[Research progress of oral allergy syndrome].

Oral allergy syndrome (OAS) is an IgE-mediated hypersensitivity. Patients with pollen allergy will experience oropharyngeal allergy after eating fresh fruits or vegetables containing homologous pathogenesis-related allergen, occasionally accompanied by systemic symptoms, it is a special type of food hypersensitivity in which respiratory allergens and food allergens are similar structurally and lead to the cross-reactivity. At present, there is little research and attention to it in China. To master the definition, epidemiological characteristics, pathological mechanism, diagnosis, prevention and treatment of OAS is very important to the prevention and control of OAS. This article reviews the research progress of OAS, providing reference and prevention basis for clinicians to improve the diagnosis and differential diagnosis of OAS.

High MEK/ERK signalling is a key regulator of diapause maintenance in the cotton bollworm, Helicoverpa armigera.

MEK/ERK signalling has been identified as a key factor that terminates diapause in Sarcophaga crassipalpis and Bombyx mori. Paradoxically, high p-MEK/p-ERK signalling induces diapause in pupae of the moth Helicoverpa armigera; however, the regulatory mechanism is unknown. In the present study, we show that p-MEK and p-ERK are elevated in the brain of diapause-destined pupae and suppression of MEK/ERK activity terminates diapause progress. Reactive oxygen species (ROS) activate MEK/ERK signalling, causing large-scale phosphorylation of downstream proteins. The levels of ubiquitin-conjugated proteins are also significantly reduced when ROS or p-ERK level decreased. Moreover, terminated diapause progress by 20-hydroxyecdysone injection significantly decreases p-MEK, p-ERK and phospho-ribosomal S6 kinase levels, while phospho-MAPK substrates and ubiquitin-conjugated protein levels increase. Our data demonstrate that high MEK/ERK signalling mediated by ROS promotes diapause maintenance via increasing phosphorylation and degradation of downstream substrates. The results of this study may provide important information for understanding the regulatory mechanisms during insect diapause.

[Detection of EDA gene mutation and phenotypic analysis in patients with hypohidrotic ectodermal dysplasia].

OBJECTIVE: To detect the ectodysplasin A (EDA) gene mutation in patients with hypohidro-tic ectodermal dysplasia (HED), and to analyze the distribution pattern of missing permanent teeth and the systemic manifestation of HED patients with EDA gene mutation. METHODS: Twelve HED families were enrolled from clinic for genetic history collection, systemic physical examination and oral examination. Peripheral blood or saliva samples were collected from the probands and the family members to extract genomic DNA. PCR amplification and Sanger sequencing were utilized to detect the EDA gene variations, which were compared with the normal sequence (NM_001399.5). The functional impact of EDA gene variants was then evaluated by functional prediction of mutation, conservation analysis and protein structure prediction. The pathogenicity of each EDA gene variation was assessed according to the stan-dards and guidelines of the American College of Medical Genetics and Genomics (ACMG). The systemic phenotype and missing permanent tooth sites of HED patients with EDA gene mutations were summarized, and the missing rate of each tooth position was analyzed and compared. RESULTS: Eight out of twelve HED families were identified to carry EDA gene mutations, including: c.164T>C(p.Leu55Pro); c.457C>T (p.Arg153Cys); c.466C>T(p.Arg156Cys); c. 584G>A(p.Gly195Glu); c.619delG(p.Gly207Profs*73); c.673C>T(p.Pro225Ser); c.676C>T(p.Gln226*) and c.905T>G(p.Phe302Cys). Among them, c.164T>C(p.Leu55Pro); c.619delG(p.Gly207Profs*73); c.673C>T(p.Pro225Ser); c.676C>T(p.Gln226*) and c.905T>G(p.Phe302Cys) were novel mutations. The HED patients with EDA gene mutations in this study were all male. Our results showed that the average number of missing permanent teeth was 13.86±4.49, the average number of missing permanent teeth in the upper jaw was 13.14±5.76, the missing rate was 73.02%. And in the lower jaw, the average number of missing permanent teeth was 14.57±3.05, the missing rate was 80.95%. There was no significant difference in the number of missing teeth between the left and right sides of the permanent dentition (P>0.05). Specifi-cally, the maxillary lateral incisors, the maxillary second premolars and the mandibular lateral incisors were more likely to be missing, while the maxillary central incisors, the maxillary and mandibular first molars had higher possibility of persistence. CONCLUSION: This study detected novel EDA gene pathogenic variants and summarized the distribution pattern of missing permanent teeth of HED patients, thus enriched the variation and phenotype spectrum of EDA gene, and provided new clinical evidence for genetic diagnosis and prenatal consultation.

