PubMed Health⌕ Search

Biomedical subjects

L Longhi

Publications and source records attributed to L Longhi.

At least 19 recordsLinked to original sources
PubMed2003

[Brain vulnerability and its modulation].

Clinical and experimental studies revealed that the injured brain is highly vulnerable to a subsequent insult. Surfery of the literature pertinent to clinical and experimental traumatic brain injury (TBI) is made. Increased vulnerability of the traumatically injured brain to an additional sub lethal ischemic, hypoxic, excitotoxic, or mechanical insult has been clearly demonstrated. Compared to traumatic brain injury alone, the double insult paradigm dramatically increases the brain damage. Brain vulnerability following TBI can be explained by a reduced ability to compensate for a reduction of cerebral blood flow (CBF) and oxygen (O(2)) delivery to the brain or inability to meet an increased metabolic demand. In addition, there is a specific increased sensitivity to delayed insults induced by the first injury. Potential mechanisms of the increased sensitivity to a second insult might be related to post-traumatic gene expression alterations leading to changes in neurotransmitters release, density of receptors and reduced thresholds for activation of pathways leading to delayed cell death. The brain is vulnerable to repetitive injuries. Derangements of compensatory mechanisms are responsible, in part, for this vulnerability. Additional work is needed to better understand the molecular pathways leading to secondary damage and to find novel therapeutic strategies to modulate the brain response to TBI.

Brain Chemistry↗
PubMed2003

[How to quantify the severity of brain injury during intensive care after adult head trauma].

Adequate early assessment of brain damage is essential. Location, extension and severity of structural damage affect brain function and ultimately determine the outcome. The extent of functional impairment, and the morphology of intracranial lesions, require specific treatment, often a combination of medical and surgical interventions. Brain damage usually evolves over time, and repeated assessments are necessary. Clinical evaluation is often biased by concomitant sedation and/or anesthesia, but remains necessary. A revision of the literature is presented. Brain damage is assessed combining clinical and instrumental data. Clinical examination is performed assessing the 3 components of the Glasgow Coma Scale. Spontaneous or stimulated (pain stimulus) eye opening, verbal and motor responses are observed after hemodynamic and respiratory stabilisation. Unfortunately a significant proportion of patients can not be properly examined for several reasons: eye opening can be altered by palpebral and facial injuries, verbal response can be impaired by maxillo-facial injuries or by endotracheal intubation, and motor response remains the most consistent parameter. Sedation, analgesia and myorelaxants, however, can profoundly diminish or abolish the motor response to maximal stimulation, so that examination should be performed after clearance of drugs. Often alcohol or other substances can further impair the neurological performances. Pupils diameter and reactivity to light should be observed, excluding pharmacologic effects (as dilation due to catecholamines) and direct ocular or orbital damage. The CT scan is necessary for disclosing surgical masses and for identifying the extent of diffuse damage and the location of focal lesions. These data should be combined with additional functional exploration, as provided by cerebral extraction of oxygen and electrophysiologic data. Early estimation of cerebral damage is complex and prone to mistakes. Accurate, repeated evaluations, based on the combination of clinical observation and imaging, are necessary.

Brain Injuries↗
PubMed2002

Effects of hyperoxia on brain tissue oxygen tension in cerebral focal lesions.

We evaluated the systemic and cerebral effects induced by an increase to 100% of the inspired oxygen fraction (FiO2) on 20 comatose patients with head injury (9 patients) and SAH (11 patients). Brain tissue oxygen tension (PtiO2) was measured through a Clark electrode inserted in penumbra-like areas. We performed 55 hyperoxia tests by increasing FiO2 from 35 +/- 8% to 100% in one second and calculating the PtiO2 index as: PtiO2 variation from baseline at 1 minute/arterial oxygen tension (PaO2) variation from baseline at 1 minute x 100. One hundred percent FiO2 caused an increase of both arterial (from 139 +/- 28 to 396 +/- 77 mmHg) and cerebral (from 22.6 +/- 14 to 65.4 +/- 60 mmHg) oxygenation after 1 minute. The range of the PtiO2 response was not uniform and two groups were identified. The change was small, 0.8 mmHg/min/100 mmHg PaO2 (+/- 0.7; range 0-2) when mean PtiO2 was 19.7 +/- 13.1 mmHg, while a stronger response, 8 mmHg/min/100 mmHg PaO2 (+/- 5; range 3-18) (p < 0.01) was found when mean PtiO2 was 31.7 +/- 14.3 mmHg. Since O2 diffusion should follow the gas diffusion law, the increase in diffusion distance due to a reduction of capillary density in focal lesions may explain this relationship.

Brain↗
PubMed2001

Brain oxygen tension, oxygen supply, and oxygen consumption during arterial hyperoxia in a model of progressive cerebral ischemia.

