteries were morphometrically assessed in anaesthetized, paralysed and mechanically ventilated pigs with respiratory distress, induced by oleic acid. Vasoconstriction was deduced from the medial thickness which was measured and expressed as a percentage of external diameter. Six pigs received oleic acid (0.12 +/- 0.07 ml/kg), dissolved 1:1 in 96% alcohol, in multiple injections of 0.1 ml. Six pigs were used as controls. After the oleic acid injections a stable hypoxaemia (PaO2 = 57 +/- 8 mmHg, at an inspiratory oxygen fraction of 0.6) and pulmonary hypertension (mean Ppa = 36 +/- 2 mmHg) were obtained for several hours. Electron microscopy revealed swelling of endothelial cells with signs of degeneration. Medial thickness was far greater in the oleic acid group than in the control group; overall mean values were 8.1 +/- 3.2 and 3.8 +/- 1.7% respectively (P < 0.001). Arteries with prominent vasoconstriction were lying in clusters. This pattern was the same in dependent and non-dependent regions. We concluded that in oleic acid induced respiratory distress active vasoconstriction of muscular pulmonary arteries is an important factor in the development of pulmonary hypertension. Besides vasoconstriction, endothelial swelling and intravascular clotting may contribute to the development of pulmonary hypertension.

Animals↗
PubMed1993

Pulmonary veno-occlusive disease and Hodgkin's lymphoma.

Pulmonary veno-occlusive disease (PVOD) is a rare cause of pulmonary hypertension, and is of unknown aetiology. It has seldom been described in association with malignant disease and cytotoxic chemotherapy, and there have been only two previous reports of an association with Hodgkin's disease [1, 2]. We report a third case which developed 14 yrs after Hodgkin's disease had been diagnosed and treated, initially with radiotherapy and subsequently with chemotherapy.

Adult↗
PubMed1990

Ultrastructural heterogeneity of lung carcinomas: representativity of samples for electron microscopy in tumor classification.

Histologic heterogeneity of tumors is a well-known phenomenon, which has been repeated studied at the light microscopic level. Electron microscopy has been advocated as an adjunct in classification of tumors which pose difficulties on light microscopic classification. However, in view of tumor heterogeneity, it might be anticipated that the problem of sample error could detract from the usefulness of electron microscopy in tumor typing. Ultrastructural heterogeneity of tumors has thus far not been systematically investigated. We performed an ultrastructural randomized and blinded study of superficial and deep samples of 44 resected lung carcinomas, tumors which are notorious for their histologic heterogeneity. Neuroendocrine and squamous differentiation, as well as adenodifferentiation, were assessed separately and semiquantitatively in each sample. Twenty-six tumors showed more than one type of differentiation in at least one sample. However, in only two cases did the main type of differentiation differ between the two samples. A further nine cases showed one predominant differentiation type in both samples, but a similarly pronounced second differentiation type in one of the samples. Thus, in terms of ultrastructural diagnosis, the two samples showed a major discrepancy in two of 44 cases, and a minor discrepancy in nine of 44 cases. We conclude that ultrastructural heterogeneity of lung tumors is a common occurrence, but that it only rarely leads to totally different ultrastructural diagnoses.

Carcinoma↗
PubMed1989

[Arterial hypertension and veno-occlusive disease. Connections with pulmonary hemorrhage].

Primary pulmonary hypertension, as defined by the World Health Organization, specifically includes three entities: primary plexogenic arteriopathy, pulmonary veno-occlusive disease, and silent recurrent thromboembolism. Pulmonary hemorrhage may occur in each of these syndromes but is not usually a prominent symptom. The hemorrhage is probably the result of a variety of causes and related to the specific morphologic characteristics of the pulmonary vasculature in these diseases. In primary plexogenic arteriopathy, hemoptysis and pulmonary hemosiderosis occur mainly in advanced disease with dilatation lesions and plexiform lesions. In veno-occlusive disease, pulmonary hemorrhage occurs chiefly in adult patients and is almost certainly capillary in origin. In recurrent thromboembolism, hemoptysis is considerably more common in the symptomatic form than in the silent form, probably because hemorrhagic infarction and anticoagulant therapy play a greater role in the former situation.

