Jukka Mäkitie

Ultrastructure of striated muscle of the rat after temporary ischemia.

SummaryTwenty-six anterior tibial muscle specimens were analyzed with the electron microscope 2h, 1, 4, 18, 45, 90 and 226 days after temporary ischaemia of the rat hind leg produced by pneumatic tourniquet for 1, 2, 3, 4 and 6 h.No ultrastructural alterations were seen after 1 h ischaemia, but reversible disappearance of muscle glycogen and swelling of muscle and nerve mitochondria occurred after 2 h ischaemia.Irreversible alterations such as disappearance of the Z-line, disruption of cell membrane and vacuolation of muscle mitochondria were observed after ischaemia of 3 h and longer in a part of the muscle fibres. Ischaemia for 6 h was followed by autolysis of all the muscle fibres within the specimens. Autolysis and phagocytosis of the remnants of the affected fibres was present on the 4th day. On that day regenerative phenomena were also observed, such as satellite cells and yound myotubes. The fine structure of the muscle fibres was normal on the 18th day after the temporary ischaemia, although some size variation of the muscle fibres was still observed.Degeneration of a part of the presynaptic nerve endings of motor end-plates with or without simultaneous degeneration of the postsynaptic muscle fibre was seen after ischaemia lasting 3 h or longer. Motor end-plates were first seen on the 45th day in the muscle subjected to 6 h ischaemia and were most likely regenerated ones.

Peripheral nerve injury and recovery after temporary ischemia

SummaryNerve (NCV) and motor (MNCV) conduction velocities of the rat sciatic nerve were examined between 1 and 90 days after ischemia for 1, 2, 3, 4 or 6 h. The results were compared to light and electron microscopy of the nerve.Slight diminution in the MNCV was observed 1 day after 1–2 h ischemia, whereas 3–6 h ischemia resulted in a complete conduction block. Diminution in the NCV occurred first after ischemia for 2 h and a complete block was seen after 4 and 6 h ischemia. Reduced NCV and MNCV were seen between 4 and 18 days only in the animals subjected to ischemia of longer duration of 3–6 h. Both the NCV and MNCV were nearly normalized at the 90th day. Ischemia of 4 and 6 h resulted in denervation of some of the muscle fibers, seen as spontaneous fibrillation at the 4th and 18th day.Electron microscopy and histometric studies showed degeneration of myelinated fibers increasingly after longer durations of ischemia; ischemia for 2 h caused a degeneration of about 5%, 3 h of about 35%, 4 h about 45%, and 6 h about 75% of the fibers. Myelinated fibers of different sizes were equally damaged. In the teased fiber preparations normal and myelin sheaths undergoing Wallerian-like degeneration was seen. Regeneration occurred, but even at the 90th day there was a tendency of the myelin/axon ratio towards values less than control values.

Histochemical studies of striated muscle after temporary ischemia in the rat

SummaryTemporary ischaemia of the hind limb of the rat was produced using a tourniquet with controlled pressure. Changes in the muscle seen after Gomori trichrome staining and after histochemical reactions for NADHdiaphorase, ATPases and phosphorylase were correlated with the duration of the ischaemia and the time of recovery.Histopathological changes were seen first after 2 h of ischaemia and increased thereafter; necrosis of most of the muscles occurred between 4 and 6 h of ischaemia.Necrosis and phagocytosis of muscle fibres and later the amount of regenerating fibres with characteristic histochemical staining properties increased linearly with increasing duration of ischaemia. Even after the most severe lesions of seemingly total necrosis of the muscle after 6 h of ischaemia most of the muscle regenerated within 18 days. Morphological alterations such as variation in fibre size, split fibres and central nuclei were still observed 226 days after ischaemia at which time the follow-up was terminated. Fibre type grouping was seen first after 45–90 days subsequent to 4 and 6 h ischaemia after incubation for ATPase, indicating concomitant neurogenic lesion in addition to the direct ischaemia of the muscle fibres.

Microvasculature of rat striated muscle after temporary ischemia.

SummaryThe structure and distribution of the capillaries of the rat anterior tibial muscle were analyzed by electronmicroscopy and microangiography 2 h and 1, 4, 18, 45 and 90 days after temporary ischaemia for 1, 2, 3, 4 and 6 h.Degeneration of some capillaries was seen first after ischaemia for 3 h, more extensive degeneration after ischaemia for 4 h, and after ischaemia for 6 h all the capillaries were undergoing degeneration when analyzed 1 day after the ischaemia. Capillaries with normal ultrastructure were seen 45 days after the ischaemia.When examined 18 and 45 days after 3–6 h of ischaemia the capillary density was increased by about twofold but it decreased thereafter. At 18th and 45th days after 3–6h of ischaemia the endothelial fraction of the capillary area was increased and the luminal fraction decreased.Microangiography of the anterior tibial muscles demonstrated the increase in the capillarization 18 and 45 days after 3–6 h of ischaemia.

The effect of temporary ischemia on the perivascular sympathetic nerves

Abstract Perivascular sympathetic nerves around the arteries on the muscle fascia of the anterior compartment were studied at various intervals after temporary ischemia of the hindlimb in the rat. Ischemia was produced by controlled-pressure tourniquet wrapped around the leg for from 1 to 6 hr. The number of noradrenergic sympathetic nerves was studied after glyoxylic acid treatment under a fluorescence microscope, and the results were correlated with electron microscopy of the fascial nerves and with light microscopy of the extensor digitorum longus and anterior tibial muscles. Ischemia for 2 hr or longer caused (i) a temporary diminution in the amount of histochemically demonstrable norepinephrine of the sympathetic nerves, the fluorescence intensity returning to normal within 4 days, and (ii) increasing diminution in the number of fluorescing nerves after 2 hr and longer periods of ischemia. The disappearance of fluorescing nerves correlated with autolysis of the perivascular sympathetic axons as observed with the electron microscope. The denervating effect of ischemia roughly paralleled the ischemic damage to the muscle fibers, even though the sympathetic nerves were more sensitive: About 35% decrease in the number of nerves occurred after 2-hr of ischemia, whereas muscle degeneration was first seen after 3-hr of ischemia.

Corneal endothelium after photocoagulation in diabetic patients

Abstract The corneal endothelium was photographed through a wide‐field specular microscope in 38 eyes, in 20 successive diabetic outpatients receiving laser therapy because of underlying proliferative or background retinopathy. Areas of 100 individual endothelial cells from each central cornea were analysed using a digitizer. No statistically significant correlations were observed between mean cell areas or standard deviations of mean and total amount of previous laser energy received. Laser therapy or the type of diabetes did not seem to cause statistically significant changes in the endothelial cell areas examined.