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Biomedical subjects

Q Gan

Publications and source records attributed to Q Gan.

18 recordsLinked to original sources
PubMed2006

Brainstem projections from recipient zones of the anterior ethmoidal nerve in the medullary dorsal horn.

Stimulation of the anterior ethmoidal nerve or the nasal mucosa induces cardiorespiratory responses similar to those seen in diving mammals. We have utilized the transganglionic transport of a cocktail of horseradish peroxidase conjugates and anterograde and retrograde tract tracing techniques to elucidate pathways which may be important for these responses in the rat. Label was seen throughout the trigeminal sensory complex after the horseradish peroxidase conjugates were applied to the anterior ethmoidal nerve peripherally. Reaction product was most dense in the medullary dorsal horn, especially in laminae I and II. Injections were made of biotinylated dextran amine into the recipient zones of the medullary dorsal horn from the anterior ethmoidal nerve, and the anterogradely transported label documented. Label was found in many brainstem areas, but fibers with varicosities were noted in specific subdivisions of the nucleus tractus solitarii and parabrachial nucleus, as well as parts of the caudal and rostral ventrolateral medulla and A5 (noradrenergic cell group in ventrolateral pons) area. The retrograde transport of FluoroGold into the medullary dorsal horn after injections into these areas showed most neurons in laminae I, II, and V. Label was especially dense in areas which received primary afferent fibers from the anterior ethmoidal nerve. These data identify potential neural circuits for the diving response of the rat.

Animals↗
PubMed2005

The central termination of sensory fibers from nerves to the gastrocnemius muscle of the rat.

Peripheral nerves innervating muscles have sensory fibers that relay information into the CNS information about proprioception, pain, and the metabolic state of the muscle. The present study shows the primary afferent projections into the spinal cord of the nerves innervating the gastrocnemius muscle of the rat using the transganglionic transport of a cocktail of horseradish peroxidase (HRP) conjugated to cholera toxin and wheat germ agglutinin; these markers have been shown to label large and small fibers, respectively. A dense projection into lamina I of the lumbar dorsal horn and a more moderate projection into lamina V were seen. Moreover, dense reaction product was found in the most medial aspect of lamina II, especially lamina II inner part, and less in lamina III and IV of levels L3-L5. Lamina VI had dense reaction product from the rostral sacral levels of the spinal cord that continued into Clarke's column at rostral lumbar levels. The nucleus gracilis also was labeled. Other nerves emerging from the popliteal fossa, including the tibial, peroneal, and sural nerves, also were injected with the HRP cocktail and their projections compared with those from the gastrocnemius muscle. Projections from the gastrocnemius muscle only partially overlapped with those from the tibial nerve, from which the nerves to the gastrocnemius muscle branch. However, the topology of projections from these nerves to laminae II-IV of the dorsal horn differed from that of the nerves of the gastrocnemius muscle, suggesting there was little spread to other nerves in the popliteal fossa. It was also noted that large labeled processes, presumably dendrites of retrogradely labeled motoneurons, entered the dorsal horn. These data provide information on the central projections of both the large and small fibers innervating the gastrocnemius muscle, and may aid in determining the circuitry utilized in the exercise pressor reflex as well as muscle pain.

Afferent Pathways↗
PubMed2004

Activation of waste MDF sawdust charcoal and its reactive dye adsorption characteristics.