Hemorrhage↗
PubMed1988

Morphological substrate for the reversibility and irreversibility of pulmonary hypertension.

The reversibility of pulmonary hypertension in hypertensive pulmonary vascular disease depends, in the first place, on the feasibility of eliminating the cause of the elevation of pressure. Equally important in this respect are the type, the severity, and the extent of the pulmonary vascular lesions. This implies that various forms of pulmonary hypertension have completely different tendencies for regression. In thrombotic arteriopathy, whether caused by primary thrombosis or by embolism, the chance of regression of pulmonary hypertension, and of the vascular lesions, is limited. On the other hand, in many patients pulmonary venous hypertension and the associated vasculopathy, even when severe, appear potentially reversible. Experimental evidence suggests that the same is true in cases of hypoxic pulmonary hypertension as long as prominent complicating vascular alterations, as often observed in chronic obstructive lung disease, are absent. In plexogenic arteriopathy regression of pulmonary hypertension, following elimination of its cause, is observed whenever the vascular lesions have not progressed beyond a certain stage that can be considered a point of no return. Thereafter, there is not only no regression but a distinct tendency to progression of pulmonary vascular disease.

Humans↗
PubMed1986

The 'grey area' between small cell and non-small cell lung carcinomas. Light and electron microscopy versus clinical data in 14 cases.

We studied 14 lung tumours which on light microscopy had posed difficulties on classification as either small cell or non-small cell carcinomas. The light and electron microscopical features were compared with patient follow-up data. Electron microscopy showed neuroendocrine granules in 12 cases, and adeno- and squamous cell differentiation but no neuroendocrine granules in the remaining two cases. The latter two cases showed prolonged patient survival (both patients alive after 2 1/2 and 2 years, respectively). Ten of the cases with neuroendocrine granules showed a rapid course of disease (death between 2 1/2 weeks and 15 months after diagnosis) and marked initial response to multiagent chemotherapy. Thus, the clinical impression of these cases was that of small cell carcinoma. The remaining two cases with neuroendocrine granules showed a more protracted course, with death after 1 1/2 and 2 1/2 years. These two tumours did not show the light microscopical features of atypical carcinoid. The results illustrate the value of electron microscopy in predicting clinical behaviour of carcinomas difficult to place into small cell or non-small cell carcinoma groups. They also point to the existence of neuroendocrine carcinomas other than carcinoids with a more protracted course than small cell carcinomas.

Adult↗
PubMed1986

Medial defects of lung vessels: a new cause of pulmonary hypertension.

Defects, abrupt thinning of the media of muscular pulmonary arteries and pulmonary veins, were observed in two female patients, one 20 and the other 11 years of age. This congenital anomaly was associated with vasoconstriction and medial hypertrophy of adjacent segments of the vascular wall, as well as with a peculiar type of intimal proliferation. The subsequent intimal fibrosis was essentially limited to the hypertrophied segments and caused arterial obstruction and pulmonary hypertension in one of the patients. The other patient had concomitant arteriovenous fistulae, probably related to the extrahepatic portal hypertension that was also present. The medial defects of the pulmonary arteries and veins are likely to be congenital. They may easily be overlooked during histologic examination.

Adult↗
PubMed1986

Misalignment of lung vessels: a syndrome causing persistent neonatal pulmonary hypertension.

The cases of two female infants with persistent neonatal pulmonary hypertension are described. Combinations of pulmonary parenchymal lesions were present, including underdevelopment of alveoli and interstitial fibrosis as well as misalignment of lung vessels. As a result of the misalignment, the pulmonary veins joined the pulmonary arteries, rather than following a course away from them. One of the infants had additional congenital malformations. This syndrome should be considered in the evaluation of infants with persistent fetal circulation.

Female↗