MiR-203 regulates DJ-1 expression and affects proliferation, apoptosis and DDP resistance of pancreatic cancer cells.

OBJECTIVE: DJ-1 is a negative regulator of PTEN and plays a role in tumorigenesis. Abnormal miR-203 expression is associated with pancreatic cancer. Bioinformatics analysis showed a targeted relationship between miR-203 and DJ-1 3'-UTR. This study investigated whether miR-203 regulates DJ-1 expression and its role in pancreatic cancer cell proliferation, apoptosis, and cisplatin (DDP) resistance. MATERIALS AND METHODS: The Dual-Luciferase reporter gene assay validated the targeted regulation between miR-203 and DJ-1. The DDP-resistant cell line SW1990/DDP was established and divided into miR-NC group and miR-203 mimic group followed by analysis of the expression of DJ-1, PTEN and p-AKT, cell apoptosis, and proliferation. RESULTS: There was a targeted relationship between miR-203 and DJ-1 mRNA. The expression of miR-203 in SW1990/DDP cells was significantly lower than that in SW1990 cells, while the expression of DJ-1 mRNA and protein was significantly higher than that in SW1990 cells. Compared with miR-NC group, the expression of DJ-1 and p-AKT protein in SW1990/DDP cells was significantly decreased in miR-203 mimic transfection group, while the expression of PTEN was significantly increased with increased cell apoptosis and decreased cell proliferation, as well as reduced DDP resistance. CONCLUSIONS: The decreased expression of miR-203 and the increased expression of DJ-1 is associated with drug resistance in pancreatic cancer cells. Elevated miR-203 can inhibit the expression of DJ-1, affect the activity of PTEN-PI3K/AKT pathway, inhibit the proliferation of pancreatic cancer cells, induce cell apoptosis, and reduce DDP resistance of pancreatic cancer cells.

[Adenosine facilitates carotid baroreflex in rats].

The effects of adenosine (Ado) on the carotid baroreflex were studied in 27 anesthetized rats with isolated carotid sinus perfusion. The results obtained were as follows: (1) By perfusing the isolated carotid sinus with adenosine (125 mumol/L), the functional curve of baroreflex was shifted to the left and downward, with the peak slope (PS) increased from 0.37 +/- 0.02 to 0.55 +/- 0.02 kPa/kPa (P < 0.001) and the reflex decrease in mean arterial pressure (RD) enhanced from 5.53 +/- 0.12 to 7.76 +/- 0.36 kPa (P < 0.001). Meanwhile, the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were significantly decreased from 8.60 +/- 0.27 to 5.63 +/- 0.11 kPa (P < 0.001), 12.53 +/- 0.30 to 10.89 +/- 0.29 kPa (P < 0.01) and 23.69 +/- 0.15 to 20.18 +/- 0.55 kPa (P < 0.001), respectively. Among the functional parameters of carotid baroreflex, the changes of RD, PS and TP induced by Ado were dose-dependent. (2) By pretreatment with (8-cyclopentyl-1, 3-dipropylxanthine, 0.134 mmol/L), a selective adenosine A1-receptor antagonist, the above effects of Ado on carotid baroreflex were abolished. (3) The Ado-induced changes of baroreflex were also eliminated as the carotid sinus was pretreated with KATP channel blocker glibenclamide (10 mumol/L). The results strongly suggest that the carotid baroreflex could be facilitated by Ado. It is proposed that the facilitatory action of Ado on carotid baroreflex may be resulted from the opening of KATP channels mediated by Ado A1-receptors.

[Adenosine facilitates carotid baroreceptor activity in rats].