This paper reports an experimental investigation of converting waste medium density fibreboard (MDF) sawdust into chars and activated carbon using chemical activation and thermal carbonisation processes. The MDF sawdust generated during the production of architectural mouldings was characterised and found to have unique properties in terms of fine particle size and high particle density. It also has a high content of urea formaldehyde resin used as a binder in the manufacturing of MDF board. Direct thermal carbonisation and chemical activation of the sawdust by metal impregnation and acid (phosphoric acid) treatment prior to pyrolysis treatment were carried out. The surface morphology of the raw dust, its chars and activated carbon were examined using scanning electron microscopy (SEM). Adsorptive properties and total pore volume of the materials were also analysed using the BET nitrogen adsorption method. Liquid adsorption of a reactive dye (Levafix Brilliant red E-4BA) by the derived sawdust carbon was investigated in batch isothermal adsorption process and the results compared to adsorption on to a commercial activated carbon (Filtrasorb F400). The MDF sawdust carbon exhibited in general a very low adsorption capacity towards the reactive dye, and physical characterisation of the carbon revealed that the conventional chemical activation and thermal carbonisation process were ineffective in developing a microporous structure in the dust particles. The small size of the powdery dust, the high particle density, and the presence of the urea formaldehyde resin all contributed to the difficulty of developing a proper porous structure during the thermal and chemical activation process. Finally, activation of the dust material in a consolidated form (cylindrical pellet) only achieved very limited improvement in the dye adsorption capacity. This original study, reporting some unexpected outcomes, may serve as a stepping-stone for future investigations of recycle and reuse of the waste MDF sawdust which is becoming an increasing environmental and cost liability.

Adsorption↗
PubMed2001

Central corticotropin releasing factor (CRF) and adrenergic receptors mediate hemodynamic responses to cocaine.

Cocaine administration evokes cardiovascular responses that are variable in rats such that the pressor response is attributable to either a large increase in systemic vascular resistance and a decrease in cardiac output (vascular responders) or a smaller increase in systemic vascular resistance and no change or an increase in cardiac output (mixed responders). This study was designed to determine the role of central corticotropin releasing factor (CRF) and adrenergic receptors in mediating specific hemodynamic response patterns. Rats were instrumented for ascending aortic blood flow determination (cardiac output) using a pulsed Doppler system, arterial pressure measurement and for intravenous and intracerebroventricular (icv) administration of drugs. After characterizing the hemodynamic response pattern in individual rats to cocaine (5 mg/kg, i.v., 4-6 trials), selective receptor antagonists were administered icv 10 min before cocaine (5 mg/kg, i.v.). Pretreatment with the CRF antagonist alpha-helical CRF(9-41) (10 microg/5 microl, icv) prevented the decrease in cardiac output in vascular responders without altering hemodynamic responses to cocaine in mixed responders. Astressin (5 microg/5 microl, icv) exerted a similar effect in vascular responders. The alpha(2) receptor antagonist, yohimbine (3 microg/microl, icv) also prevented the decrease in cardiac output in vascular responders. Lower doses of alpha-helical CRF(9-41) (1 and 3 microg) were ineffective whereas higher doses of either CRF antagonist were lethal within 24 h. In contrast, propranolol (3 or 30 microg, icv) pretreatment enhanced the cocaine-induced decrease in cardiac output and increase in systemic vascular resistance noted in vascular responders and resulted in a decrease in cardiac output in mixed responders. We conclude that CRF and adrenoceptors in the CNS play an important role in determining the hemodynamic response pattern to cocaine. Furthermore, central beta-adrenoceptors may be responsible for the reported effects of intravenous propranolol on cocaine-induced responses.

Adrenergic beta-Antagonists↗
PubMed2001

Hemodynamic response pattern predicts susceptibility to stress-induced elevation in arterial pressure in the rat.

Cocaine or air jet stress evokes pressor responses due to either a large increase in systemic vascular resistance (vascular responders) or small increases in both cardiac output and vascular resistance (mixed responders) in conscious rats. Repeated cocaine administration results in elevated arterial pressure in vascular responders but not in mixed responders. The present study examined the hypothesis that the pattern of cardiovascular responses to an unconditioned stimulus (UCS; air jet) is related to responses to a conditioned stimulus (CS; tone followed by brief foot shock) in individual rats. Our data demonstrate that presentation of the UCS produced variable cardiac output responses that correlated with responses to the CS (n = 60). We also determined whether individual cardiovascular response patterns to acute stress correlated with predisposition to a sustained stress-induced elevation in arterial pressure. Rats were exposed to three different stressors presented one per day successively for 4 wk and during a poststress period of 3 wk while arterial pressure was recorded periodically. Mean arterial pressure was elevated in all rats during chronic stress but, during the poststress period, remained at significantly higher levels in vascular responders but not mixed responders. Therefore, we conclude that acute behavioral stress to a conditioned stimulus elicits variable hemodynamic responses that predict the predisposition to a sustained stress-induced elevation in arterial pressure.

