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M Marsala

Publications and source records attributed to M Marsala.

69 records · Page 4Linked to original sources
PubMed1993

Panmyelic epidural cooling protects against ischemic spinal cord damage.

The neuroprotective effect of epidural cooling before and during spinal cord ischemia on the neurological, neurophysiological, and histopathological outcome was evaluated after 40 min of proximal and distal thoracic aorta crossclamping in dogs. In the normothermic group (n = 12), no attempt was made to change the spinal cord temperature. Four of eight animals showed complete paraplegia and four had partial recovery. The N3 component of spinal somatosensory-evoked potentials recovered to only 11.7 +/- 1.4% after 2 hr of recirculation and to 45% of control value after 2 days of survival. In the transverse sections taken from L1-L7 segments, apparent interneuronal damage in the intermediate zone was found after 2 hr of reperfusion followed by a heavy loss of interneurons after 2 days of survival and functionally defined as fully developed paraplegia. In the hypothermic group (n = 12), the spinal cord temperature was lowered 3 min before aortic crossclamping with a bolus of epidurally administered 0.9 N saline solution (8 ml/kg at 5 degrees C) to 28.5 +/- 1.3 degrees C and was maintained throughout the crossclamping time with the additional infusion of the same solution (20 ml/kg/40 min) using a peristaltic pump. Seven of eight animals had no neurological deficit and one animal showed partial recovery, which was significantly better than the motor score for the normothermic group (P < 0.05). The SSEP revealed 55% of postsynaptic (N3) wave recovery after 2 hr of recirculation and 92% recovery after 2 days survival, which was significantly higher than those for the normothermic animals (P < 0.05). Histological analysis showed almost full protection of interneurons and A-motoneurons verified after 2 hr and 2 days, respectively. We conclude that spinal cord epidural cooling has a highly protective effect against ischemic spinal cord damage under experimental conditions of high thoracic aorta crossclamping in dogs.

Animals↗
PubMed1993

Epidural perfusion cooling protection against protracted spinal cord ischemia in rabbits.

The protective effect of a modified epidural cooling technique was assessed in a rabbit spinal cord ischemia model. The epidural space around the lumbar segments with induced ischemia was continually perfused with cold (5 degrees C) isotonic saline via two communicating spinal canal openings. This procedure allowed the spinal cord to be kept deeply hypothermic (< 15 degrees C within central gray matter) during the ischemic period. The animals were subjected to either normothermic ischemia (Group A) or hypothermic ischemia (Group B). Each group contained three subgroups of animals undergoing 20, 40, or 60 minutes of aortic ligation. Their neurological outcomes were evaluated up to 48 hours postischemia, and the intergroup differences were compared. Two days postischemia, all of the animals were sacrificed by transcardial perfusion-fixation and their lumbar segments were processed for histopathological examination. In addition, in animals with 60-minute ischemia, spinal somatosensory evoked potentials were recorded during surgical intervention and again after 48 hours. In the normothermic animals, a high incidence of paraplegia was detected: in 40% after 20 minutes of ischemia, in 75% after 40 minutes, and in 100% after 60 minutes. In contrast, all of the hypothermic animals exhibited full neurological recovery even after 60 minutes of ischemia. Both electrophysiological and histological observations clearly correlated with the neurological findings. The results suggest that deep spinal cord hypothermia produced by epidural perfusion cooling provides effective protection against protracted spinal cord ischemia in rabbits.

Animals↗
PubMed1993

A new applicability of the suppressive Nauta method in the early phase of neuronal damage.

A new applicability of the suppressive Nauta impregnation method was tested allowing the detailed mapping of early neuronal damage expressed in the form of somatodendritic argyrophilia. Two spinal cord ischemia-reperfusion models of rabbit and dog, a model of canine global brain ischemia-reperfusion, involving cardiac arrest followed by resuscitation, and a canine spinal cord compression-decompression model were used. Early phases of neuronal damage are characterized by conspicuous somatodendritic argyrophilia permitting an exact evaluation of acute neuronal damage according to soma size, dendritic ramifications and localization of the affected neuronal neuronal pool. By its high sensitivity to somatodendritic damage the suppressive Nauta method appears to be a valuable neuropathological technique.

