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PubMed1998

Alterations in swim stress-induced analgesia and hypothermia following serotonergic or NMDA antagonists in the rostral ventromedial medulla of rats.

Serotonergic, NMDA, or opioid antagonists in the rostral ventromedial medulla (RVM) reduce morphine analgesia elicited from the periaqueductal gray (PAG). Continuous (CCWS) and intermittent (ICWS) cold-water swims elicit respective naltrexone-insensitive and naltrexone-sensitive analgesic responses. CCWS analgesia is reduced by systemic NMDA receptor antagonism and by systemic, but not intrathecal serotonergic antagonism. ICWS analgesia is reduced by both systemic and intrathecal serotonergic antagonism, but unaffected by systemic NMDA antagonism. The present study evaluated whether serotonergic (methysergide: 5-10 microg) or competitive [AP7 (2-amino-7-phosphonoheptanoic acid): 0.01-0.1 microg] or non-competitive [MK-801 (dizocilipine maleate): 0.3-3 microg] NMDA antagonists in the RVM altered CCWS and ICWS analgesia and hypothermia as well as basal nociceptive latencies. Methysergide in the RVM significantly potentiated CCWS, but not ICWS analgesia. In contrast, AP7 in the RVM significantly potentiated ICWS analgesia. Antagonist-induced changes in either hypothermia or basal nociception failed to account for any alterations in stress-induced analgesia. These data suggest that serotonergic, but not NMDA, receptors in the RVM may mediate collateral inhibition between mesencephalic morphine analgesia and naltrexone-insensitive CCWS analgesia.

Animals↗
PubMed2005

Epileptogenic insult causes a shift in the form of long-term potentiation expression.

The relationship between epilepsy, modeled here by pentylenetetrazol kindling, and learning deficits, modeled here by long-term potentiation (LTP), was studied. The field excitatory postsynaptic potentials and population spikes (PS) were recorded from strata radiatum and pyramidale, respectively, in urethane-anesthetized rat dorsal hippocampus CA1 area upon stimulation of Schaffer collaterals. To induce LTP, a 100 Hz primed-burst stimulation protocol was used. Experiments were carried out at approximately 30 days after the last pentylenetetrazol dose. The effects of voltage dependent calcium channel blocker verapamil and N-methyl-D-aspartate receptor antagonist MK-801 on LTP expression were examined. Tetanic stimulation elicited both field excitatory postsynaptic potential LTP and PS LTP in control animals, and LTP-induction of the PS in control animals was attenuated by MK-801, but not by verapamil. By contrast, kindled rats showed LTP of the PS only. MK-801 reduced the extent of potentiation of PS amplitude and verapamil inhibited the PS amplitude potentiation, completely. The results suggest that seizure induction modifies mechanisms underlying LTP induction and causes a shift in the form of LTP expression. The pentylenetetrazol-kindling-induced increase in PS LTP is sensitive to verapamil and not to MK-801 and therefore primarily dependent on activation of voltage dependent calcium channels rather N-methyl-D-aspartate receptors. Kindling may lead to a shift in synaptic plasticity thresholds much like the shift that occurs during aging, and such alterations may contribute to deficits in learning and memory.

Animals↗
PubMed1987

Effects of phencyclidine, SKF 10,047 and related psychotomimetic agents on N-methyl-D-aspartate receptor mediated synaptic responses in rat hippocampal slices.