Animals↗
PubMed2001

Hemodynamic response patterns to acute behavioral stressors resemble those to cocaine.

Hemodynamic responses to cocaine vary greatly between animals, and the variability is related to the incidence of cocaine-induced cardiomyopathies and hypertension. The variability in cardiac output and systemic vascular resistance responses to cocaine in individuals is correlated with the responses to acute startle (air jet). This experiment was designed to determine whether responses to cocaine and to air jet are related to those evoked by a conditioned stimulus (tone preceding foot shock) and to an unconditioned stimulus (cold water). We verified the relationship in hemodynamic response patterns between cocaine and cold stress using selective receptor antagonists. Rats were instrumented with a pulsed Doppler flow probe on the ascending aorta for determination of cardiac output and with an arterial cannula for recording arterial pressure and heart rate. After recovery, some rats were tested multiple times with four different stimuli: air jet (6 trials), 15-s tone preceding 1-s foot shock (12 trials), cold water exposure (1 cm deep for 1 min, 4-12 trials), and cocaine (5 mg/kg iv, 4-6 trials) while hemodynamic parameters were recorded. Each stimulus was capable of eliciting a pressor response that was associated with variable changes in cardiac output. The cardiac output response to cocaine was correlated with the initial responses to each stressor in individual rats. Responses evoked by cold stress were most similar to those elicited by cocaine. Furthermore, nicardipine (25 microg/kg iv) or atropine methylbromide (0.5 mg/kg iv) pretreatment prevented the cardiac output differences to acute cold stress, as noted after cocaine administration. On the other hand, propranolol (1 mg/kg iv) exacerbated both the decrease in cardiac output and the stress-induced increase in systemic vascular resistance as previously reported with cocaine. Therefore, the initial response to cold water exposure is a reliable method of evoking characteristic hemodynamic response patterns that, as seen with cocaine, may provide a suitable model for identifying the causes for predilection to stress-induced cardiovascular disease.

Acute Disease↗
PubMed1999

Role of cholinergic receptors and cholinesterase activity in hemodynamic responses to cocaine in conscious rats.

It has been suggested that toxicity to cocaine is related to the relative rate of cocaine metabolism by cholinesterases and to activation of cholinergic receptors either directly or by reflex mechanisms. We examined these possibilities by altering cholinesterase activity and blocking cholinergic receptors in rats prone or resistant to cocaine-induced cardiovascular toxicity. Rats were instrumented with a pulsed Doppler flow probe on the ascending aorta for measurement of cardiac output and cannulated for arterial pressure and heart rate determination. In conscious rats, cocaine (5 mg/kg iv) elicited pressor responses and a delayed bradycardia but cardiac output and systemic vascular resistance responses varied greatly between rats. Pretreatment with the nonspecific cholinesterase inhibitors physostigmine (0.1-0.2 mg/kg) or neostigmine (0.1 mg/kg) reduced the pressor response by diminishing the increase in systemic vascular resistance. In contrast, inhibition of cocaine metabolism with the selective plasma cholinesterase inhibitor tetraisopropyl pyrophosphoramide (0.5 mg/kg) or increasing cholinesterase activity with human butyryl cholinesterase (9.9 mg/kg iv) did not alter hemodynamic responses to cocaine. Administration of atropine methyl bromide (0.5-1 mg/kg iv) alone or with physostigmine to prevent the cholinomimetic effects of physostigmine reduced the cocaine-induced decrease in cardiac output noted in some animals. These data suggest that the cocaine-induced decrease in cardiac output observed in some rats is, at least in part, dependent on activation of muscarinic receptors. In addition, the rate of cocaine metabolism is not critical for the initial hemodynamic responses to cocaine in conscious rats.

