Non-injured Tissue Research Articles

Fleischner lecture. Biokinetic impacts on structure and imaging of the lung: the concept of biologically closed electric circuits.

The corona complex of the lung is a collection of radiographic features surrounding a pulmonary mass. Each of its 12 components may be explained by a recently described subset of biologically closed electric circuits, the vascular-interstitial closed electric circuit (VICC) system. This system is activated both by normal metabolism of tissue and by local degrading processes, such as spontaneous necrosis or hemorrhage, that lead to local electrochemical polarization of a lesion in relation to surrounding noninjured tissue. Ions, cells, and water are transported electrically in the VICC system, leading to the development of the corona complex. The VICC system is conceived to exist with the walls of arteries and veins functioning as insulators around the electrically conducting medium of blood, the plasma. Blood vessels therefore connect electrically the injured and noninjured tissues. At the capillary level, electric junctions connect plasma and interstitial fluid, which functions as an electrical conductor comparable to blood plasma. The interstitial fluid therefore completes the circuit. The VICC system can be regarded as an additional circulatory system for selective electrogenic transports, coupled directly to the mechanical circulation of blood and lymph. The injury potential represents an important energetic factor in the activation of the VICC system. It is a slowly fluctuating, attenuating, electrochemical potential inducing ebb and flow of time-dependent anionic and cationic transports. The corona structures are special effects of the healing of injured tissue. The 12 radiologic signs of the corona complex have each been produced experimentally in vitro in animals and in vivo in humans during electrochemical treatment of cancers. The "A" zone is characterized radiographically by radiolucency around an electrically polarizing focal lesion. Peripheral to the A zone, a "B" zone is seen as a radiopaque region. The A and B zones are predominantly the result of an electroosmotic outflow of water from a lesion during its electropositive phase. At the interface between the A and B zones, small arches sometimes form an arcade. This configuration develops when the polarizing lesion has small protrusions at its surface. As a result of electrical edge enhancement, various elements of the interstitial tissue are transformed into radiating fibrous structures. They grow out at right angles to the surface of the lesion and serve as supporting columns for the arches. When necrotic material from a tumor is evacuated through a bronchus, ensuing collapse of the tumor will displace those radiating structures already produced.(ABSTRACT TRUNCATED AT 400 WORDS)

Changes in Respiratory Metabolism during Aging in Seeds and Isolated Axes of Soybean<xref ref-type="fn" rid="fn1"><sup>1</sup></xref>

Cyanide-sensitive O2 uptake was observed in the isolated embryonic axis of soybean [Glycine max L. merr. cv. ‘Essex’] within 5 min after wetting and the O2 uptake rate during the first h of imbibition was directly proportional to axis moisture content. Within 10 min after wetting, O2 uptake was lower in aged low vigor (LV) axes than in high vigor (HV) axes imbibed either in water (LV axes sustain imbibition injury) or in 30% w/v polyethylene glycol (LV axes do not sustain imbibition injury). Mitochondria isolated from LV axes after 4- and 24-h imbibition were characterized by lower O2 uptake, ADP:O, and respiratory control ratios relative to HV mitochondria. A plot of O2 uptake vs temperature between 10 and 25°C revealed a break in the slope between 13 and 16°C for HV, but not LV, axes. Since LV axes sustained water uptake injury at all temperatures tested, whereas HV axes sustained chilling injury only below 16°C, the data indicate two temperature-O2 uptake relationships: one for injured tissues and one for non-injured tissues. We conclude that deterioration per se involves impairment of respiratory metabolism in the soybean embryonic axis. Chilling (10°C; HV and LV axes) and imbibitional (25°C; LV axes) injuries during the initial min of inbibition further disrupt respiratory metabolism and interfere with subsequent mitochondrial development and axis growth.

Injury-induced neuronotrophic activity in adult rat brain: correlation with survival of delayed implants in the wound cavity

Mechanical or chemical injury to adult rat brain elicited the accumulation in the affected area of trophic activity for cultured parasympathetic, sympathetic, and sensory neurons. Neuronotrophic activity was relatively low both in noninjured brain tissue extracts and in extracts prepared from the tissue surrounding an injury immediately after the lesion was made. However, trophic titers increased considerably over time, first in the brain tissue that formed the walls of the wound and then in the Gelfoam filling the wound cavity. In the tissue adjacent to the injury, trophic titers began to rise immediately after the lesion, reached a maximum 10 days later, and decayed thereafter. In the wound cavity, occupied by Gelfoam, neuronotrophic activity began to increase 6 days postlesion, reached a maximum at day 16 after injury, and decreased at later times. The levels of induced trophic activity appeared to be proportional to the size of the wound. Injury to various brain areas including temporal, entorhinal, occipital, parietal, and frontal cortices, hippocampus, corpus striatum, and cerebellum, all induced a similar increase in neuronotrophic factor(s). Damage to the myelinated fibers of the corpus callosum did not. High trophic titers decayed rapidly with distance from the wound except in areas heavily deafferented by the lesion, where activity also reached high levels. Extracts from all of the above-mentioned brain areas contained toxic activity for cultured spinal cord neurons. The level of neuronotoxic activity was similar both before the lesion and 15 days postlesion, with the possible exception of the corpus callosum. Intraventricular injections of kainic acid at doses which destroy areas CA4, CA3, and part of CA1 of the hippocampus also induced a time-dependent rise of neuronotrophic activity in this structure, comparable to that achieved by mechanical damage. Both kainic acid treatment and mechanical injury cause extensive glial proliferation in the injured and/or deafferented area. The apparent concurrence of glial reaction and increase in neuronotrophic activity suggests that glial cells may be a major source of the induced trophic activity. As an in vivo correlate of cell culture data, the survival of striatal transplants into host cortical wounds was examined. Fragments of embryonic corpus striatum did not survive when transplanted into a freshly made cavity in the entorhinal/occipital cortex of adult rats. Survival was enhanced by introducing a delay between the time at which the wound cavity was made and that at which the striatal tissue was implanted in it.(ABSTRACT TRUNCATED AT 400 WORDS)

