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Cardiac catheterization is important in the diagnosis and risk stratification of pulmonary hypertensive vascular disease (PHVD) in children. Acute vasoreactivity testing provides key information about management, prognosis, therapeutic strategies, and efficacy. Data obtained at cardiac catheterization continue to play an important role in determining the surgical options for children with congenital heart disease and clinical evidence of increased pulmonary vascular resistance. The Pediatric and Congenital Heart Disease Task Forces of the Pulmonary Vascular Research Institute met to develop a consensus statement regarding indications for, conduct of, acute vasoreactivity testing with, and pitfalls and risks of cardiac catheterization in children with PHVD. This document contains the essentials of those discussions to provide a rationale for the hemodynamic assessment by cardiac catheterization of children with PHVD.

Damaged mesenteric arterioles from rats made hypertensive with intravenous injections of angiotensin showed a production of Van Gieson positive connective tissue which was proportional to the infiltration of mononuclear cells (lymphocytes and monocytes). Rats treated with antithymocyte serum before hypertensive damage of the arterioles showed no or only a very sparse cellular reaction and corresponding to this decreased cellular reaction no production of connective tissue fibrils was observed. As some fibroblast-like cells contained carbon particles in their cytoplasm it is highly probable that they were transformed lymphocytes and/or monocytes, which had phagocytized carbon particles from the hypertensively damaged arterioles.

Following the induction of three different forms of experimental hypertension, deposits of amyloid were found in the spleens of 5-20 per cent of the mice late in the course of the hypertension, Amyloidosis was found in nude (with genetical aplasia of the thymus) as well as in haired (normal) mice. The highest frequency of amyloidosis was observed in mice with hypertension due to partial infarction of one kidney and contralateral nephrectomy. The hypertensive vascular disease, involving lesion of the vessels and of the organs supplied by the affected vessels, is believed, to represent a stimulus for the reticulo endothelial system (RES) with development of amyloidosis as a secondary event.

NZB nice spontaneously develop a high blood pressure and hypertensive vascular disease in the heart and the kidney. Treatment with cyclophosphamide decreased the level of blood pressure; congenital athymic nude NZB mice failed to develop a high blood pressure. These findings suggest that thymus and the thymus-dependent immune reactions have pathogenic importance for the spontaneous hypertension in these mice.

It is demonstrated that an inflammatory mononuclear cellular infiltration into hypertensively damaged arterioles and small arteries takes place in man, independent of the aetiology of the systemic hypertension. This cellular infiltration was observed both in vessels in which marked degenerative changes were recognized and in vessels in which no degenerative changes could be observed under the light microscope. The mononuclear cellular infiltration is possibily due to a hypersensitivity of the delayed type.

The degree of round cell infiltration around hypertensively damaged heart arteries in one kidney Goldblatt hypertensive mice is more pronounced in haired mice with normal thymus function than in their nude littermates with genetic aplasia of the thymus. The level of hypertension and the prognoses for the hypertensive mice are, however, not influenced by the presence of thymus and thymus derived T cells. The results give evidence that delayed type immune reactions are involved in the hypertensive vascular disease in mice, but fail to support the assumption that they have pathogenic importance for either the level of hypertension or the prognoses of the one kidney Goldblatt hypertensive mice.

Hypertensive vascular disease was studied in acute experimental angiotensin induced hypertension. If the hypertension was induced in rats pretreated with injection of thoracic duct lymphocytes the quantity of the mononuclear inflammatory cellular reaction in the damaged arterioles was 2–9 times higher and more prolonged than in control rats. This difference in the cellular reaction is in agreement with the cellular reaction in cases of hypersensitivity of the delayed type.

Experimentally-induced acute angiotensin hypertension has been shown to increase the permeability of cardial arteries and arterioles to plasma components within a few hours. Only in one of the coronary arteries was an increased and focal permeability for plasma components demonstrated, the penetration taking place into the entire thickness of the vessel wall. However, the permeability observed in intramyocardial small arteries and arterioles showed a distinct deposition of plasma components, both in the tunica intima and the tunica media and usually in the entire circumference of the vessels. The results support the view that an increased arterial permeability of the myocardial vessels for plasma components is an important initial stage in the development of hypertensive vascular disease of the heart.

SUMMARY 1. Study of kidney weights in post-mortem material defined the limits of normal variation in weight between the members of pairs of healthy kidneys. 2. There is an almost identical variation in the areas of pairs of kidneys in normal pyelograms. 3. In a large series of pyelograms it was found that abnormally small kidneys were found more frequently on the right side than on the left. 4. This preponderance of contracted kidneys on the right side cannot be explained by hypo-plasia, dysplasia or hypertensive vascular disease. 5. Post-mortem weights of pairs of pyelonephritic kidneys show a disproportionate number of contracted kidneys on the right side.