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Biomedical subjects

J J Neil

Publications and source records attributed to J J Neil.

26 records · Page 2Linked to original sources
PubMed1991

Sepsis does not impair tricarboxylic acid cycle in the heart.

Sepsis has been reported to cause mitochondrial dysfunction and inhibition of key enzymes that regulate the tricarboxylic acid (TCA) cycle. We investigated the effect of sepsis on high-energy phosphates, glycolytic and TCA cycle intermediates, and specific amino acids that are involved in regulating the size of the TCA cycle pool during changes in metabolic state of the heart. Sepsis was induced in 12 female rats by the cecal ligation and perforation technique under halothane anesthesia; seven control rats underwent cecal manipulation without ligation. At 36-42 h postsurgery, the rats were reanesthetized, the chest was opened, and the hearts were freeze-clamped. Perchloric acid extracts of the hearts were analyzed with fluorometric enzymatic methods and 31P nuclear magnetic resonance spectroscopy. There were no significant differences in the levels of the TCA cycle intermediates or high-energy phosphates between the septic and control rats. The major metabolic changes were the 28% decrease in alanine and the 31% decrease in glutamate in the septic hearts compared with control (P less than 0.05 and P less than 0.005, respectively). Phosphocholine, a component of membrane phospholipids, was increased by 91% in the septic hearts (P less than 0.01). We conclude that sepsis does not impair the TCA cycle or induce significant cellular ischemia in the heart. The increase in phosphocholine may represent significant cellular membrane disruption during sepsis.

Adenosine Triphosphate↗
PubMed1984

Changes in regional blood flow and cardiac output after L-glutamate stimulation of A5 cell group.

Changes in regional blood flow and cardiac output were measured by the reference organ method in pentobarbital-anesthetized rats with radioactive microspheres (15 microns) before and after chemical stimulation of the A5 cell group with the excitatory amino acid L-glutamate an agent that excites cell bodies but not fibers of passage. This stimulation caused a decrease in mean arterial pressure, heart rate, cardiac output, and calculated stroke volume. The limb skeletal muscles showed a large increase in blood flow and decrease in vascular resistance, whereas the trunk musculature showed no change in flow or resistance. The blood flow of the entire gastrointestinal tract decreased. Blood flow in the skin decreased with no change in resistance. The cardiac muscle of the ventricles showed a decrease in flow without a change in resistance. The ipsilateral half of the brain showed a decrease in blood flow, while the contralateral side showed no change. The kidneys exhibited no change in blood flow and a decrease in resistance. A5 stimulation in guanethidine-sympathectomized rats caused no change in regional blood flow. In contrast, an increase in cardiac output was observed, and the possible interpretations for this change are discussed. Rats treated with intraventricular injections of 6-hydroxydopamine showed no changes in regional blood flow or cardiac output, indicating that catecholamine neurons are involved in these responses.

Animals↗
PubMed1982

Actions of N-methyl aspartate and its antagonist aminophosphonovalerate on the A5 catecholamine cell group in rat.

When N-methyl-D,L-aspartic acid was injected into the A5 catecholamine cell group of the rat, a dose-dependent decrease in blood pressure and heart rate was obtained. These cardiovascular changes were subsequently blocked by the (-) and (+) isomers of the aspartate receptor blocker 2-amino-5-phosphonovalerate (2-amino-5-phosphonopentanoic acid). The (-) isomer was 2-4 times more potent than the (+) form.

2-Amino-5-phosphonovalerate↗
PubMed1982

Substance P neurons project from the ventral medulla to the intermediolateral cell column and ventral horn in the rat.

The descending substance P projections from the ventral medulla were studied in the rat. Electrolytic lesions which included the nucleus interfascicularis hypoglossi decreased the substance P-like immunoreactivity (SP-I) in both the intermediolateral cell column and the ventral horn of the spinal cord. Lesions of other ventral medullary areas and midbrain hemisections did not change spinal cord SP-I levels. Intracerebroventricular administration of the serotonin neurotoxin, 5,7-dihydroxytryptamine, reduced the SP-I content of the ventral horn but not of the intermediolateral cell column.