The effects of representative drugs from three classes of psychotomimetic compounds (arylcyclohexylamines, benzomorphan opioids and dioxolanes) have been examined on synaptic transmission at an identified monosynaptic pathway in rat hippocampal slices. The compounds tested were phencyclidine (PCP) and ketamine, the racemate and isomers of SKF 10,047 (N-allylnormetazocine), and the isomers of dioxadrol (dexoxadrol and levoxadrol). In the absence of added magnesium ions (Mg) in the perfusion medium low frequency stimulation of the Schaffer collateral-commissural pathway evoked a burst of population spikes in the CA1 cell body region. The secondary components of this response could be abolished by the selective N-methyl-D-aspartate (NMDA) antagonist D-2-amino-5-phosphonovalerate (APV). PCP (1 microM) or ketamine (10 microM) selectively blocked the secondary components of the synaptic response. The effect of PCP was neither mimicked nor prevented by hexamethonium and atropine, phentolamine and propranolol, or clonidine and was therefore unlikely to involve cholinergic or adrenergic neurotransmitter systems. The sigma opiate, (+/-)-SKF 10,047 (10 microM) also abolished selectively the secondary components of the synaptic response. There was no apparent difference between the potency of the stereoisomers of this compound. The action of (+/-)-SKF 10,047 was not affected by either naloxone or haloperidol, indicating that this effect did not involve opioid receptors or the haloperidol-sensitive sigma site. Dexoxadrol (10 microM), but not levoxadrol (10 microM), also selectively blocked the secondary components of the synaptic response. It is concluded that these psychotomimetic agents can block an NMDA receptor-mediated component of synaptic transmission in the hippocampus and that this effect is mediated by a specific PCP/sigma site.

Analgesics↗
PubMed1992

Myocardial protective effects of adenosine. Infarct size reduction with pretreatment and continued receptor stimulation during ischemia.

BACKGROUND: We hypothesized that 1) endogenous adenosine released during ischemia conferred an inherent cardioprotection, and 2) a pretreatment dose of adenosine before ischemia would provide additional protection independent of hemodynamic effects. METHODS AND RESULTS: Thirty-six anesthetized New Zealand White rabbits underwent 30 minutes of regional ischemia produced by coronary occlusion followed by 2 hours of reperfusion. The adenosine group (ADO, n = 9) received a 5-minute pretreatment infusion of 140 micrograms/kg/min of adenosine before ischemia. A control group (SAL, n = 9) received saline before ischemia. To separate the effects of adenosine used as a pretreatment versus the effects during ischemia, a third group (ADO+SPT, n = 9) received adenosine as pretreatment followed by 10 mg/kg 8-p-sulfophenyl theophylline (8-SPT), an A1/A2-receptor antagonist given before ischemia, thus allowing pretreatment with adenosine but antagonizing its effects during ischemia. To preclude any protection from endogenous adenosine released during ischemia, the fourth group (SAL+SPT, n = 9) received saline as pretreatment and 8-SPT before ischemia. Area of necrosis within the area at risk (infarct size) was determined with tetrazolium and Evans blue stains, and transmural blood flow was measured using radioactive microspheres. Collateral blood flow in the area at risk was similar in all groups, as was the size of the area at risk. Infarct size was reduced by adenosine pretreatment (ADO, 8.4 +/- 7.2%) in contrast to saline vehicle (SAL, 27.8 +/- 6.3%; p less than 0.05 versus ADO). alpha 1/alpha 2-Receptor blockade after adenosine pretreatment abolished the ischemic protection provided by pretreatment adenosine (ADO+SPT, 42.7 +/- 8.3%; p less than 0.05 versus ADO). Finally, receptor blockade of endogenously released adenosine without adenosine pretreatment increased infarct size by 24% over the nonpretreated saline group (SAL+SPT, 51.5 +/- 9.0%; p less than 0.05 versus SAL). CONCLUSIONS: We conclude that 1) endogenous adenosine building up during ischemia is cardioprotective, and 2) pretreatment with adenosine confers cardioprotection independent of hemodynamic effects. Whether pretreatment effects of adenosine subsequently modulate the effects of endogenous adenosine (through alterations in receptor population or sensitivity) or endogenous and exogenous adenosine represent additive compartments is unclear.

Adenosine↗
PubMed1993

Spatial features of focal infarction after hydralazine treatment in stroke-prone spontaneously hypertensive rats.

