PubMed Health⌕ Search

Biomedical subjects

H C Lin

Publications and source records attributed to H C Lin.

At least 73 records · Page 4Linked to original sources
PubMed2001

Effects of intravenous lidocaine overdose on cardiac electrical activity and blood pressure in the horse.

This study aimed to identify blood serum lidocaine concentrations in the horse which resulted in clinical signs of intoxication, and to document the effects of toxic levels on the cardiovascular and cardiopulmonary systems. Nineteen clinically normal mature horses of mixed breed, age and sex were observed. Lidocaine administration was initiated in each subject with an i.v. loading dose of 1.5 mg/kg bwt and followed by continuous infusion of 0.3 mg/kg bwt/min until clinical signs of intoxication were observed. Intoxication was defined as the development of skeletal muscle tremors. Prior to administration of lidocaine, blood samples for lidocaine analysis, heart rate, mean arterial blood pressure, systolic blood pressure, diastolic blood pressure, respiratory rate and electrocardiographic (ECG) data were collected. After recording baseline data, repeat data were collected at 5 min intervals until signs of intoxication were observed. The range of serum lidocaine concentrations at which the clinical signs of intoxication were observed was 1.85-4.53 microg/ml (mean +/- s.d. 3.24 +/- 0.74 microg/ml). Statistically significant changes in P wave duration, P-R interval, R-R interval and Q-T interval were observed in comparison to control values, as a result of lidocaine administration. These changes in ECG values did not fall outside published normal values and were not clinically significant. Heart rate, blood pressures and respiratory rates were unchanged from control values. This study establishes toxic serum lidocaine levels in the horse, and demonstrates that there were no clinically significant cardiovascular effects with serum lidocaine concentrations less than those required to produce signs of toxicity.

Anesthetics, Local↗
PubMed2001

Upregulation of inducible nitric oxide synthase and cytokine secretion in peripheral blood monocytes from pulmonary tuberculosis patients.

SETTING: Peripheral blood monocytes (PBM) are the main source of alveolar macrophages, which have an upregulation of inducible nitric oxide synthase (iNOS) in pulmonary tuberculosis (TB). TNF-alpha and IL-1 beta are thought to be involved in the immune response to mycobacterial infection. OBJECTIVE: To identify whether iNOS expression and cytokine release of PBM are upregulated and have a connection in TB infection. DESIGN: The expression of iNOS immunoreactivity on PBM from TB patients and normal subjects was measured by loading with anti-macrophage iNOS polyclonal primary antibody analyzed by flow cytometry. Expression of iNOS mRNA in PBM was detected by RT-PCR. The spontaneous generation of nitrite and cytokines (IL-1 beta and TNF-alpha) by cultured monocytes was also determined. RESULTS: Compared to normal subjects, iNOS immuno-reactivity, the capacity for spontaneous nitrite generation and the level of TNF-alpha or IL-1 beta secretion of PBM were significantly higher in TB patients. The amount of nitrite, TNF-alpha and IL-1 beta released from PBM of TB patients was inhibited by NG-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of NOS. The level of iNOS immunoreactivity on PBM was highly correlated with nitrite generation both in all the subjects studied and in TB patients alone. Spontaneous TNF-alpha production showed a stronger correlation with nitrite production than with IL-1 beta. CONCLUSION: The NO and cytokine synthase activities of monocytes appear to be concomitantly upregulated in response to mycobacterial infection. The enhanced NO generation by monocytes in TB patients may play an autoregulatory role in amplifying the synthesis of pro-inflammatory cytokines.

Female↗
PubMed2001

Relationship between six-minute walking test and pulmonary function and ventilatory drive in patients with airflow limitation.