We investigated the changes in brain oxygen tension (ptiO2) after ventilation with pure O2 in order to (1) clarify the pathophysiology of O2 exchange in the cerebral microcirculation; and (2) investigate the relationship between brain O2 tension, O2 delivery, and consumption in steady-state conditions during stepwise cerebral blood flow (CBF) reductions. A swine model was developed to reduce CBF in three stable steps: (1) baseline (CBF 100%), (2) CBF of 50-60% of baseline, and (3) CBF of <30% of baseline. CBF was reduced by infusing saline into the left lateral ventricle through a catheter connected with an infusion pump. At each step, hyperoxia was tested by increasing the inspired oxygen fraction up to 100%, PtiO2 reflected the CBF reductions, since it was respectively 27.95 (+/-10.15), 14.77 (+/-3.58), and 3.45 (+/-2.89) mm Hg during the three CBF steps. Hyperoxia was followed by an increase in ptiO2, although the increase was significantly lower when hyperoxia was applied during progressive ischemia. O2 supply to the brain did not change during hyperoxia. Arteriovenous oxygen difference (AVDO2) decreased during the phases of intact CBF and moderate impairment, but not during the phase of severe CBF reduction. In conclusion, ptiO2 reductions closely reflect the imbalance between oxygen delivery and demand; this implies a link between low ptiO2 and defective O2 supply due to impaired CBF. However, this relation is not necessarily reciprocal, since manipulating brain oxygen tension does not always influence brain oxygen delivery, as in the case of ventilation with pure oxygen.

Animals↗
PubMed2001

A review and rationale for the use of genetically engineered animals in the study of traumatic brain injury.

The mechanisms underlying secondary cell death after traumatic brain injury (TBI) are poorly understood. Animal models of TBI recapitulate many clinical and pathologic aspects of human head injury, and the development of genetically engineered animals has offered the opportunity to investigate the specific molecular and cellular mechanisms associated with cell dysfunction and death after TBI, allowing for the evaluation of specific cause-effect relations and mechanistic hypotheses. This article represents a compendium of the current literature using genetically engineered mice in studies designed to better understand the posttraumatic inflammatory response, the mechanisms underlying DNA damage, repair, and cell death, and the link between TBI and neurodegenerative diseases.

Animals↗
PubMed2001

Mild head injury increasing the brain's vulnerability to a second concussive impact.

OBJECT: Mild, traumatic repetitive head injury (RHI) leads to neurobehavioral impairment and is associated with the early onset of neurodegenerative disease. The authors developed an animal model to investigate the behavioral and pathological changes associated with RHI. METHODS: Adult male C57BL/6 mice were subjected to a single injury (43 mice), repetitive injury (two injuries 24 hours apart; 49 mice), or no impact (36 mice). Cognitive function was assessed using the Morris water maze test, and neurological motor function was evaluated using a battery of neuroscore, rotarod, and rotating pole tests. The animals were also evaluated for cardiovascular changes, blood-brain barrier (BBB) breakdown, traumatic axonal injury, and neurodegenerative and histopathological changes between 1 day and 56 days after brain trauma. No cognitive dysfunction was detected in any group. The single-impact group showed mild impairment according to the neuroscore test at only 3 days postinjury, whereas RHI caused pronounced deficits at 3 days and 7 days following the second injury. Moreover, RHI led to functional impairment during the rotarod and rotating pole tests that was not observed in any animal after a single impact. Small areas of cortical BBB breakdown and axonal injury. observed after a single brain injury, were profoundly exacerbated after RHI. Immunohistochemical staining for microtubule-associated protein-2 revealed marked regional loss of immunoreactivity only in animals subjected to RHI. No deposits of beta-amyloid or tau were observed in any brain-injured animal. CONCLUSIONS: On the basis of their results, the authors suggest that the brain has an increased vulnerability to a second traumatic insult for at least 24 hours following an initial episode of mild brain trauma.

Animals↗
PubMed2000

Brain oxygen tension during hyperoxia in a swine model of cerebral ischaemia.