Animals↗
PubMed1998

Mechanisms of hemodynamic responses to cocaine in conscious rats.

Several agents have been used to treat cocaine-related cardiovascular complications and toxicity occurring in sensitive individuals, yet the causes of hemodynamic responsiveness and differential sensitivity to cocaine are unknown. In this study, we sought to examine the role of different mediators in a model of variable cardiovascular responses to cocaine. As noted previously in conscious rats, cardiac output (CO) and systemic vascular resistance (SVR) responses to cocaine (5 mg/kg, i.v.) varied widely. Twenty of 34 rats exhibited cocaine-induced decreases in CO of > or =8% and large increases in SVR (designated vascular responders). The remaining rats with little change or an increase in CO and smaller increases in SVR were named mixed responders. Pretreatment with propranolol (1 mg/kg) or metoprolol (1 mg/kg) reduced heart rate. In mixed responders, propranolol or metoprolol reversed the cocaine-induced increase in CO and stroke volume and enhanced the increase in SVR, making these rats respond like vascular responders. Nicardipine (25 microg/kg) reduced the pressor response and selectively reversed the CO responses in vascular responders. N omega-nitro-L-arginine methyl ester (L-NAME; 2.7 mg/kg) increased arterial pressure by increasing SVR. Cocaine induced greater pressor and SVR responses apparently because of a shift in baseline values elicited by L-NAME alone. Therefore, differences in hemodynamic responses patterns may be the result of differences in beta-adrenergic activation or subsequent calcium channel activation or both. We predict that calcium channel antagonists may be useful to treat cocaine-induced cardiovascular complications, whereas beta-adrenergic antagonists are not likely to be beneficial.

Adrenergic beta-Antagonists↗
PubMed1997

Ethanol alters hemodynamic responses to cocaine in rats.

Cocaine is often used while consuming ethanol despite evidence that this combination may enhance the toxicity of cocaine. In the present study, we examined the cardiovascular effects of ethanol (475 or 950 mg/kg, i.v.) alone and in combination with cocaine (5 mg/kg, i.v.) in conscious rats. Ethanol or cocaine administration produced a consistent pressor response but highly variable cardiac output and systemic vascular resistance responses. The hemodynamic response patterns in individual rats to either drug were similar and related within rats. After ethanol pretreatment, cocaine produced greater decreases in cardiac output. We have proposed that this pattern of responses may reflect a predisposition in individual rats to cocaine-induced cardiomyopathies and hypertension. Furthermore, these data suggest that ethanol administration elicits a similar pattern of hemodynamic responses as previously reported for cocaine or amphetamine administration or acute behavioral stress.

Animals↗
PubMed1997

Effects of proposed treatments for cocaine addiction on hemodynamic responsiveness to cocaine in conscious rats.

Several agents may treat cocaine addiction and toxicity including bromocriptine, desipramine, GBR 12909 [1-(2-(bis(4-fluorphenyl)-methoxy)-ethyl)-4-(3-phenyl-propyl) piperazine], diazepam, buprenorphine and dizocilpine. In this study, we sought to determine whether these specific therapeutic agents alter cardiovascular responses to cocaine in conscious rats. Arterial pressure responses to cocaine (5 mg/kg, i.v.) were similar in all rats whereas cardiac output responses varied widely. In 26 of 33 rats (named vascular responders), cocaine induced a decrease in cardiac output of 8% or more. The remaining rats with little change or an increase in cardiac output were classified as mixed responders. Pretreatment with bromocriptine (0.1 mg/kg) or desipramine (1 mg/kg) increased cardiac output in mixed responders and increased systemic vascular resistance in vascular responders similar to the differential effects noted with cocaine. GBR 12909 (0.5-10 mg/kg) elicited a decrease in cardiac output at higher doses. Diazepam (0.1 and 0.5 mg/kg) had small, short-lasting effects on cardiovascular parameters. Buprenorphine (0.3 mg/kg) or the NMDA (N-methyl-D-aspartic acid) receptor antagonist, dizocilpine (0.05 mg/kg), increased arterial pressure, heart rate and cardiac output in vascular responders. Bromocriptine and desipramine prevented the difference in cardiac output responses in vascular and mixed responders by reducing the cocaine-induced decrease in cardiac output in vascular responders. Pretreatment with GBR 12909 (1 mg/kg) had little effect on cardiovascular responses to cocaine except to depress the increase in cardiac output noted in mixed responders. Buprenorphine selectively enhanced the increase in systemic vascular resistance whereas dizocilpine enhanced the pressor response. These data suggest that several treatment regimens for cocaine addiction alter the cardiovascular responses to cocaine and that dopamine D2 receptor activation may be necessary for the decrease in cardiac output noted in vascular responders.