5,7-Dihydroxytryptamine↗
PubMed1982

Effects of kainic acid applied to the ventral surface of the medulla oblongata on vasomotor tone, the baroreceptor reflex and hypothalamic autonomic responses.

Application of an excitotoxic amino acid, kainic acid, to the ventral medullary surface just caudal to the trapezoid bodies (at Feldberg and Guertzenstein's glycine-sensitive area) led to the following observations. (1) Blood pressure began to rise within 25 s and by 10 min rose to high levels (200-240 mm Hg). Blood pressure subsequently fell to levels at or approaching those of a spinal animal. (2) Sympathetic vasomotor activity became insensitive to baroreceptor inhibition shortly after the peak in blood pressure, and the cardioinhibitory action of the reflex was enhanced during this time. (3) The autonomic effects of hypothalamic stimulation were differentially affected--pupillary dilatation and retraction of the nictitating membranes were unaffected, while the increases in blood pressure and renal nerve activity were blocked. (4) Recovery from these effects was observed on two occasions, when the animals were infused with a pressor agent and allowed to survive beyond 6 h after the kainic acid application. These results support the view that vasomotor tone is dependent upon the activity of relatively superficial cells in the ventral medulla. We further suggest that baroreceptor inhibition of sympathetic vasomotor activity acts via these cells and that descending hypothalamic autonomic pathways are organized at this level in terms of separate end organs.

Animals↗
PubMed1981

The role of descending monoaminergic systems in central control of blood pressure.

The descending projections to the intermediolateral cell column arise from several sources. The serotonergic inputs come from the raphe pallidus, raphe obscurus, raphe magnus nuclei, and ventral medulla. The A5 cell group provides a norepinephrine input to the intermediolateral cell column and the A1 cell group appears to be the main source of the epinephrine input. The functional role of monoamines on sympathetic preganglionic neurons is unclear. Iontophoresis studies indicate that serotonin excites and norepinephrine inhibits sympathetic preganglionic neurons. Pharmacological studies indicate that an alpha-2 receptor is located on or near these neurons. In contrast, electrical stimulation of the monoamine cell bodies produces opposite results. Stimulation of the raphe nuclei causes an inhibition of the sympathetic outflow whereas stimulation of some of the noradrenergic cell groups causes pressor responses. The role of monoamines in various cardiovascular reflexes and in experimental hypertension is discussed.

Animals↗
PubMedDate not supplied

Diffusion MRI: precision, accuracy and flow effects.

After a decade of evolution and application of diffusion imaging, a large body of literature has been accumulated. It is in this context that the accuracy and precision of diffusion-weighted and quantitative diffusion MRI are reviewed. The emphasis of the review is on practical methods for clinical human imaging, particularly in the brain. The requirements for accuracy and precision are reviewed for various clinical and basic science applications. The methods of measuring and calculating diffusion effects with MRI are reviewed. The pulse gradient spin echo (PGSE) methods are emphasized as these methods are used most commonly in the clinical setting. Processing of PGSE data is reviewed. Various PGSE encoding schemes are also reviewed in terms of the accuracy and precision of isotropic and anisotropic diffusion measurements. The broad range of factors impacting the accuracy of the PGSE methods and other encoding schemes is then considered. Firstly, system inaccuracies such as background imaging gradients, gradient linearity, refocusing RF pulses, eddy currents, image misregistration, noise and dynamic range are considered. A second class of inaccuracies is contributed by the bulk effects of the imaged object, and include sample background gradients, subject motion of cerebrospinal fluid and organs, and aperiodic organ motion. A final category of potential inaccuracies is classified as being contributed by microscopic, biophysical tissue properties and include partial volume effects, anisotropy, restriction, diffusion distance, compartmentation, exchange, multiexponential diffusion decay, T2 weighting and microvascular perfusion. Finally, the application of diffusion methods to studies of blood flow in the microvasculature (i.e. the arterioles, capillaries and venules) are reviewed in detail, particularly in terms of feasibility and the stringent accuracy and precision requirements. Recent provocative studies examining the use of PGSE approaches to suppress microvascular signals in brain functional MRI (fMRI) are also reviewed.

Animals↗