J. V. Hurley

The effects of cooling on experimental free flap survival

Cooling to 6-7 degrees significantly increases ischaemic tissue survival to 48 and, probably, 72 hours. Inflammatory changes develop in direct proportion to the duration of the cold ischaemia time. The skin and vessels within the flap appear to be minimally affected by cold ischaemia while fat and muscle demonstrate significant necrosis, inflammation and ultimate fibrosis. Very little, if any, muscle survives the ischaemic insult studied in this model.

Relationship between lymphocyte emigration and vascular endothelium in chronic inflammation.

Summary Small blood vessels within areas of chronic inflammation which contain large numbers of lymphocytes develop unusually thick walls. Combined histological and electron microscope study shows that the thickening is due to hypertrophy of endothelial cells which come to resemble the endothelium of post‐capillary venules in lymphoid tissue. Vessels of this type have been found in experimental granulomas induced by injection of Freunds adjuvant or killed tubercle bacilli and in human biopsy material from cases of rheumatoid arthritis and Hashimotos disease of the thyroid. Comparison with the developing Peyers patch in young rats shows that the unusual vessels in granulomas are very similar in endothelial cell size, pattern of distribution, extent of lymphocyte migration and degree of carbon leakage to post‐capillary venules of the immature Peyers patch. Study of the time at which lymphocytes appear in large numbers within the granuloma or developing Peyers patch and the time at which thickened vessels are first seen suggests that the endothelial changes are a consequence and not a cause of lymphocyte emigration. The stimulus to endothelial hypertrophy appears to be massive sustained migration of lymphocytes, but the functional significance of this change in vascular structure is not clear.

Delayed and prolonged vascular leakage in inflammation: the effects of dehydromonocrotaline on blood vessels in the rat cremaster

Summary Local application of dehydromonocrotaline to the rat cremaster produces a delayed prolonged increase in vascular permeability with a time course similar to that of the pulmonary oedema seen after intravenous injection of the same substance. Study of the injured area by the carbon labelling technique and by electron microscopy shows that the increased permeability involves both capillaries and venules of all sizes within the region exposed to dehydromonocrotaline. The vascular leakage appears to be due to a direct effect on the endothelium of small blood vessels. Carbon deposition in labelled capillaries and venules is predominantly intramural and indicative of increased vascular permeability. Accumulation of carbon within the lumen of capillaries is uncommon, and accounts for only a small fraction of total capillary labelling. The findings indicate that capillaries are a major source of inflammatory exudate in this type of injury and suggest that the importance of leakage from capillaries has been underestimated in other types of delayed prolonged increase in vascular permeability.

Aspects of increased vascular permeability following the intradermal injection of histamine in the rat

Summary In rats 131I‐labelled serum albumin can be detected in extravascular tissues within one minute of intradermal injection of histamine. The rate of accumulation of labelled protein is approximately constant during the period 0‐15 minutes after histamine injection. During the first 3 minutes of this period, the protein content of accumulating oedema fluid is substantially less than that of plasma, but the results allow no conclusion as to the composition of oedema formed at later stages of the reaction. Concurrent or recently completed emigration of leucocytes into the site of histamine injection has no effect on the rate of escape of the labelled albumin. This finding suggests that the vascular basement membrane does not significantly delay protein leakage from histamine‐stimulated vessels.

Functional anatomy of early atherosclerosis

The histological and ultrastructural appearances of the normal arterial wall and of the two early lesions of atherosclerosis, the fatty streak and the fibrous plaque, will be described, and an account given of present knowledge of the functional capabilities of endothelial cells and of the magnitude and mechanism of leakage of macromolecules into the wall of normal arteries. With this background the basic features of the following hypotheses of atherogenesis will be discussed: a the lipid theory b the insudation theory c the focal injury theory of Ross and Mustard, and the possible causes of injury to arterial endothelium d the fatigue concept of arterial injury e Benditts monoclonal hypothesis.