BACKGROUND: We studied the correlation between exercise tolerance and pulmonary function, arterial blood gases, and ventilatory drive in patients with airflow limitation (AFL). METHODS: Forty-one patients (36 men, 5 women, mean age 63.6 +/- 10.3 years) with forced expiratory volume in one second (FEV1) < 75% and FEV1/forced vital capacity (FVC) < 75% were enrolled. All patients were clinically stable with no impairment of the lower extremities. On the first day of the study, pulmonary function test (PF), including FVC, FEV1, diffusion capacity (DLCO), and residual volume (RV)/total lung capacity (TLC) was measured by plethysmography. On the next day, ventilatory drive P0.1 were measured before drawing blood gases. Then, a 6-minute walking test with pulse-oxymetry and end tidal CO2 monitoring was performed. Ventilation efficiency (O2SATp & ETCO2) was recorded every 6 seconds during exercise. RESULTS: The walking distance (WD) was significantly correlated to PF: FVC%, FEV1%, DLCO%, and RV/TLC. There was also a significant correlation between resting arterial blood gases (PaO2, PaCO2, SatO2) and PF (FVC%, FEV1%, DLCO% and RV/TLC). The SatO2 at the end of exercise was highly correlated to PF (FVC%, FEV1%, DLCO% and RV/TLC). Gas exchange parameters: PaO2, PaCO2, O2SATa, O2SATp at rest, and O2SATp at the end of exercise were also significantly related to WD. CONCLUSION: The magnitude of exercise intolerance in patients with AFL was not only significantly correlated to the impairment of pulmonary function, but also closely related to gas exchange during exercise. Therefore, limitation of ventilation could be identified earlier using an exercise test.

Aged↗
PubMed2001

Frequency doubling technology perimetry in retinal diseases--preliminary report.

The role of frequency doubling technology perimetry (FDT) in glaucoma has been promising in speed and simplicity as well as in its high sensitivity and specificity compared to conventional automatic perimetry. In this study, we evaluate the role of frequency doubling technology perimetry (FDT) in a variety of retinal diseases. FDT using full-threshold C-20 mode was performed in thirty-three patients with a variety of retinal diseases [16 cases of rhegmatogenous retinal detachment (RRD), nine cases of age-related maculopathy (AMD) and eight cases of central serous chorioretinopathy (CSCR)]. The fundus was scored by the extent of disease on each quadrant and macular area (central five degree visual angle). Then the retinal scores were compared with the points depressed to 2% on total deviation plots in FDT C-20 full-threshold mode using Spearman's rank correlation method. The correlation was statistically significant in the group of RRD (R = 0.57, P = 0.01), whereas the correlation was not significant in the group of macular diseases (AMD & CSCR, R = 0.47 & 0.32, P = 0.12 & 0.20). In conclusion, our results suggest that FDT might be a useful and simple technique for functional evaluation in RRD, but not in the macular disease group under this scoring system.

Adult↗
PubMed2001

Hemodynamic effects of Salvia miltiorrhiza on cirrhotic rats.

Salvia miltiorrhiza (Sm) administration has been shown to reduce hepatic fibrosis in rats. We investigated the hemodynamic effects of Sm on bile duct ligated (BDL) rats. Hemodynamic, histological, and vascular contractile studies were conducted in rats 4 weeks after bile duct ligation. An aqueous extract of Sm (0.2 g twice per day) or vehicle was administered for 4 weeks to BDL rats. Sm treatment in BDL rats significantly reduced histological grades of fibrosis and ameliorated the portal hypertensive state (including portal venous pressure, superior mesenteric artery blood flow, cardiac index, and total peripheral resistance) as compared with vehicle treatment. Moreover, Sm treatment enhanced the vascular sensitivity of mesenteric arteries to phenylephrine in BDL rats. Sm treatment had no effect on plasma biochemical profiles of either BDL or normal rats. Our results suggest that 4-week Sm treatment ameliorates the portal hypertensive state in BDL rats.

Animals↗
PubMed2001

Hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure: role of endotoxin and tumor necrosis factor-alpha.