BACKGROUND AND PURPOSE: Rapid occlusion of the middle cerebral artery above the rhinal fissure produces a large ischemic infarct in hypertensive rats, but this occlusion results in a minimal lesion in young normotensive rats. Our purpose was to attenuate rising blood pressure in young stroke-prone spontaneously hypertensive rats with hydralazine before the occlusion to determine if the gross infarct volume is smaller, and if it is, to determine whether length, width, depth, or surface area of the infarct changes, which could suggest a mechanism of protection. METHODS: Untreated rats (n = 6) and rats receiving hydralazine for 1.5 (n = 6) or 5 (n = 5) weeks were anesthetized, and the middle cerebral artery was rapidly occluded with a ligature. One day later the rats were killed and the brains were fixed in formalin. Fine-grain-release film that is sensitive to spectral properties of the infarct was used to photograph the tissue. Infarcted areas were traced on paper and then digitized for measurements and computations with a microcomputer. RESULTS: Compared with untreated rats, tail systolic blood pressure (120 +/- 3 versus 138 +/- 4 mm Hg), infarct volume (61 +/- 4 versus 93 +/- 6 mm3), infarct surface area (39 +/- 1 versus 54 +/- 2 mm2), infarct width (3.8 +/- 0.1 versus 4.8 +/- 0.2 mm), and infarct length (6.0 +/- 0.3 versus 8.1 +/- 0.3 mm) were less in rats receiving hydralazine for 5 weeks (p < 0.05). No change was detected in infarct depth. CONCLUSIONS: Treatment of young stroke-prone spontaneously hypertensive rats with hydralazine for 5 weeks before middle cerebral artery occlusion results in a smaller infarct. The narrower, shorter dimensions indicate increased protection against lateral enlargement of the infarct and the possibility that protection was due to increased collateral blood flow through modified blood vessels.

Animals↗
PubMed2000

Vascular complications in acute pancreatitis assessed by color duplex ultrasonography.

We determined the sensitivity of computed tomography and color duplex ultrasonography in the detection and characterization of vascular complications in acute pancreatitis. The relationship of these complications with the etiology and activity of the disease was assessed. In a prospective study, 189 patients with acute pancreatitis seen in the Department of Gastroenterology. Charité Hospital in Berlin over a period of 38 months underwent color duplex ultrasonography every second day for 3 weeks and thereafter at least once a week for 2 months. Dynamic computed tomography was performed within 72 hours after admission, and follow-up computed tomography scans were obtained. In 45 patients (23%), at least temporary thromboses of portal venous vessels were demonstrated by color duplex ultrasonography. The incidence of venous thromboses was 30% in severe acute pancreatitis with fluid collections without necroses and 57% in necrotizing pancreatitis. In 27 of those 45 patients, a formation of collaterals was documented. In 13 patients, arterial pseudoaneurysms were demonstrated. Vascular complications were significantly more frequent in alcohol-induced than in gallstone-induced pancreatitis. Only 62% of all sonographically diagnosed thromboses and only 32% of all collaterals were demonstrated by computed tomography. The prevalence of vascular complications in acute pancreatitis was much higher as suspected. The risk of gastrointestinal bleeding was lower than previously reported. Color duplex sonography is the method of choice for the detection of vascular complications in acute pancreatitis.

Acute Disease↗
PubMed2002

Gene therapy techniques for peripheral arterial disease.

Somatic gene therapy is the introduction of new genetic material into selective somatic cells with resulting therapeutic benefits. Vascular wall and, subsequently, cardiovascular diseases have become an interesting target for gene therapy studies. Arteries are an attractive target for gene therapy since vascular interventions, both open surgical and endovascular, are well suited for minimally invasive, easily monitored gene delivery. Promising therapeutic effects have been obtained in animal models in preventing post-angioplasty restenosis and vein graft thickening, as well as increasing blood flow and collateral development in ischemic limbs. First clinical trials suggest a beneficial effect of vascular endothelial growth factor in achieving therapeutic angiogenesis in chronic limb ischemia and the efficacy of decoy oligonucleotides to prevent infrainguinal vein graft stenosis. However, further studies are mandatory to clarify the safety issues, to develop better gene delivery vectors and delivery catheters, to improve transgene expression, as well as to find the most effective and safe treatment genes.