Animals↗
PubMed1992

Post cardiac arrest hyperoxic resuscitation enhances neuronal vulnerability of the respiratory rhythm generator and some brainstem and spinal cord neuronal pools in the dog.

Selective neuronal vulnerability of the motor cortex, basal ganglia, brainstem, medulla, cerebellum, C6 and L6 segments of the spinal cord were studied after 15 min of cardiac arrest followed by 1 h of normoxic or hyperoxic resuscitation using the suppressive Nauta method in dogs. Hyperoxic resuscitation causes characteristic somatodendritic argyrophilia of the interneuronal pool in the spinal cord and lower medulla. Cuneate, lateral reticular, supraspinal, and caudal trigeminal nuclei as well as the dorsal and ventral respiratory neuronal groups were heavily involved. Similarly, the Purkinje cells, neurons in the middle and deep portions of the mesencephalic tectum, perirubral, pretectal, posterior commissure, middle-sized striatal and giant pyramidal (Betz's) neurons in the motor cortex became argyrophilic. Hyperoxic resuscitation versus normoxic resuscitation causes statistically significant somatodendritic argyrophilia of the dorsal respiratory group, cuneate, dorsal lateral geniculate and thalamic reticular nuclei.

Animals↗
PubMed1992

Graded postischemic reoxygenation reduces lipid peroxidation and reperfusion injury in the rabbit spinal cord.

The effect of graded postischemic reoxygenation on lipid peroxidation, neurological recovery and the degree of spinal cord damage after 20 min abdominal aorta ligature was tested in the rabbit. In comparison with normoxic recirculation, the graded postischemic reoxygenation (GPIR) during early phase of reperfusion (30 min) significantly reduced the level of lipid peroxidation products (LPP) in vivo and in vitro after 1 h survival. Neuropathological changes in animals with normoxic reperfusion showed gradual deterioration ranging from appearance of heavy argyrophilic neurons after 1 h reperfusion followed by neuronal necroses after 12 h survival to the development of an extensive spongy lesion reaching ventral horn and intermediate zone 2 days postoperatively. The neuroprotective effect of graded postischemic reoxygenation was evident even after 2 days survival with preserved structural integrity of the gray matter as confirmed by light and electron microscopy. The results indicate that graded postischemic reoxygenation during 1 h reperfusion can reduce lipid peroxidation and suppress irreversible neuronal damage using developing during the early reperfusion phase.

Animals↗
PubMed1992

Prolonged postischemic hyperventilation reduces acute neuronal damage after 15 min of cardiac arrest in the dog.

Hyperventilation is commonly used as a constituent of antiedematous therapy after global cerebral ischemia. The effect of hyperventilation on brain functions, however, is complex, and a number of mechanisms involved remains unclear. In this study, we attempted to determine whether postischemic hyperventilation influences acute neuronal changes developing during recirculation. Two groups of dogs underwent 15 min of cardiac arrest and cardiopulmonary resuscitation with an 8 h survival. After resuscitation, in group A the internal environment was maintained in the physiological ranges. In group B the animals were artificially hyperventilated maintaining a high level of respiratory alkalosis during recirculation. Histopathological examination of the vulnerable structures was performed using the Nauta degenerating method and the argyrophilic neurons were counted. Statistically significant amelioration in group B suggests that postischemic hyperventilation may act as a neuroprotective factor.

Animals↗
PubMed1992

Silver impregnability of ischemia-sensitive neocortical neurons after 15 minutes of cardiac arrest in the dog.

The development of postischemic neuronal argyrophilia and the subsequent fate of argyrophilic neurons were studied in dogs after 15 min of complete cerebral ischemia and survival varying from 1 h to 7 days. Histopathological examination of the vulnerable neocortical region was performed using the Nauta degeneration method, and the time course of cellular changes was described. Clear-cut neuronal argyrophilia was found to precede cell body shrinkage and gradual disintegration corresponding to selective neuronal death. To clarify this initial stage of neuronal impregnability, the samples from the animals surviving 8 h postarrest were stained with toluidine blue or processed for electron microscopy, and the distribution of argyrophilic cells was confirmed to be identical with that of hyperchromatic or electron-dense cells. On the other hand, infrequently observed "tissue infarctions" exhibited no silver affinity in spite of apparent cellular damage. These findings indicate that enhanced impregnability is related to cytochemical processes incidental to the phenomenon of "selective neuronal death", which can be readily detected by the Nauta method.