BACKGROUND: Hepatic encephalopathy, a complex neuropsychiatric syndrome secondary to acute liver failure, chronic parenchymal liver disease or portal-systemic shunting, may possibly develop through mediators of endotoxin and tumor necrosis factor-alpha (TNF-alpha). However, there are no published data concerning the relationships between the severity of encephalopathy and the plasma levels of endotoxin and TNF-alpha. METHODS: Male Sprague-Dawley rats weighing about 300-350 g were used. Fulminant hepatic failure was induced by intraperitoneal injection ofthioacetamide (350 mg/kg/day) for 3 consecutive days. Severity of encephalopathy was assessed by measuring motor counts using an Opto-Varimex animal activity meter. Plasma levels of endotoxin and TNF-alpha were determined by chromogenic Limulus assay and ELISA method, respectively. RESULTS: Our study revealed that higher plasma levels of endotoxin (> 5.9 pg/ml) and TNF-alpha (> 18.8 pg/ml) were significantly associated with more blunted motor activities in rats with fulminant hepatic failure (p < 0.05). A significant correlation was observed between plasma concentrations of endotoxin and TNF-alpha (r = 0.59, p < 0.001). Plasma levels of endotoxin were weakly correlated with the total movements in an open field (r = -0.34, p = 0.032) and the counts of ambulatory (r = -0.38, p = 0.014) and vertical movements (r = -0.40, p = 0.010). There were no correlations between the motor counts and plasma levels of TNF-alpha (p > 0.05). CONCLUSIONS: In addition to endotoxin and TNF-alpha, other factors may participate in the pathogenesis of hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure.

Animals↗
PubMed2001

Matrilysin cleavage of corneal collagen type XVIII NC1 domain and generation of a 28-kDa fragment.

PURPOSE: To localize endostatin and collagen type XVIII in human corneas and to characterize the enzymatic action of matrix metalloproteinases (MMPs) in the cleavage of collagen type XVIII and generation of endostatin in the cornea. METHODS: Anti-endostatin and anti-hinge antibodies were generated using peptide fragments corresponding to the endostatin region and the adjacent nonendostatin hinge region of collagen XVIII noncollagenous (NC)1 domain, respectively. Confocal immunostaining was performed to localize collagen XVIII in human corneas. SV40-immortalized corneal epithelial cells were immunoprecipitated and incubated with active MMP-1, -2, -3, -7, or -9, and Western blot analysis was performed to study collagen XVIII cleavage. Incubation with MMP-7 was performed at various concentrations (0, 2, 4, and 6 microg/ml) and time intervals (0, 1, 5, and 12 hours). Purified recombinant NC1 fragment of collagen XVIII was also digested with MMP-7, and the cleavage product was sequenced. RESULTS: Collagen XVIII was immunolocalized to the human corneal epithelium, epithelial basement membrane, and Descemet membrane. Western blot analysis demonstrated a 180- to 200-kDa band corresponding to collagen XVIII. MMP-7 (but not MMP-1, -2, -3, and -9) cleaved corneal epithelium-derived collagen XVIII to generate a 28-kDa endostatin-spanning fragment in a time- and concentration-dependent fashion. MMP-7 cleaved purified recombinant 34-kDa NC1 fragment of collagen XVIII in the hinge region to generate a 28-kDa fragment. CONCLUSIONS: Collagen XVIII is present in human cornea. MMP-7 cleaves the collagen XVIII NC1 domain to generate a 28-kDa fragment in the cornea.

Amino Acid Sequence↗
PubMed2001

Risk factors of wheeze and allergy after lower respiratory tract infections during early childhood.

Lower respiratory tract infections (LRIs) during early childhood can lead to bronchial hyperreactivity or recurrent obstructive bronchitis. The role of LRIs in the pathogenesis of allergic diseases such as allergic rhinoconjunctivitis, atopic eczema, and bronchial asthma is less clear. The aim of this retrospective study was to determine the incidence of subsequent wheezing and atopy, and the known risk factors for allergic sensitization in 74 children hospitalized for acute LRIs of various etiologies from January 1994 through December 1994. Results showed that there are no differences in outcomes between patients with respiratory syncytial virus LRI, Chlamydia pneumoniae LRI, and LRIs caused by other agents. Although lower respiratory tract illnesses, especially those caused by respiratory syncytial virus during infancy, were associated with an increased risk of subsequent wheezing during early childhood, wheezing tended to disappear with increasing age in many children. This study also found recurrent episodes of wheezing during the first 5 years of life, and symptoms suggestive of allergic rhinoconjunctivitis were the only factors predictive of subsequent diagnosis of asthma for children who had LRIs during early childhood. In conclusion, this study suggests that prevention of recurrent wheezing LRIs and good control of allergic rhinoconjunctivitis is critical for preventing subsequent development of bronchial asthma.

