Early cerebrovascular response to head injury in immature and mature rats.

Clinical studies suggest that children respond to head injury with more pronounced cerebral edema and hyperemia than do adults. We hypothesized that these age-related differences could be demonstrated in an animal model. Anesthetized and ventilated mature (2-3 months) and immature (3.

Effect of phorbol myristate acetate on cerebral blood flow in normal and neutrophil-depleted rats.

Background And Purpose: Recent evidence suggests a possible role for leukocytes in ischemic brain injury. This study examined the effect of activation of endogenous circulating leukocytes on cerebral blood flow in normal and neutrophil-depleted rats.

Methods: Leukocytes were activated by rapid injection of either 50 micrograms/kg phorbol 12-myristate 13-acetate, a protein kinase C activator, or an equimolar amount of the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine, into the right carotid artery.

Rat liver lipids during ex vivo warm and cold ischemia and reperfusion.

Rat livers were flushed and stored ex vivo in Krebs-Henseleit buffer at 37 degrees C for 3 hr or in University of Wisconsin solution at 2 degrees C for 48 hr. After this they were perfused with recirculated Krebs-Henseleit solution at 37 degrees C for 1 hr. Levels of phospholipids (PL), free fatty acids (FFA), and conjugated dienes were determined at various times during ischemia and after 1 hr of reperfusion.

Substantia nigra damage after fluorothyl-induced seizures in rats worsens after post-seizure recovery: no exacerbation with hyperglycaemia.

The substantia nigra pars reticularis (SNPR) of rats is highly susceptible to both seizure- and ischaemia-mediated damage. Hyperglycaemic exacerbation of brain damage similar to that observed after global brain ischaemia may also occur in rats with status epilepticus. We tested the hypotheses that hyperglycaemia exacerbates seizure-induced SNPR damage in rats and that SNPR lesions develop rapidly post-seizure.

Local cerebral blood flow measured by xenon-enhanced CT during cryogenic brain edema and intracranial hypertension in monkeys.

We developed a closed-skull model of freeze injury-induced brain edema, a model classically thought to produce vasogenic edema, and observed the natural course of changes in edema and blood flow using xenon-enhanced computed tomography (CT) in five rhesus monkeys before and for up to 6 h post insult. Intracranial pressure (ICP) gradually rose throughout the duration of the experiment. CT scans and CBF images permitted direct observation of the evolution of the lesion and revealed early ischemia in the periphery of the injury zone that progressed over time in association with edema.

Membrane lipid degradation during ischemia and impact on the monolayer surface pressure area diagram (SPAD).

This article briefly reviews the importance and relevance of membrane lipid degradation to the pathogenesis of ischemic brain damage ranging from the liberation and accumulation of free fatty acids (FFA) to their consequences on the biophysical characteristics of membrane lipids. The rapid accumulation of brain FFA during cerebral ischemia is a hallmark of the evolution and pathogenesis of ischemic brain damage: It signals the degradation of membrane lipids; it generates the precursors to the metabolically and physiologically potent eicosanoids; and it promotes the generation of lipid oxidizing free radicals, which could propagate the destruction of membrane lipids. The impact of ischemia-induced changes in cerebral membrane lipid composition on membrane function is difficult to assess in vivo.

Elevated production of interleukin 6 by hepatic MNC correlates with ICAM-1 expression on the hepatic sinusoidal endothelial cells in autoimmune MRL/lpr mice.

MRL/lpr mice, which are a model of SLE and rheumatoid arthritis in humans, develop profound lymphadenopathy resulting from the accumulation of CD3+ 4-8- double-negative (DN) alpha beta T cells in peripheral lymphoid tissues. We previously indicated that these DN alpha beta T cells preferentially proliferate in the liver and migrate to the periphery. In this study, we analyzed whether any kind of cytokine was produced by hepatic mononuclear cells (MNC) in MRL/lpr mice.

Regional lipid composition in the rat brain.

The lipid composition of the brain is of great importance to its metabolism and function. Although much research has been done on regional brain lipid composition, studies usually suffer from limited brain regions or from limited lipids analyzed. We modified a previously described method for the separation of brain phospholipids and glycolipids, improving the separation and sensitivity of the method.

[Thallium-201 and gallium-67 scintigraphies in the diagnosis of pneumoconiosis combined with lung cancer].

Thallium-201 (201Tl) and Gallium-67 (67Ga) scintigraphies were performed on 62-year-old male with silicosis combined with lung cancer (squamous cell carcinoma). In 67Ga and early 201Tl images, radiotracer uptakes were observed in both sites of cancer and silicosis, and thus, it was impossible to differentiate cancer mass from the large opacity of pneumoconiosis. On the other hand, in the 201Tl delayed images, 201Tl was localized only in cancer mass, while it was washed out from the large opacity.

Effect of 80% Xe on whole brain blood flow and metabolism in awake monkeys.

We previously reported that 33% xenon (Xe) did not activate cerebral blood flow (CBF) and metabolism in monkeys as it appears to do in humans. However, monkeys may be less sensitive to Xe than humans are, which would explain the discrepancy in the results, but no one has studied the effects of higher concentrations of Xe on CBF and metabolism in monkeys. Therefore, we studied the effect of 80% Xe on whole-brain CBF, cerebral metabolic rate for oxygen (CMRO2) and glucose (CMRG) in five awake rhesus monkeys.