The effects of adenosine (Ado) on the carotid baroreceptor were studied in 36 anesthetized rats with isolated carotid sinus perfusion by recording the sinus nerve afferent activity. The results obtained were as follows: (1) By perfusing the isolated carotid sinus with 75 mumol/L Ado, the functional curve for intrasinus pressure(ISP)-integral of sinus nerve activity (ISNA) relation was shifted to the left and upward with peak slope (PS) increased from (18.75 +/- 0.12)%/kPa to (22.21 +/- 0.11)%/kPa (P < 0.001) and the peak integral value (PIV) enhanced from (209.83 +/- 2.57)% to (239.17 +/- 1.75)% (P < 0.001), while the threshold pressure (TP) and saturation pressure (SP) were significantly decreased from 8.57 +/- 0.24 to 7.15 +/- 0.23 kPa (P < 0.001) and from 22.99 +/- 0.34 to 21.21 +/- 0.43 kPa (P < 0.01). By perfusing with high concentrations of Ado (125 and 175 mumol/L), the curves for ISP-ISNA relation were shifted to the left and upward further and the changes of the functional parameters such as PS, TP and SP were dose-dependent. (2) By pretreatment with 8-cyclopentyl-1,3-dipropylxanthine (0.134 mmol/L), a selective adenosine A1-receptor antagonist, the above mentioned effects of Ado on carotid baroreceptor activity were abolished. (3) The Ado-induced increase in sinus nerve afferent activity could be eliminated by pretreatment with KATP channel blocker glibenclamide (10 mumol/L). The above results suggest that Ado exerts a facilitatory action on the isolated carotid baroreceptor and such an action of Ado may be attributed to the opening of KATP channels, which is mediated by A1-receptors.

[17beta -estradiol inhibits carotid sinus baroreflex in male rats].

By perfusing isolated carotid sinus, the effect of 17beta-estradiol (E(2)) on carotid sinus baroreflex was observed in anesthetized male rats. The results obtained are as follows. (1) By perfusing with E(2) (10 micromol/L), the functional curve of baroreflex was shifted to the right and upward, with a peak slope (PS) decrease from 0.49+/-0.03 to 0.25+/-0.01 (P<0.01) and a reflex decrease in mean arterial pressure (reflex decrease, RD) from 7.37+/-0.42 kPa to 3.49+/-0.20 kPa (P<0.001), while the threshold pressure (TP) and saturation pressure (SP) were significantly increased from 9.52+/-0.68 kPa to 13.3+/-0.11 kPa (P<0.001) and 24.53+/-0.48 kPa to 27.52+/-0.20 kPa (P<0.01) respectively. Among the functional parameters of carotid baroreflex, the changes of RD, PS, TP and SP were dose-dependent. (2) Pretreatment with different doses of tamoxifen (1, 5, 10, 30 micromol/L), an inhibitor of estrogen receptor, did not block the effect of E(2) on carotid baroreflex. (3) Preperfusion with an inhibitor of NO synthase L-NAME (100 micromol/L) could completely abolish the effect of E(2) on carotid baroreflex. It is concluded that the inhibitory effect of E(2)on carotid sinus baroreflex may be mediated by NO release from endothelial cells, but not by a genomic mechanism.

[Modulatory effects of endothelin on carotid baroreflex in anesthetized rats].

Modulatory effects of endothelin (ET) on carotid baroreflex were examined in 27 anesthetized rats with isolated carotid sinus perfusion. The results obtained were as follows: (1) By perfusing with 1 nmol/L ET-1, the functional curve of carotid baroreflex (FCCB) was shifted to the left and downward with an increase in its peak slope (PS) from 0.40 +/- 0.02 to 0.51 +/- 0.02 kPa/kPa (P < 0.01), while the reflex decrease of mean arterial pressure (RD) was increased from 5.66 +/- 0.23 to 6.76 +/- 0.22 kPa (P < 0.01). The above results indicated that this dose of ET-1 facilitated the carotid baroreflex. (2) On the contrary, by perfusing with 10 nmol/L of ET-1, FCCB was shifted to the right and upward with a decrease of PS to 0.28 +/- 0.01 kPa/kPa (P < 0.01), while RD was decreased to 4.16 +/- 0.19 kPa (P < 0.01). In response to perfusion with 100 nmol/L ET-1, FCCB was further shifted to the right and upward with a marked decrease of PS to 0.19 +/- 0.03 kPa/kPa (P < 0.001), and RD was conspicuously decreased to 3.33 +/- 0.38 kPa (P < 0.001). These results showed that ET-1 at the doses of 10 or 100 nmol/L exerted an inhibitory action on baroreflex. (3) Selective ETA receptor blocker BQ123 (0.15 mumol/L) might abolish the effects of ET-1 (10 nmol/L) on baroreflex. (4) Preperfusing with KATP channel antagonist glibenclamide (10 mumol/L) could also eliminated the effects of ET-1. Taken together, it is suggested that ET-1 exerts a dual effects on baroreflex, being facilitatory at lower dose and inhibitory at higher dose. The latter effect is mediated by ETA receptor, in which KATP channels may be involved.