Animals↗
PubMed1997

[The experimental study of Pseudomonas contamination in soft drinks].

Bymeans of this study, we have found out about the situation of Pseudomons contamination in the soft drinks which are manufactured and sold at the area of Nanchang City. In the course of this study, we examined total 416 specimens, in which we found that 69 specimens were positive reaction. The positive rate made up 16.59% of the total specimens. From these 69 positive specimens we separate isolated andidentified the following Pseudomonas 111 strains including 16 different species: P. aeruginosa, 9; P. fluorescens biovars; 11; P. putida biovars, 14; P. syringae pathovars, 5; P. mendocina, 5; P. alcaligenes, 23; P. pseudoalcaligenes, 10; P. cepacia, 17; P. solanacearum, 1; P. testosteroni, 1; P. delafieldii, 3; P. facilis, 6; P. flava 1; P. psenudoflava, 2; P. palleronii, 1; and a new species of Pseudomonas--P. halosensibilis. The achievement of this study will provide scientific basis for working out the standards of food safety control and inspection, raising the level of food hygieneinspection, and directing the drinks menufacturers and selling units to strengthen the food safety control and inspection.

Carbonated Beverages↗
PubMed1994

Central sympathetic control of spinal endothelin release in the rat.

Endothelin and its receptors have been identified in the spinal cord. Intrathecal administration of endothelin-3 produces hypotension in anesthetized rats. The present study was designed to identify whether endothelin-3 is released upon changes in sympathetic nervous activity. Endothelin-3-like immunoreactivity in spinal superfusates was directly correlated with resting arterial pressure. Endothelin-3 levels were enhanced by hypothalamic stimulation and by hemorrhage-induced hypotension and reduced by nitroprusside-induced hypotension. These findings suggest that sympathetic activation enhances endothelin-3 release but that nitroprusside may act directly to suppress release. We propose that endothelin-3 plays a role in spinal regulation of sympathetic outflow.

Anesthesia↗
PubMed1994

Nonadrenergic mechanisms of cocaine-induced regional vascular responses in rats.

The pressor response to cocaine is a consequence of mesenteric vasoconstriction and hindquarters vasodilation as a result of activation of alpha 1- and beta-adrenergic receptors, respectively. In the present study, evidence for additional, nonadrenergic effects of cocaine-induced changes in regional blood flow was obtained using pulsed Doppler flowmetry in conscious rats. Cocaine produced dose-dependent initial peaks (within 1 min) in mean arterial pressure concomitant with an increase in hindquarters and mesenteric vascular resistance. The sustained, modest pressor response was associated with hindquarters vasodilation and bradycardia. The cocaine-induced vasodilation was enhanced by pretreatment with indomethacin (5 mg/kg), prevented by ibuprofen (12.5 mg/kg) or 3-amino-1-[m-(trifluoromethyl)-phenyl]-2-pyrazoline (BW755C, 10.5 mg/kg) pretreatment, and unaffected by meclofenamate administration (2.5 mg/kg). Equipotent local anesthetic doses of procaine produced equivalent hindquarters vasodilator responses and more modest pressor responses. Dial-urethane anesthesia did not affect hindquarters vasodilation in response to cocaine or procaine but did reduce the mesenteric vasoconstrictor and pressor responses. These data demonstrate that the cocaine-induced hindquarters vasodilation is not mediated solely by beta-adrenergic receptors but is also dependent upon eicosanoids. Furthermore, the cocaine-induced vasodilation may be due, in part, to a direct local anesthetic effect but is not dependent upon a locomotor or behavioral stress induced increase in blood flow.