UNLABELLED: Arterial hyperoxia improves oxygen tension measured into the cerebral tissue (ptiO2). The extent of this improvement in ameliorating O2 delivery to the cerebral tissue, when cerebral blood flow (CBF) is reduced, is still unclear. The present experiment was developed to investigate the effect of arterial hyperoxia at normal or reduced CBF (baseline, CBF = 50-60%, and CBF = 20-30% of the baseline). CBF reduction was achieved in 7 pigs by saline infusion in a lateral ventricle. PtiO2 was measured by Licox equipment. Arterovenous oxygen difference (AVDO2) was calculated as the difference between arterial oxygen content and superior sagittal sinus oxygen content. Hyperoxia was induced by increasing inspired oxygen fraction to 100%. PtiO2 moved respectively from 27.95 (+/- 10.15) to 45.98 (+/- 15.31), from 14.77 (+/- 3.58) to 30.71 (+/- 12.2), and from 3.45 (+/- 2.89) to 11.1 (+/- 12.6) mmHg at normal CBF, after the first reduction and after the second reduction. O2 supply showed only a negligible increase. AVDO2 decreased during the phases of intact and moderate CBF impairment, while it did not change during the phase of severe CBF impairment. IN CONCLUSION: an increase of ptiO2 does not necessarily correspond to an improvement of brain oxygen delivery. The small increase in oxygen delivery due to hyperoxia may cause a slight improvement in the balance between O2 delivery and consumption during mild CBF reduction, but such improvement is negligible when severe CBF reduction occurs.

Animals↗
PubMed1999

[Cerebral tissue oxygen monitoring: a useful thing?].

Monitoring cerebral oxygenation has been one of the main fields of interest in neurointensive care during the past few years. In fact it is strongly believed that restoring adequate cerebral oxygenation is the premise to maintaining the viability and restoring the function of the damaged CNS. Global monitoring provides an indirect estimation of adequacy of substrates supply to the brain. Local measurement of brain oxygen tension (ptiO2) is possible through a Clark electrode implanted into the cerebral parenchyma. The paper describes the physical basis of the monitoring, the pathophysiology of ptiO2 and its clinical use.

Brain Chemistry↗
PubMed1999

[Cranial trauma and multiple trauma: from the street to the operating room].

Brain injury occurs with a range of severity: even less severe cases should be carefully observed since they may deteriorate. By definition severe head injury has a Glasgow Coma Scale score of 8 or less; comatose patients are defined as cases who do not obey commands, do not open their eyes and do not speak. Very often (50% of case in our series) brain injury is associated with relevant extracranial injuries that may add to the severity of cases and may worsen outcome. The conceptual framework for treating head injury is based on the evidence that after the impact, the initial damage may be exacerbated by insults capable of further disturbing cerebral metabolism, leading to a final damage defined as secondary damage. Secondary damage represents the final end of many pathways that can be studied at the biochemical level and are centered in a calcium influx into the neuronal cell. Most probably there is a genetic susceptibility to secondary damage leading to a range of cellular dysfunctions for any given level of insult. The management of traumatic brain injury is aimed at interrupting the chain of events leading to secondary brain damage and from this perspective the fact that damage may develop over time can be seen as a window of opportunity for timely treatment. The milestone of treatment is the removal of surgical masses. This surgical treatment can be performed only in a brain that is properly perfused and once coagulation is preserved. Therefore the organization of treatment from rescue to neuro-traumatological centers should provide appropriate restoration of the volume and a normal oxygen delivery to the brain and to the overall organism.

Craniocerebral Trauma↗
PubMed1992

Multicenter evaluation of a new enzyme immunoassay for detection of Clostridium difficile enterotoxin A.

The Premier Clostridium difficile toxin A enzyme immunoassay (PTA EIA) (Meridian Diagnostics, Inc., Cincinnati, Ohio) for rapid diagnosis of antibiotic-associated colitis (AAC) was evaluated in a multicenter study. Stool samples from 421 patients suspected of having AAC were tested for toxin A by the PTA EIA and for toxin B by three tissue culture assays (TCA) employing WI-38 cells (New England Deaconess Hospital) in conventional tubes or foreskin fibroblasts (Children's Hospital) or Vero cells (Beth Israel Hospital) in microwells. The tubes and plates were examined at 24 and 48 h for cytotoxicity. Clinical criteria, repeat testing at another site, and culture of frozen stool samples for C. difficile were used to evaluate discrepant results. Of 504 samples, 66 were positive and 409 were negative by both tests. Eight samples had indeterminate PTA EIA results and were excluded from this analysis. Of 21 discrepancies, 9 were PTA EIA positive and TCA negative and 12 were PTA EIA negative TCA positive. Following resolution of the discrepancies, 11 of 12 PTA EIA-negative-TCA-positive and 5 of 9 PTA EIA-positive-TCA-negative samples were considered true positive for AAC. The sensitivity and specificity were, respectively, 86.6 and 99.0% for the PTA EIA and 93.9 and 99.8% for TCA. The predictive values of positive and negative tests were, respectively, 94.7 and 97.4% for the PTA EIA and 98.7 and 98.8% for TCA. We conclude that the PTA EIA is a rapid, simple EIA technique whose accuracy in detecting enterotoxin A approaches that of reference TCA methods for detection of cytotoxin B.

Bacterial Proteins↗