[Effects of endothelin on carotid baroreceptor activity in anesthetized rats].

The effects of endothelin (ET-1) on carotid baroreceptor activity were examined in 33 anesthetized rats with perfused isolated carotid sinus by recording sinus nerve afferent discharge. The results obtained were as follows: (1) By perfusing with 1 nmol/L ET-1, the functional curve of carotid baroreceptor (FCCB) was shifted to the left and upward with increase of peak slope (PS), while the peak integral value of carotid sinus nerve discharge (PIV) was increased, indicating that the carotid baroreceptor activity was facilitated. (2) On the contrary, by perfusing with 10 nmol/L ET-1, FCCB was shifted to the right and downward with a decrease of PS and PIV. In response to perfusion with 100 nmol/L ET-1, FCCB was further shifted to the right and downward with a marked decrease of PS and PIV. These results showed that ET-1 at 10 or 100 nmol/L exerted an inhibitory action on the baroreceptor activity. (3) Selective ETA receptor blocker-BQ-123 (0.15 mumol/L) could abolish the inhibitory effects of ET-1 (10 nmol/L) on baroreceptor. (4) Preperfusing with KATP channel antagonist-glibenclamide (10 mumol/L) could also eliminated the effects of ET-1. All the above results suggested that ET-1 exerts the dual effects on baroreceptor, facilitation at low doses and inhibition at high doses. The later effect may be mediated by ETA through KATP channels.

Differential responses of regional vascular beds to local injection of agmatine in rats.

In 66 anaesthetized rats, the effects of local injection of agmatine on femoral, renal, and mesenteric vascular beds were investigated respectively by constant flow perfusion method. The results are as follows. (1) Agmatine (0.1, 0.5, 1 mg/kg) increased the perfusion pressure (PP) of femoral vascular bed in a dose dependent manner. The effect of agmatine (1 mg/kg) was completely blocked by pretreatment with idazoxan (0.5 mg/kg), an antagonist for imidazoline receptors (IR) and alpha(2)-adrenergic receptors (alpha(2)-AR), and yohimbine (1 mg/kg), a selective alpha(2)-AR antagonist. (2) Agmatine also increased the PP of renal vascular bed in a dose-dependent manner, and agmatine at high dose (1 mg/kg) caused a biphasic increase of PP in renal vascular bed. Idazoxan blocked these effects completely, while yohimbine led the agmatine induced effect to a decrease in the PP of renal vascular bed. (3) Agmatine decreased the PP of mesenteric vascular bed in a dose-dependent manner, an effect which was completely blocked by idazoxan, but unaffected by yohimbine. From the results obtained, it is concluded that agmatine differentially affects the vascular tone in the femoral, renal, and mesenteric vascular beds.

[Agmatine inhibits the afferent activity of carotid baroreceptor in rats].

The effect of agmatine (Agm) on the carotid baroreceptor activity was examined in 24 anesthetized rats with perfused isolated carotid sinus by recording sinus nerve afferent discharges. The results are as follows. (1) By perfusing with 1 mmol/L Agm, the functional curve for the intrasinus pressure (ISP)-integral of sinus nerve activity (ISNA) relation was shifted to the right and downward with decreases in peak slope (PS) and peak integral value of carotid sinus afferent discharge (PIV). By perfusing with high concentrations of Agm (5 and 10 mmol/L), the curves were shifted to the right and downward further with marked decreases of PS and PIV. These results showed that Agm exerted an inhibitory action on the baroreceptor activity in a dose-dependent manner. (2) The Agm-induced decrease in sinus nerve afferent activity was eliminated by pretreatment with IR and alpha 2-AR blocker idazoxan (0.1 mmol/L). (3) Selective alpha 2-AR blocker yohimbine (15 mumol/L) partly abolished the inhibitory effect of Agm on baroreceptor. (4) Preperfusing with Bay K 8644 (500 nmol/L), an agonist of calcium channels, also eliminated the effect of Agm on carotid baroreceptor activity. These results indicate that Agm exerts an inhibitory action on carotid baroreceptor and such an action may be attributed to the reduction in calcium influx in carotid baroreceptor, which is mediated by IR and alpha 2-AR.