Animals↗
PubMed1991

The blood-brain barrier permeability in graded postischemic spinal cord reoxygenation in rabbits.

Postischemic blood-brain barrier permeability changes were studied using a rabbit spinal cord ischemia model followed by normoxic recirculation (group I) or graded postischemic reoxygenation (group II). No signs of Evans blue leakage were found in lumbar segments 3 h after normoxic blood recirculation. After 6 h, the fluorescence was apparent in the perivascular space and in the pericytes, followed by a massive penetration of the tracer into the neuropil and perikarya at 12 h survival; 18 h after normoxic reperfusion, the fluorescence was localized in the cytoplasm of the middle-sized and large neurons. Graded postischemic reoxygenation of lumbar segments applied during the same survival periods had a highly protective effect on vascular membrane permeability. The structural components of the vascular wall as well as neuropil and perikarya remained after its application entirely tracer free.

Animals↗
PubMed1991

Mapping of the canine lumbosacral spinal cord neurons by Nauta method at the end of the early phase of paraplegia induced by ischemia and reperfusion.

The Nauta impregnation method was used to map the neuronal changes in the canine lumbosacral segments following ischemia and reperfusion. The early perikaryal changes ensuing during the first phase after 30 min of thoracic aorta cross-clamping alone or followed by 30 min of reperfusion were mapped. During the second phase (one to six postischemic reperfusion days) the dendritic, preterminal and synaptic degeneration developed. The influence of 30 min cross-clamping immediately followed by perfusion fixation is characterized by the occurrence of flocculent argyrophilic clusters in the cytoplasm of middle-sized and large neurons of L3-S1 segments. Declamping of the thoracic aorta followed by 30 min of reperfusion basically modifies the susceptibility of lumbosacral neurons to Nauta impregnation promoting somatic and dendritic argyrophilia mainly of small (less than 15 microns) neurons, localized mostly in the fifth, sixth and seventh layers, respectively. This early appearing somatic and dendritic argyrophilia is not abolished by a pretreatment of sections with acetone in which cholesterol and its esters are highly soluble, or chloroform-methanol which extracts total lipid. After 24 h of reperfusion the somatic and dendritic argyrophilia is lost but the first signs of drop-like degeneration are detected in all but three superficial dorsal horn layers. At the end of the third reperfusion day, an atypical form of bouton degeneration was found, consisting of massive occurrence of enlarged (greater than 4 microns) boutons encircled by a clear halo. Laminar distribution of enlarged degenerating boutons coincides with laminar quantitative distribution of small argyrophilic neurons detected 30 min after reperfusion. The basic orientation of the many terminal fibres attached to enlarged boutons suggests that they belong to the axons localized mainly in the lateral and anterior columns. Despite a dense argyrophilic network pervading the gray matter of lumbosacral segments only pale shadows of middle-sized and large neurons were found at the end of the sixth reperfusion day and neither somatic nor vessel wall argyrophilia could be detected. All animals surviving one, three and six days postoperatively suffered from fully developed paraplegia.

Animals↗
PubMed1991

Graded postischemic reoxygenation ameliorates inhibition of cerebral cortical protein synthesis in dogs.

The purpose of this study was to determine the effect of normoxic reperfusion and graded postischemic reoxygenation on cerebral protein synthesis in a cell-free system. Ischemia alone produced a relatively small decrease (15-17%) in activity in all the subcellular systems studied. After a 15-min interval of normoxic reperfusion (75-90 mmHg O2 in arterial blood), a 40% decrease (p less than 0.01) in [14C]leucine incorporation was observed. Reoxygenation with hypoxemic blood containing 37.5 mm Hg O2 at 0-5 min and 56 mm Hg O2 at 6-10 min of recirculation followed by 5 min of normoxic reperfusion resulted in a significant increase (p less than 0.05) of polypeptide chain synthesis in vitro when compared with normoxic reperfusion. The results obtained by this experimental approach tend to show that graded postischemic reoxygenation could be used as a simple and effective neuroprotective tool that substantially diminishes the secondary postischemic damage in nervous tissue, including the newly synthesized proteins.

