Tissue Perfusion

Perfusion is flow per unit tissue mass, conventionally millilitres per minute per hundred grams, and it is not the same as flow in the artery feeding a region. What reaches cells depends on perfusion pressure divided by microvascular resistance, on capillary density, and on how much flow is nutritive rather than shunted past the exchange vessels. Autoregulation, metabolic vasodilators and endothelial nitric oxide adjust resistance continuously, and oxygen delivery is the product of perfusion and arterial oxygen content.

The thresholds used clinically are concrete. Transcutaneous oxygen tension below roughly thirty millimetres of mercury predicts failure of a wound to heal, and an ankle-brachial index under about 0.9 defines peripheral arterial disease. Tissues differ enormously at baseline: articular cartilage has no blood supply and depends on diffusion through synovial fluid, tendon is sparsely vascularised, and skeletal muscle can raise perfusion many-fold during exercise. This is the physiology behind revascularising a limb before expecting an ulcer to close.

Perfusion therefore constrains every other intervention. A compound with impeccable in vitro activity still has to arrive, and the tissues most often targeted for repair are least able to receive it. The same limit applies to the healing tissue itself, which cannot build matrix without oxygen for collagen hydroxylation.

The misreading is to treat vasodilation as perfusion. Raising total limb blood flow, or producing visible erythema and a muscular pump, does not establish that nutritive capillary flow in the target tissue rose, since flow can be shunted. Peptide claims of improved blood supply typically come from rodent flap or ischaemia models with laser Doppler readouts, which measure superficial skin flow, rarely from human measurement.