Neuronotrophic activity in brain wounds of the developing rat. Correlation with implant survival in the wound cavity

Neuronotrophic activity accumulates in a wound cavity created in the entorhinal/occipital cortex of developing rats. These trophic factors support the survival of neurons in monolayer cultures of chick embryo spinal cord, ciliary ganglion, sympathetic ganglion and dorsal root ganglion, as well as of mouse dorsal root ganglion. Trophic activity was very low both in non-injured brain tissue and in the wound cavity 1 day post-lesion, but it increased 15- to 300-fold during the subsequent 2–5 days. Together with the trophic activity in the wound fluid were other substances which interfered with the survival of spinal cord neurons. The neuronotrophic factors appeared to be proteins immunologically distinct from mouse submaxillary nerve growth factor. Fragments of rat embryo corpus striatum placed in the cortical wound cavity immediately after its formation showed very poor subsequent survival and no innervation of the host hippocampus. However, if implantation was delayed by 3 or 6 days with respect to the time at which the receiving cavity was made, the survival was greatly improved and innervation of the host took place. The time course for the accumulation of the trophic factors in the cavity paralleled the delay leading to increased survival of brain grafts. It is suggested that the neuronotrophic activity accumulating in the wound cavity during the delay period may be responsible for the increased survival of the implants.

Phospholipase A2 stimulated release of prostanoids from the isolated, perfused rabbit liver: implications in regional cellular injury.

We have previously demonstrated a direct relationship between the activity of the arachidonic acid cascade in vivo and the extent of cellular damage following several types of experimental injury. Since phospholipase activity has been shown to regulate arachidonic acid availability, we tested the ability of circulating phospholipase A2 (PLA2) of pancreatic origin to stimulate prostanoid production or induce cellular injury in the isolated, perfused rabbit liver. Experimental conditions were similar to those present during pancreatitis or early splanchnic artery occlusion shock. The administration of PLA2 at a rate of 100 U/min for 10 min resulted in enhanced rates of thromboxane B2 and 6-ketoprostaglandin F1 alpha release between 1 and 5 min into the infusion period. No changes in hepatic perfusion pressure, vascular resistance, wet tissue weight, or release of lactic dehydrogenase or acid phosphatase into the effluent were observed in either vehicle or PLA2-treated livers. This indicates that cellular injury was not a factor in the prostanoid release. These data suggest that circulating PLA2 can directly stimulate de novo prostanoid synthesis in noninjured tissues. Thus, enhanced plasma prostanoid concentrations in intact animals during periods or regional cellular injury may be due in part to circulating PLA2 released from damaged tissues.

Foliar Response of Six Clones of Hybrid Poplar

After exposure to simulated acid rain at pH levels from 2.7 to 3.4, lesions of several types were produced on foliage of six clones of Populus spp. hybrids. The types of adaxial leaf surface lesions were observed at low magnification by scanning electron microscopy, and via leaf histology. On two clones, galls resulting from hyperplasia and hypertrophy of parenchyma cells predominated. In contrast, two clones exhibited neither hyperplasia nor hypertrophy. In these clones the upper epidermis, palisade parenchyma, and sponge parenchyma were injured in succession. In a third set of two clones, hyperplasia and hypertrophy were present in areas between injured and apparently noninjured tissues. In general, percent leaf area with lesions and percent leaves injured were similar among all six clones at all pH levels tested. At pH 2.7 up to 10% of the leaf area was injured after 5 daily exposures of 6 min each. Injury decreased to about 1.0% at pH 3.4. Lesions developed mostly near stomata and prior to maximum leaf enlargement. Very young and older leaves were less affected. The results support the hypothesis that the adaxial leaf surface is the most affected after exposure to simulated acid rain.

Autoradiographic evaluation of gingival response to injury. IV. Surgical trauma in low-protein-fed young adult rats.

Low-protein-fed rats demonstrated lower levels of proliferative activity in non-injured periodontal tissues than was noted in ad-libitum-fed or pair-fed rats. Gingival wounding resulted in tissue compensation, at the site of injury, for the reduction in proliferative activity present in low-protein-fed young adult rats.

The responses of injured and noninjured rat periodontal tissues to a single administration of dihydrotachysterol

The responses of injured and noninjured rat periodontal tissues to a single administration of dihydrotachysterol