Asthma↗
PubMed2001

Use factor analysis to identify difficulties in implementing a case payment reimbursement system in Taiwan.

BACKGROUND: Taiwan's National Health Insurance Program (NHIP) began on March 1, 1995. The major purpose of National Health Insurance is to remove financial barriers to care and enhance accessibility to comprehensive health care for all citizens in Taiwan. However, due to the rapid rise in medical expenses and unanticipated accumulation of overdue premiums, the program went into debt in 1999. In response to this financial crisis, the Bureau of National Health Insurance proposed to change hospital financing from a cost-based to a case-based reimbursement system. The major purpose of this study is to identify the difficulties in implementing a case payment reimbursement system in Taiwan. METHODS: This study was conducted in four stages: structured interviewing, questionnaire development and testing, surveying, and data analysis. In this study, the sampling surgeons were selected based on availability from 7 teaching hospitals and 10 regional hospitals. RESULTS: The results of factor analysis indicated that a five-factor structure has emerged in the use of the newly developed survey administered to 372 surgeons in Taiwan. These five factors accounted for approximately 97% of the overall variance. The alpha coefficient for this 22-item scale was 0.914. The researchers concluded that these five factors are considered evidence of adequate internal consistency for use in measuring difficulty in the implementation of case payment. CONCLUSIONS: These five factors were named as follows: perceived barriers to compliance, perceived barriers to quality assurance, perceived financial pressure, perceived threats to physicians' autonomy, and inadequate allowance for patient severity. Policy recommendations including annual revision of coding system, physician education, and hospital specialization were also made to address the perceived difficulties identified in this study.

Adult↗
PubMed2000

Activation of group II metabotropic glutamate receptors induces long-term depression of synaptic transmission in the rat amygdala.

An animal model most sensitive for measuring anticipatory anxiety is fear conditioning, which is expressed by an enduring increase in synaptic strength in the amygdala. A converse view predicts that agents that induce long-term depression (LTD) of synaptic efficacy in the amygdala may be useful in the amelioration of stress disorders. In the present study, we show that activation of group II metabotropic glutamate receptor (mGluR II) by (2S,3S, 4S)-2-(carboxycyclopropyl) glycine (l-ccg) induces an LTD in the basolateral amygdala neurons. The effect was concentration-dependent with a maximal inhibition of approximately 30%. The induction of l-CCG LTD required concurrent synaptic activity, required presynaptic but not postsynaptic Ca(2+) increases, and was independent of NMDA receptors. l-CCG LTD was associated with an increase in the ratio of paired-pulse facilitation and was not occluded by low-frequency stimulation-induced LTD, suggesting that these two forms of LTD did not share a common underlying mechanism. After eliciting LTD with l-CCG, application of isoproterenol increased the synaptic responses back to its original baseline, demonstrating that chemically depressed synapses could be potentiated by another chemical. A selective PKA inhibitor, KT 5720, by its own caused a depression of synaptic transmission and blocked l-CCG LTD, presumably by mimicking and thereby occluding any further depression. Together, these results suggest that l-CCG LTD is induced by presynaptically mGluR II-mediated inhibition of Ca(2+)-sensitive adenylyl cyclase, resulting in a decrease in cAMP formation and PKA activation, which leads to a long-lasting decrease in transmitter release.

Adenylyl Cyclase Inhibitors↗
PubMed2000

Prolonged exposure to hyperbaric oxygen induces neuronal damage in primary rat cortical cultures.

