Carl-Evert Jonsson

Decreased Survival of Experimental Critical Flaps in Rats after Sensory Denervation with Capsaicin

The role of capsaicin-sensitive primary sensory neurons on the survival of experimental critical flaps was studied in the rat. Pretreatment with capsaicin, which depletes neuropeptide transmitter content from primary sensory neurons, caused a dramatic decrease in flap survival area compared to normal animals. In contrast, pretreatment with reserpine, which depletes catecholamines from adrenergic neurons, including the sympathetic post-ganglionic fibers, resulted in a significant increase in the survival area. It was concluded that both capsaicin-sensitive primary sensory neurons and sympathetic postganglionic adrenergic neurons play a role in systemic vascular regulation and that intact primary sensory neurons are of importance for the survival of ischemic tissue.

Effects of indomethacin on the transcapillary leakage of macromolecules and the efflux of prostaglandins in the paw lymph following experimental scalding injury.

Transport of macromolecules (dextrans and proteins) from blood to lymph and efflux of prostaglandins into lymph were studied in dogs following scalding injury of the paw and treatment with indomethacin. Indomethacin inhibited the efflux of prostaglandins following scalding injury, indicating an inhibition of the biosynthesis of prostaglandins. A pronounced suppression of the increased lymph flow and transcapillary transport of macromolecules following scalding was found after treatment with indomethacin. The increased microvascular permeability in scalded tissue was not significantly altered by indomethacin. These results indicate that the major effect of indomethacin on the microcirculation in the scalded tissue is a reduction of the capillary surface area available for exchange due to a reduced number of capillaries perfused with blood. The results also support the hypothesis that some of the vascular reactions following thermal injury may be mediated by prostaglandins.

Prostaglandins and Thromboxanes in Burn Injury in Man

The main urine metabolite of prostaglandin F2 alpha (5 alpha, 7 alpha-dihydroxy-11-ketotetranor-phostane-1, 16-dioic acid, PGF-metabolite) was determined by mass spectrometry (MS) and radioimmunoassay (RIA) in burned patients treated under routine conditions. The amount of the PGF-metabolite as determined by MS was 130 and 67 microgram/24 h (normal value 24 +/- 17 microgram/24 h) on days 3 and 5 respectively in one patient. In serial determinations using RIA the urine level of the PGF-metabolite was within normal values during the first days and rose to a broad peak 1-4 weeks after the injury. Thromboxane B2 (TXB2) was identified and quantitated in burn blister fluid. The amount of TXB2 was 1.7 ng/ml.

Sensory neuropeptides contribute to oedema formation in experimental burns.

The role of primary sensory neuropeptides in experimental burns was investigated. It was shown that after scalding, substance P-like immunoreactivity is released into the lymphatic fluid of dogs. Substance P, injected intravenously, was shown to cause dose-dependent oedema formation in rat skin, as measured with the Evans blue-technique. Furthermore, capsaicin pretreatment, which depletes the neuropeptide content of primary sensory neurons, was shown to inhibit late oedema formation in rats.

A study of the cutaneous sensory reinnervation after burn injury using antibodies to neurofilament

SummaryThe reinnervation of neurofilament-positive sensory nerve fibers in human skin after burn injury was investigated using an indirect immunohistochemical technique. In superficial burns, which healed spontaneously, a dense innervation pattern of neurofilament positive fibers were seen after 3–5 weeks. After 1–2 years the innervation pattern resembled that of normal nonburned skin. In deep burns, subjected to early or late excision and skingrafting, neurofilament positive fibers were seen in the dermis after 3–5 weeks and after 1–2 years a less dense innervation was observed, compared to non-burned skin. In these patients fibers were often seen running in parallel to the dermis-epidermis boundary with only a few fibers entering the epidermal layer. In deep burns that healed with hypertrophic scars only sparse neurofilament positive fibers were encountered 1–2 years after the injury.