Anesthesia, General↗
PubMed1994

[A new species of Pseudomonas].

A strain No. 9191 isolated from fruit juice mineral drink is gram-negative short-rod. It differs from reported species of Pseudomonas in morphological, physiological and biochemical characteristics. Main characteristics of No. 9191 are single polar flagelled, oxidase and catalase positive, no acid from glucose but producing alkali, nitrate reduced to nitrite, inability to hydrolize gelatin and starch, arginine dihydrolase absent, no growth in presence of 0.85% NaCl. The G+C mol% of DNA is 65.15. It is named Pseudomonas halosensibilis Zou & Cai nov. sp. by the sensibility property for salt.

Beverages↗
PubMed1993

Cocaine-induced myocardial ultrastructural alterations and cardiac output responses in rats.

Cocaine use has been associated with profound functional and pathological myocardial responses in otherwise asymptomatic humans, yet a number of individuals appear to tolerate large doses of the drug. This study was designed to determine whether there is a relationship between the differential effects of cocaine administration on cardiovascular responses and on the development of cardiomyopathies in rats. After instrumentation for determination of cardiac output, conscious, freely moving rats were treated with cocaine (5 mg/kg) or saline intravenously twice daily for 14 days before removing the myocardium for analysis. Although most cardiovascular responses were similar, cocaine administration elicited consistent decreases in cardiac output in some rats, whereas others showed little change or an increase. While little change was evident at low magnification, electron microscopy revealed diffusely distributed myocardial lesions including focally dilated sarcoplasmic reticulum and myofibrillar derangement, early signs of mitochondrial alterations, and foci of myocardial fibrosis. The incidence of these alterations was greater in rats with a decrease in cardiac output. We also observed these lesions in a subset of rats treated with cocaine without cardiac output instrumentation. These data represent the first evidence that there is a relationship between cocaine-induced functional and pathological alterations and that rats, like humans, may be differentially sensitive to these effects.

Animals↗
PubMed1993

Stress and cocaine elicit similar cardiac output responses in individual rats.

Cocaine use and behavioral stress elicit variable cardiovascular responses in individuals. In the present study, we examined the effects of cocaine or stress on arterial pressure, heart rate, and cardiac output in conscious rats. Rats were instrumented for determination of ascending aortic blood flow as an index of cardiac output using pulsed Doppler flow-metry. Cocaine administration elicited consistent decreases in cardiac output in some rats, whereas others had increases. In contrast, the pressor and heart rate responses were similar in these two groups of animals. Air jet stress also elicited a decrease in cardiac output only in a subset of conscious rats, yet produced equivalent pressor responses in all rats. Cardiac output responses to cocaine and air jet stress were closely correlated in individual rats, indicating that these stimuli evoke similar hemodynamic responses in individual rats. These observations suggest that the rat may provide a model for understanding differential cardiovascular sensitivity to cocaine and/or stress in humans.

Animals↗
PubMed1992

Neural modeling with dynamically adjustable threshold and refractory period.

A variant of the FitzHugh-Nagumo model is proposed in order to fully make use of the computational properties of intraneuronal dynamics. The mechanisms of threshold and refractory periods resulting from the double dynamical processes are qualitatively studied through computer simulation. The results show that the variant neuron model has the property that its threshold, refractory period and response amplitude are dynamically adjustable. This paper has also discussed some problems relating to collective property, learning and implementation of the neural network based on the neuron model proposed. It is noted that the implicit way to describe threshold and refractory period is advantageous to adaptive learning in neural networks and that molecular electronics probably provides an effective approach to implementing the above neuron model.

Animals↗