Angiography↗
PubMed1998

Afferent and efferent connections of nucleus praeeminentialis in the channel catfish: a reevaluation.

Nucleus praeeminentialis (nPr) is an isthmic nucleus that has been described in the brains of electrosensory teleost fishes and a single non-electrosensory species. The nucleus receives axon collaterals of ascending medullary sensory lemniscal neurons. Axons of nPr neurons project in turn back down onto those same populations of medullary projection neurons via a descending parallel fiber system (the molecular layer or cerebellar crest). Thus nPr forms a link in a sensory feedback loop that modulates the activity of neurons that relay information from medulla to midbrain. The purpose of this study is to investigate the nature of the afferent and efferent connections of the nPr with the specific aim of investigating other sources of input into this modulatory circuit. Transport of neuronal tracers (horseradish peroxidase, DiI and dextran amines) revealed that nPr has extensive interconnections with nuclei in the basal metencephalon, cerebellum, octavolateralis column and basal medulla. A previously described source of afference, the torus semicircularis in the mesencephalon, was not indicated by our studies. Our studies suggest that in addition to regulating the sensitivity and resolution of electrosensory and mechanosensory lateral line systems, the nPr may play a role in the resolution of signal ambiguities posed by auditory or vestibular stimulation of the saccular endorgan of the inner ear.

Afferent Pathways↗
PubMed2005

Bedside emergency transcranial Doppler diagnosis of severe carotid disease using orbital window examination.

BACKGROUND: Identifying internal carotid artery (ICA) stenosis in the acute stroke setting can provide clinically useful information. Transcranial Doppler (TCD) through the orbital window is an easy test to perform and to track and identify different vessels. Previous TCD studies have suggested that a reversed ophthalmic artery (OA) flow is a useful collateral pattern to predict ICA disease. The authors sought to evaluate the TCD orbital window for predicting cervical ICA (cICA) stenosis in the setting of acute stroke and TIA. METHOD: Power M-mode/TCD was performed in acute stroke and transient ischemic attack patients at 2 institutions. Each orbital window depth was detected on M-mode and evaluated for the direction of flow and resistance pattern. Gold standard for comparison was carotid evaluation using carotid duplex, computed tomography angiogram, or conventional angiography. The assessment of cICA disease was categorized by degree of stenosis or occlusion. RESULTS: A total of 216 transorbital exams were performed in 117 patients. Twenty-five cICA occlusions and 8 critical cICA stenoses (>or=95%) were identified by gold standard imaging. Reversed OA flow at 50 to 60 mm depth revealed high specificity (100%; confidence interval [CI], 97.6%-100.0%) and good sensitivity (75%; CI, 53.3%-90.2%) for identifying cICA occlusion or critical stenosis (>or=95%). Low pulsatility index (<1.2) and mean flow velocity (<15 cm/s) discriminated critical severe ICA stenosis or occlusion when OA flow was anterograde with good sensitivity (87.2%) and specificity (95.2%). CONCLUSION: The reversed OA sign at 50 to 60 mm depth is very specific for identifying cICA occlusion or critical stenosis. When OA flow is anterograde, a low mean flow velocity or pulsatility index is also useful to identify cICA critical stenosis or occlusion.

Carotid Artery, Internal↗
PubMed1999

The significance and management of the leaking endograft.