Effect of stable xenon inhalation on internal carotid artery blood flow in unanesthetized monkeys.

Stable xenon (Xe) gas, at inspired concentrations above 30%, reportedly increased cerebral blood flow (CBF) in animals and humans. An unpredictable Xe-induced elevation of CBF could result in erroneous CBF values being measured by Xe-enhanced computed tomography (Xe-CT). In order to detect a potentially rapid and transient effect of Xe on CBF, estimations of supratentorial CBF were obtained by Doppler flow probes chronically and bilaterally implanted on the internal carotid arteries of five adult monkeys.

Effects of dobutamine and dopamine on whole brain blood flow and metabolism in unanesthetized monkeys.

Dobutamine (DO) and dopamine (DA) are positive inotropic agents used clinically to improve cardiac output in patients in acute or chronic heart failure or to counteract intracranial vasospasm. These patients are also at risk for cerebrovascular disease, but studies on the effects of DA on cerebral blood flow (CBF) and metabolism are few and for DO nonexistent. We evaluated the effects on DO and DA on whole brain CBF and cerebral metabolic rates of oxygen (CMRO2) and glucose (CMRglc) in unanesthetized rhesus monkeys.

Uncoupled cerebral blood flow and metabolism after severe global ischemia in rats.

In a rat model of complete global brain ischemia (neck tourniquet) lasting either 3 min or 20 min, we monitored global CBF (sagittal sinus H2 clearance) and CMRO2 for 6 h to test the hypothesis that delayed postischemic hyperemia and uncoupling of CBF and CMRO2 occur depending on the severity of the insult. Early postischemic hyperemia occurred in both the 3-min and 20-min groups (p less than 0.05 vs.

Regional differences in rat brain lipids during global ischemia.

Background And Purpose: Membrane lipid degradation plays an important role in the pathogenesis of ischemic brain damage, but there is little information on changes in cerebrosides, sulfatides, and sphingomyelin. We studied regional changes in the quantities of these lipids during complete global brain ischemia in rats.

Methods: Nitrous oxide-anesthetized rats were subjected to ischemia by a high-pressure neck cuff and arterial hypotension for 0 (control), 3, 10, or 30 minutes (n = 5 at each time).

Hepatic dysoxia commences during O2 supply dependence.

Hepatic O2 consumption (VO2) remains relatively constant (O2 supply independent) as O2 delivery (DO2) progressively decreases, until a critical DO2 (DO2c) is reached below which hepatic VO2 also decreases (O2 supply dependence). Whether this decrease in VO2 represents an adaptive reduction in O2 demand or a manifestation of tissue dysoxia, i.e.

Effect of 33% xenon inhalation on whole-brain blood flow and metabolism in awake and fentanyl-anesthetized monkeys.

Background And Purpose: Despite the documented diagnostic value of local cerebral blood flow maps by xenon-enhanced computed tomography, reports of cerebral blood flow activation by inhaled 33% Xe raised concerns about the method's safety and accuracy. We evaluated the effect of 33% Xe inhalation on cerebral blood flow and cerebral metabolic rates for oxygen and glucose in four awake and six fentanyl-anesthetized rhesus monkeys.

Methods: Platinum microelectrodes and catheters in the torcular Herophili were used to measure cerebral blood flow by hydrogen clearance, and oxygen and glucose concentrations.

Assessment of posttraumatic polymorphonuclear leukocyte accumulation in rat brain using tissue myeloperoxidase assay and vinblastine treatment.

Polymorphonuclear leukocytes (PMN) are implicated in the pathogenesis of traumatic brain injury. We tested the following hypotheses: (1) leukocyte accumulation is present in brain tissue 24 h posttrauma, (2) leukocyte accumulation represents PMN, and (3) prior systemic PMN depletion attenuates brain tissue PMN accumulation. Trauma was induced in exposed right parietal cortex by weightdrop in anesthetized Wistar rats (n = 24).

Brain glutamine synthetase activity and hyperoxia in neonatal rats.

We have previously shown that exposure to 100% oxygen for 2 h results in a two-fold decrease in the brain glutamine synthetase activity of neonatal rats. The present study examines whether this decrement in enzyme activity leads to a global accumulation of glutamate, an excitotoxin which is a substrate for this enzyme. Despite a demonstrable decrement in whole brain glutamine synthetase activity, whole brain glutamate content is unaltered in animals exposed to 100% oxygen for 2 h.

Blood flow and electrolytes in spinal cord ischemia.

The contribution of reoxygenation-reperfusion injury to ischemic brain damage has been clearly demonstrated but not in the spinal cord. To evaluate this phenomenon in spinal cord ischemia, we measured spinal cord blood flow (SCBF) by [14C]iodoantipyrine and electrolytes in rabbits after 10 or 40 min ischemia followed by 30 min or 4 days recirculation. Ischemia for 10 or 40 min reduced blood flow in the lower lumbar segments L5-L7 (30 ml/100 g/min) to 5 and 10% of control.