While seizure attack is one of the serious complications during the hyperbaric oxygen (HBO) therapy, there is still no direct evidence showing that HBO can induce neuronal damage in the brain. The objective of this study was first to investigate whether HBO would lead to neurotoxicity in the primary rat cortical culture. Second, since alterations in neurotransmitters have been suggested in the pathophysiology of central nervous system (CNS) oxygen toxicity, the protective effects of the N-methyl-D-aspartate (NMDA) receptor antagonism and nitric oxide (NO) synthase inhibition on the HBO-induced neuronal damage were examined. The results showed that HBO exposure to 6 atmosphere absolute pressure (ATA) for 30, 60, and 90 min increased the lactate dehydrogenase (LDH) activity in the culture medium in a time-dependent manner. Accordingly, the cell survival, measured by the 3,(4,5-dimethyl-2-thiazolyl)2, 5-diphenyl-tetrazolium bromide (MTT) assay, was decreased after HBO exposure. Pretreatment with the NMDA antagonist MK-801 protected the cells against the HBO-induced damage. The protective effect was also noted in the cells pretreated with L-N(G)-nitro-arginine methyl ester, an NO synthase inhibitor. Thus, our results suggest that activation of NMDA receptors and production of NO play a role in the neurotoxicity produced by hyperbaric oxygen exposure.

Animals↗
PubMed2000

Reciprocal regulation of nitric oxide and glutamate in the nucleus tractus solitarii of rats.

Nitric oxide (NO) and glutamate are both important mediators of the central cardiovascular regulation in the nucleus tractus solitarii. Our previous studies revealed that the central cardiovascular effects of NO in the nucleus tractus solitarii could be inhibited by glutamate receptor blockade. On the other hand, nitric oxide synthase (NOS) inhibitor attenuated the cardiovascular effects of glutamate. Thus, NO and glutamatergic systems appear to interact in central cardiovascular regulation. The present study examined whether NO and glutamate may affect each other's release/production in the nucleus tractus solitarii. A microdialysis probe was implanted into the nucleus tractus solitarii of male Sprague-Dawley rats, and the changes in the extracellular levels of glutamate and NO were determined by high performance liquid chromatography coupled with electrochemical detection and an NO analyzer, respectively. The results showed that NO solution elicited >10 fold increases in the extracellular level of glutamate, which returned to normal 60 min after the end of NO perfusion. The NO donor N-acetyl-penicillamine (SNAP) had an effect similar to NO solution. Furthermore, the glutamate level was reduced to 61% of basal value by perfusion with the NOS inhibitor, N(G)-monomethyl-L-arginine (L-NMMA). When glutamate receptor agonist N-methyl-D-aspartic acid (NMDA) or alpha-amino-3-hydroxy-5-methylixoxazole-4-propionic acid (AMPA) was administered into the nucleus tractus solitarii, the extracellular NO level was increased by 70-100%, whereas glutamate receptor antagonists (MK-801 hydrogen maleate and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)) did not alter the basal levels of NO. These results suggest that NO and glutamate may enhance each other's release/production in the nucleus tractus solitarii. This reciprocal regulation of NO and glutamate may be important in central cardiovascular control in the nucleus tractus solitarii.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2000

Identification of intestinofugal neurons projecting to the coeliac and superior mesenteric ganglia in the rat.

Intestinofugal neurons are parts of the afferent limbs of inhibitory intestino-intestinal reflexes. These neurons have been mapped in guinea-pigs, where they have a gradient of increasing frequency of occurrence from oral to anal, but not in other species. In the present work in the rat, a species that is more amenable to physiological study than the guinea-pig, we have used retrograde tracing to map the distribution of the cell bodies of intestinofugal neurons projecting to the coeliac-superior mesenteric ganglion complex. Labelled nerve cells were found in the myenteric, but not the submucosal plexus. They were mono-axonal neurons, most with Dogiel type I morphology, and were immunoreactive for choline acetyltransferase, implying that they are cholinergic, which is consistent with functional studies. The cells increased in number per unit area from the stomach, through the small intestine, to the caecum. The results are consistent with physiological studies that reveal distal to proximal inhibitory reflexes that are more potent from distal compared to proximal sites.

Afferent Pathways↗
PubMed2000

Nomifensine attenuates d-amphetamine-induced dopamine terminal neurotoxicity in the striatum of rats.