Endoleak is the persistence of blood flow outside the lumen of an endograft, but within an aneurysm sac or adjacent vessel being treated by the graft. Diagnosis may be difficult, and treatment remains somewhat controversial. The purpose of this article is to discuss the clinical significance and appropriate management of endoleaks within the context of our current understanding of this phenomenon. The diagnosis of an endoleak can be made by conventional angiography, duplex ultrasound, intravascular ultrasound (IVUS), and computed tomography (CT) angiography. All of these modalities are effective, although CT angiography may be the most sensitive. Endoleaks can be categorized into 5 classes: (1) perigraft flow around the proximal end of the endograft; (2) perigraft flow around the distal end of the endograft; (3) flow through a defect in the body of the endograft; (4) flow between segments of a multicomponent endovascular graft; and (5) flow between arterial branches within an aneurysm sac. The first 4 classes have been shown to represent a clinical situation in which systemic arterial pressure is transmitted to an inadequately excluded aneurysm sac, placing the sac at risk of rupture. In contrast, branch-flow leaks do not appear to carry an increased risk of rupture, provided there is no increase in aneurysm sac diameter. However, an increase in the diameter of an aneurysm sac after endograft implantation may be a sign of occult endoleak, even if not visualized by current imaging techniques. Thus, we believe that collateral branch leaks with no associated aneurysm sac expansion may be observed with regular follow-up by CT angiography. All other endoleaks should be treated with adjunctive endovascular maneuvers or explanation of the endograft with standard open repair-in short, routine follow-up imaging on endografts to detect the presence of late endoleaks or aneurysm sac expansion.

Aneurysm↗
PubMed1997

Assessment of myocardial distribution of retrograde and antegrade cardioplegic solution in the same patients.

OBJECTIVE: In order to clarify intramyocardial delivery and distribution of retrograde cardioplegic solution in humans, we induced both ante- and retrograde methods in the same patients to compare their respective delivery and distribution using myocardial contrast echocardiography during surgery. METHODS: 15 patients consisting of nine patients with valvular heart diseases and six patients with coronary artery diseases (including two patients with myocardial infarcted areas and two patients with areas supplied by coronary collateral situation associated with totally occluded coronary arteries without myocardial infarction). Induction of cardioplegia was initially accomplished antegradely and thereafter retrogradely. RESULTS: In valvular heart disease, retrograde cardioplegic solution was distributed less homogeneously, and was not delivered to the midportion of the interventricular septum in two-thirds of the patients (6/9). The transmural myocardial distribution in the anterior, lateral, and posterior walls in the left ventricle were similar for both ante- and retrograde cardioplegic solution, while delivery to the endocardial halves was better than to the epicardial halves (endo-/epicardial intensity ration in antegrade versus retrograde: 1.31 +/- 0.24 versus 1.29 +/- 0.26; 1.19 +/- 0.05 versus 1.36 +/- 0.23; 1.33 +/- 0.28 versus 1.44 +/- 0.35, respectively (all NS)). For delivery to the right ventricle, the existence of small cardiac vein was important. In patients with small cardiac vein (34% in our study), the delivery to the right ventricular dorsal walls was shown. In coronary heart disease, retrograde cardioplegic solution was well delivered to the areas by coronary collateral situation associated with totally occluded coronary arteries, but antegrade solution was not. Neither ante- nor retro grade solution was delivered to myocardial infarcted areas. CONCLUSIONS: These results have important implications for planning strategies for myocardial protection. We think that it is necessary to fully grasp the coronary arterial and venous anatomy of individual patients and to know how to use either ante- or retrograde cardioplegia properly.

Aged↗
PubMed2007

Structural imaging reveals anatomical alterations in inferotemporal cortex in congenital prosopagnosia.

Congenital prosopagnosia (CP) refers to the lifelong impairment in face recognition in individuals who have intact low-level visual processing, normal cognitive abilities, and no known neurological disorder. Although the face recognition impairment is profound and debilitating, its neural basis remains elusive. To investigate this, we conducted detailed morphometric and volumetric analyses of the occipitotemporal (OT) cortex in a group of CP individuals and matched control subjects using high-spatial resolution magnetic resonance imaging. Although there were no significant group differences in the depth or deviation from the midline of the OT or collateral sulci, the CP individuals evince a larger anterior and posterior middle temporal gyrus and a significantly smaller anterior fusiform (aF) gyrus. Interestingly, this volumetric reduction in the aF gyrus is correlated with the behavioral decrement in face recognition. These findings implicate a specific cortical structure as the neural basis of CP and, in light of the familial history of CP, target the aF gyrus as a potential site for further, focused genetic investigation.

Adult↗
PubMed2003

Genetic modification removes an immunodominant allergen from soybean.