Animals↗
PubMed1990

Postischemic hypoxia improves metabolic and functional recovery of the spinal cord.

We studied the effect of graded postischemic reoxygenation on the tissue concentrations of adenylates, glucose, and lactate in the rabbit lumbar spinal cord after 10, 20, and 30 minutes of ischemia. In comparison with recirculation without manipulated PaO2, a decrease of PaO2 to 40 to 45 mm Hg upon reestablishment of blood circulation after ischemia led to an amelioration of the energy metabolism in the spinal cord tissue as determined by measuring the ATP concentration and energy charge. The protective effect of postischemic hypoxia was also reflected by the improvement of neurologic functions in animals after 10 and 20 minutes of ischemia.

Adenosine Triphosphate↗
PubMed1989

Early neurohistopathological changes of canine lumbosacral spinal cord segments in ischemia-reperfusion-induced paraplegia.

Mapping the canine lumbosacral spinal cord neurons damaged by ischemia-reperfusion after high thoracic aorta ligation was performed using the Nauta degenerating method. Highly Nauta-positive perikarya of the long ascending projection systems in the 4th to 6th dorsal layer, interneurons in the 7th layer and motoneurons in the 8th and 9th layers in L3-S3 segments subjected to 30 min of ischemia and 30 min of reperfusion were localized and their laminar distribution was specified. Spastic paraplegia fully developed 2 days postoperatively after 30 min of aortic ligation is neurohistopathologically characterized by occurrence of enlarged Nauta-positive boutons with prevailing localization in the 4th to 8th layer of the gray matter.

Animals↗
PubMed1989

Improvement of energy state and basic modifications of neuropathological damage in rabbits as a result of graded postischemic spinal cord reoxygenation.

The role of graded postischemic reoxygenation applied at the end of 20 min of spinal cord ischemia was studied with respect to the intraspinal pO2 tension, energy state, and histopathological sequelae. Graded postischemic reoxygenation can induce a positive shift in the intraspinal pO2 tension, but normal postischemic reoxygenation with normotensive pO2 blood tension inevitably causes the postischemic intraspinal pO2 overshoot. Graded postischemic reoxygenation significantly improves the energy state expressed by higher adenosine triphosphate (ATP), phosphocreatine (PCr) and glucose levels. Using the Nauta impregnating degenerating method, clear histopathological differences were found in the L3-S3 segments after 20 min of ischemia. Apparently divergent damage was observed when normal reoxygenation or graded postischemic reoxygenation was used. Diametrically different histopathological outcomes were obtained with normal reoxygenation and graded postischemic reoxygenation 2 and 4 days postoperatively.

Animals↗
PubMedDate not supplied

Epidural perfusion cooling protects against spinal cord ischemia in rabbits. An evaluation of cholinergic function.

The protective effect of regional epidural spinal cord cooling was evaluated in a rabbit spinal cord ischemia model. Hypothermia was performed by the continual perfusion of 2-4 degrees C cold saline in the epidural space around the ischemic lumbar segments, 4 min before and during ischemia. The spinal cord was deeply hypothermic (21 degrees C) throughout the whole ischemic period. Ischemia was induced by the occlusion of the abdominal aorta for 40 min under normothermic or hypothermic conditions. Recovery of motor and sensory functions, spinal cord-evoked potentials, and motor-evoked potentials were then evaluated up to 24 h postischemia. After this period, choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were measured, in particular, zones of the lumbar spinal cord. AChE was also investigated histochemically. Animals in the normothermic group displayed fully developed spastic paraplegia with near complete loss of spinal somatosensory and motor-evoked potentials. AChE histochemistry showed extensive necrotic changes affecting lumbosacral gray matter. These changes corresponding with the pronounced losses of ChAT and AChE activities indicated irreversible injury of the spinal cord. In contrast, after hypothermic ischemia, animals survived without any sign of neurological impairment with almost full recovery of the spinal cord-evoked potentials. ChAT and AChE activities in the gray matter showed near control values corresponding with histochemical analysis of fully preserved gray matter. Hypothermia under the present experimental conditions efficiently protected the spinal cord against ischemic injury.

Acetylcholinesterase↗