Long-term or high dose administration of d-amphetamine (AMPH) in the rat has been shown to result in dopamine terminal neurotoxicity in the striatum of rats. This phenomenon includes depletion of dopamine content, decreased activity of tyrosine hydroxylase and diminish in the number of dopamine reuptake transporter. Recent studies implicate a role of oxidative stress induced by dopamine in the AMPH-induced neurotoxicity. However, the primary source of dopamine responsible for radical formation during AMPH challenge has remained elusive. To elucidate this issue, the study was designed to examine the effects of nomifensine, a dopamine transporter blocker, and deprenyl, a monoamine oxidase B (MAO-B) inhibitor, on the prevention of striatal dopamine neurotoxicity in AMPH-treated rats. The results showed that nomifensine but not deprenyl protected against AMPH-induced long-term dopamine depletion. Correspondingly, the hydroxyl radical formation caused by AMPH in the striatum was attenuated by nomifensine, whereas its formation was not abolished by deprenyl. In conclusion, this study suggests that intracellular oxidative stress is more likely involved in the AMPH-induced dopamine terminal toxicity in the rat striatum, while this phenomenon is not mediated by MAO-B pathway.

Animals↗
PubMed2000

Systemic administration of d-amphetamine induces long-lasting oxidative stress in the rat striatum.

The long-term effect of d-amphetamine (AMPH) on the induction of oxidative stress was examined in vivo in the rat brain. In this study, 2,3-dihydroxybenzoic acid (2,3-DHBA) and malonaldehyde (MDA) were used as the index of the hydroxyl radical and lipid peroxidation, respectively. The levels of 2,3-DHBA, MDA and dopamine (DA) in striatal homogenates were examined 7 days following injection of a single large dose of AMPH (7.5 mg/kg, i.p.) in rats pretreated with desipramine (10 mg/kg, i.p.), an agent that inhibits the metabolism of AMPH. Our results showed that 2,3-DHBA and MDA levels were significantly increased by AMPH, whereas DA and its metabolites, DOPAC and HVA were depleted in the striatum. Pretreatment with the glutamate NMDA receptor subtype antagonist MK-801 (1 mg/kg, i.p.) attenuated the increases of 2,3-DHBA and MDA, and provided partial protection against the long-lasting loss of DA produced by AMPH. Overall, the results demonstrate that AMPH could induce sustained production of free radical and oxidative damage, and lead to DA terminal degeneration in the striatum of the rat.

Animals↗
PubMed2000

Intra-striatal infusion of D-amphetamine induces hydroxyl radical formation: inhibition by MK-801 pretreatment.

Recent evidence suggests that free radicals can be produced in the brain following systemic administration of repeated or high doses of D-amphetamine (AMPH). However, it has been proposed that the toxic effects of AMPH are mostly secondary to AMPH-induced hyperthermia, and agents that protect against AMPH neurotoxicity do so by blocking AMPH-induced hyperthermia or causing hypothermia. In this study, we examined the effects of AMPH on the formation of hydroxyl radicals (*OH) following its infusion into the rat striatum via a microdialysis probe. We found that intra-striatal perfusion of AMPH (10 microM) caused an increased formation of hydroxyl radicals but did not raise the core temperatures of the rats. Pretreatment with the NMDA antagonist MK-801 (0.5 mg/kg) attenuated hydroxyl radical production elicited by AMPH infusion, although core body temperatures in AMPH-treated rats were not significantly altered. Additionally, infusion of AMPH in the striatum increased extracellular dopamine concentration and this effect was potentiated by MK-801 pretreatment. Thus, these results demonstrate that direct infusion of AMPH in the striatum induces hydroxyl radical production without causing hyperthermia, and also imply that activation of glutamate NMDA receptors mediates, at least in part, AMPH-induced hydroxyl radical formation in the rat striatum.

Animals↗
PubMed2000

Diterpenoids from Salvia miltiorrhiza.

The abietane diterpenoid, neocryptotanshinone II, and the known 6,12-dihydroxyabieta-5,8,11,13-tetraen-7-one were isolated as minor components from the roots of Salvia miltiorrhiza. Their structures were established on the basis of spectral evidence.

Abietanes↗