The increasing use of soybean (Glycine max) products in processed foods poses a potential threat to soybean-sensitive food-allergic individuals. In vitro assays on soybean seed proteins with sera from soybean-sensitive individuals have immunoglobulin E reactivity to abundant storage proteins and a few less-abundant seed proteins. One of these low abundance proteins, Gly m Bd 30 K, also referred to as P34, is in fact a major (i.e. immunodominant) soybean allergen. Although a member of the papain protease superfamily, Gly m Bd 30 K has a glycine in the conserved catalytic cysteine position found in all other cysteine proteases. Transgene-induced gene silencing was used to prevent the accumulation of Gly m Bd 30 K protein in soybean seeds. The Gly m Bd 30 K-silenced plants and their seeds lacked any compositional, developmental, structural, or ultrastructural phenotypic differences when compared with control plants. Proteomic analysis of extracts from transgenic seed detected the suppression of Gly m Bd 30 K-related peptides but no other significant changes in polypeptide pattern. The lack of a collateral alteration of any other seed protein in the Gly m Bd 30 K-silenced seeds supports the presumption that the protein does not have a role in seed protein processing and maturation. These data provide evidence for substantial equivalence of composition of transgenic and non-transgenic seed eliminating one of the dominant allergens of soybean seeds.

Allergens↗
PubMed1996

[Roentgen diagnosis and computerized tomography in inflammatory rheumatic diseases. Methods with a future?].

Plain-film radiography is an important and basic element in the assessment of inflammatory rheumatic diseases. Its various uses include assessment of inflammatory osseous destruction and the activity of inflammatory changes. Furthermore, the inflammatory collateral phenomena can indicate an acute clinical phase, and the articular soft tissue swelling and tenosynovitis are shown directly and indirectly very clearly. On the other hand, high-resolution computed tomography is very capable of showing cortical structures of bone complementary to MR. In some special clinical questions and anatomical regions, especially the axial skeleton, it delivers information of high specifity, partly for definitive diagnosis and partly for planning surgical procedures. The assessment of changes in the sacroiliac joints, sternoclavicular joints and craniocervical junction are domains of computed tomography.

Arthritis, Rheumatoid↗
PubMed1984

Functional evidence for sprouting or decentralized parasympathetic neurons in rat urinary bladder.

The pelvic nerve, carrying parasympathetic nerve fibres, distributes bilaterally in the rat urinary bladder. Preganglionic parasympathetic denervation (decentralization) on one side and postganglionic parasympathetic denervation on the other are followed by an initial decrease in acetylcholine forming capacity and in number of acetylcholinesterase positive nerves in the bladder. However, within a few weeks a marked recovery in acetylcholine synthesis and in number of nerves, based on collateral sprouting, occurs. In this study muscle strips of the rat urinary bladder exposed to the combined surgical procedure was studied. The strips were taken from "denervated" and "decentralized" halves of the bladder. Their contractile responses to methacholine and transmural electrical field stimulation were isometrically recorded in vitro. A supersensitivity to methacholine was found to have developed, of about the same degree, in the two halves 1 week postoperatively. In the denervated halves 4 weeks postoperatively, the supersensitivity was even more marked, whereas in the decentralized halves it tended to be less than after 1 week. The responses of denervated halves to electrical stimulation were reduced 1 week postoperatively. This was also the case for decentralized halves, although the reduction was not large enough to be significant. When examined 4 weeks postoperatively the responses, in particular in denervated halves, were enlarged compared to those 1 week postoperatively. The atropine-sensitive portion of the responses increased with time. Increases in contractile responses to electrical stimulation accompanied by a tendency to desensitization to methacholine are taken as functional evidence for outgrowth of decentralized parasympathetic neurones in the decentralized halves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

The transient depression of hippocampal CA1 LTP induced by chronic intermittent ethanol exposure is associated with an inhibition of the MAP kinase pathway.

