Transfer of arterial hypertension by splenic cells from DOCA-salt hypertensive and renal hypertensive rats to normotensive recipients. Acta path. microbiol. scand. Sect. C, 88:Arterial hypertension was transferred from DOCA-salt hypertensive and renal hypertensive rats to normotensive rats by intravenous injection of splenic cells. Thirteen normotensive recipients were injected intravenously with splenic cells from the hypertensive donors. Eleven developed arterial hypertension ( 8 5 % ) , that is, with a systolic blood pressure exceeding 140 mm Hg. Three of the recipients developed hypertensive levels up to 155-1 60 mm Hg, which was almost up to the levels in the donors. The increase of the blood pressure in the recipients was significant when compared to controls injected intravenously with splenic cells from normotensive donors (p < 0.00 I ). Skin tests, performed by intracutaneous injection of homogenized common carotid arteries in half of the recipients, showed positive reactions 24 hours after the injection. Microscopical examination of heart and kidney from the other half demonstrated mononuclear infiltration into arterial and arteriolar walls and exudative changes in these walls. Due to exudative thickening of the vessel walls the lumina were narrowed. The hypothesis is advanced that the recipient rats developed arterial hypertension as a result of a transferred delayed hypersensitivity directed against the arterial walls. This hypersensitivity reaction caused insudation of plasma components into the arterial walls, narrowing of their lumina and an increased peripheral resistance to the blood flow, so that arterial hypertension developed.

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.

This study aimed to determine the relationship between improvement in lung function and changes in transthoracic electrical bioimpedance (TEB) after thoracentesis in patients with pleural effusions. Fifteen patients with pleural effusions due to either malignant (n = 8) or cardiac (n = 7) diseases were included. Pulmonary function was assessed before and after thoracentesis. During thoracentesis the patients were monitored with TEB. Using linear correlation analysis, the increases for each litre of aspirated thoracic fluid were: forced expiratory volume in 1 s (FEV1) 0.261; forced vital capacity (FVC) 0.331; total lung capacity (TLC) 0.58; and the lung diffusing capacity (DLCO); 2.4 ml min-1 mmHg-1. Baseline impedance increased by 2.3 Ohm l-1 aspirated thoracic fluid. The relative increase in baseline impedance was twice as high for patients with cancer as for patients with heart failure (P < 0.05). We found only minor changes in systolic blood pressure and mean arterial pressure. The improvements in diffusing capacity, airflow, and lung volumes after thoracentesis are correlated to an increase in baseline impedance, but changes are dependent on the primary disease.

The inflammatory cellular reaction in arterioles damaged by acute experimental angiotensin‐hypertension in rats has been examined 1, 3, 6, 12, 24 and 48 hours after the termination of the hypertensive period. The cellular reaction was predominantly composed of mononuclear cells derived from the blood. The majority of these cells, which were able to phagocytize, looked like lymphocytes, and the rest like typical monocytes. The cellular reaction began as a sticking phenomenon corresponding to the damaged endothelium followed by a penetration of mononuclear cells into the arteriolar walls. The cells left the walls of the arterioles after having carried out the macrophage function, returning directly to the circulation or penetrating through the arteriolar wall to the connective tissue surrounding the arteriole. A marked periarteriolar cellular infiltration like that seen in cases of chronic hypertensive vascular disease in different experimental animals was produced by prolonging the number of days (from one to four) in which experimental angiotensin‐hypertension was induced. Rats treated with cortisone showed absence of or decreased inflammatory cellular reaction and a 2–3 times slower elimination of fluorescent proteins deposited in the arterioles as compared with that found in controls. The delayed elimination is thought to be caused by the decrease in or lack of cellular reaction.

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