Using electrophysiological and biochemical approaches, we investigated the effects of chronic, intermittent ethanol (CIE) treatment on activation of the mitogen activated protein kinase (MAPK), also known as extracellular signal regulated protein kinase 1 and 2. In hippocampal slices taken from control rats, brief high-frequency stimulation to Schaffer collateral fibers induced a large post-tetanic potentiation (PTP) in the CA1 region that decayed to stable long-term potentiation (LTP) of field extracellular postsynaptic potentials. Western blot analyses showed that phosphorylation of MAPK was increased during PTP and returned to baseline levels during LTP. In slices from the rats removed immediately from CIE treatment, PTP and MAPK activation during the PTP was significantly less than that observed in control slices and LTP was absent. In slices from rats subjected to 1 day withdrawal from CIE treatment, both the reduction in MAPK phosphorylation during PTP and the impairment of PTP and LTP were still evident. Recovery of PTP and partial recovery of LTP was observed in slices obtained from 5-day withdrawn rats. However, MAPK activation during PTP was still attenuated significantly. Interestingly, MAPK activation was enhanced significantly during LTP in 5-day withdrawn rats as well as the sensitivity to MAPK inhibitor PD 098059. In addition to these changes in HFS-induced MAPK activation, we also observed a significant reduction in the basal phosphorylation of MAPK in slices removed from rats immediately after CIE treatment. These results implicate the MAPK signal transduction pathway as a potential cellular target of ethanol. Alterations in MAPKs could play an important role in the alcohol-induced changes in synaptic plasticity associated with the effects of alcohol abuse on learning and memory processes.

Alcoholism↗
PubMed1989

ECF pH dynamics within the ventrolateral medulla: a microelectrode study.

Using pH-sensitive microelectrodes, we evaluated pH dynamics of extracellular fluid (ECF) within the ventrolateral medulla (VLM) beneath the central chemoceptive areas in anesthetized, spontaneously breathing cats. Static ECF pH was acid in the superficial layers (less than 1 mm), compared with the overlying cerebrospinal fluid pH that became alkaline gradually during the experiments. In the deeper VLM areas (1-3 mm), no systematic gradients of ECF pH were observed. We found various, isolated regions where intravertebral artery injections of CO2-saturated saline evoked acidic shift of ECF pH in the time course analogous to ventilatory augmentation. Those responsive regions were found to be scattered not only in the superficial layers but also in the deeper VLM areas, although many nonresponsive regions were also intermingled among them. Occlusions of the principal vessels supplying the tested VLM regions diminished but failed to abolish the ECF pH responses to the CO2 loadings, suggesting a collateral blood flow by fine pial vessels. The present study suggests a possibility that the pH-dependent central chemoreceptors, if any, would be scattered in the deeper VLM areas as well as the superficial layers.

Animals↗
PubMed2004

High-resolution MR imaging of the elbow using a microscopy surface coil and a clinical 1.5 T MR machine: preliminary results.

OBJECTIVE: To obtain high-resolution MR images of the elbow using a microscopy surface coil with a 1.5 T clinical machine and to evaluate the feasibility of its use for elbow injuries. DESIGN AND PATIENTS: Five asymptomatic normal volunteers and 13 patients with elbow pain were prospectively studied with MR imaging using a microscopy surface coil 47 mm in diameter. High-resolution MR images using a microscopy coil were obtained with fast spin echo (FSE) proton density-weighted sequence, gradient recalled echo (GRE) T2*-weighted sequence, and short tau inversion recovery (STIR) sequence, with a 1-2 mm slice thickness, a 50-70 mm field of view, an imaging matrix of 140-224 x 512 using zero fill interpolation, and 2-6 excitations. RESULTS: High-resolution MR images of normal volunteers using a microscopy coil clearly showed each structure of the medial and lateral collateral ligaments on GRE T2*-weighted images and FSE proton-density weighted images. Partial medial collateral ligament injury, a small avulsion of the medial epicondyle, and osteochondritis dissecans were well demonstrated on high-resolution MR images. CONCLUSION: High-resolution MR imaging of the elbow using a microscopy surface coil with a 1.5 T clinical machine is a promising method for accurately characterizing the normal anatomy of the elbow and depicting its lesions in detail.

Adolescent↗