[Effects of intraventricular and epicardial application of adenosine on electrical activity of medullary PGL neurons].

The effects of intraventricular injection and epicardial application of adenosine on spontaneous electrical activity of nucleus paragigantocellularis lateralis (PGL) neurons in rostral ventrolateral medulla (RVLM) were examined in 35 anesthetized rats with sinoaortic denervation and vagotomy. The results obtained were as follows: (1) The spontaneous discharge of 121 PGL neurons (mean discharge rate: 22.5 +/- 1.9 spikes/s) were recorded in 35 rats. (2) In response to intraventricular injection of adenosine (0.5 mumol/kg), mean arterial pressure (MAP) was initially increased by 1.7 +/- 0.2 kPa(P < 0.001) and subsequently decreased by 4.6 +/- 0.5 kPa(P < 0.001), while the heart rate (HR) was decreased by 126.5 +/- 12.3 bpm (P < 0.001). Of 35 PGL spontaneous discharge units responsive to intraventricular injection of adenosine, 30 showed an average increase from 21.9 +/- 2.6 to 29.2 +/- 3.4 spikes/s (P < 0.001), 3 with no change, while 2 with a decrease. (3) Following epicardial application of 20 mmol/L adenosine, the BP and HR were not significantly changed, while the spontaneous discharge of 22 PGL neurons were increased from 18.8 +/- 1.9 to 26.9 +/- 2.8 spikes/s (P < 0.001), and that of 3 neurons was not changed. (4) The excitatory response of PGL neurons to intraventricular injection or epicardial application of adenosine was completely inhibited by pretreatment with selective adenosine A1-receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX, 500 micrograms/kg). (5) Following epicardial application of phenol or bilateral stellate ganglionectomy, adenosine failed to affect the activity of PGL neurons. The results obtained indicate that adenosine may stimulate cardiac sympathetic afferents through adenosine A1-receptor, thereby resulting in the activation of PGL neurons.

Sequential therapy for non-thalamus supratentorial hypertensive intracerebral hemorrhages.

OBJECTIVE: We sought to assess the effectiveness of sequential therapy for non-thalamus supratentorial hypertensive intracerebral hemorrhage (NTS-HICH). PATIENTS AND METHODS: We retrospectively analyzed clinical data of 110 patients with HICH. The patients were admitted 72 hours after disease onset, and 43 patients received sequential therapy. The length of hospital stay, treatment costs, incidence of pulmonary infections, mortality rates and Modified Rankin Score (mRS) 1 and 3 months after NTS-HICH were compared between patients who received sequential or non-sequential therapies. RESULTS: The length of hospital stay, treatment costs, and 1-month mortality rates were not significantly different between both groups. However, mortality rates at 3 months, incidence of pulmonary infection, and mRS at both 1 and 3 months were significantly better in patients who received sequential therapy. CONCLUSIONS: Sequential therapy significantly improves the prognosis for patients with NTS-HICH.

Signal transduction pathways and transcriptional mechanisms of ABCB1/Pgp-mediated multiple drug resistance in human cancer cells.

Multiple drug resistance (MDR), defined as the ability of tumour cells to survive exposure to many chemotherapeutic agents, is a major cause of treatment failure in human cancers. The membrane transporter P-glycoprotein (Pgp, encoded by the ABCB1 [adenosine triphosphate-binding cassette, subfamily B, member 1] gene) is the main mechanism for decreased intracellular drug accumulation in human MDR cancer. ABCB1/Pgp-mediated MDR involves several signal transduction pathways and transcription factors. Activation of these signal transduction pathways influences the prognosis of MDR human cancer. Signalling pathways involved in ABCB1/Pgp-mediated MDR include the mitogen-activated protein kinase (MAPK), c-Jun NH(2)-terminal kinase (JNK), p38, cyclic adenosine monophosphate-dependent protein kinase, phosphatidylino sitol 3-kinase and protein kinase C signalling pathways. This review summarizes the biological characteristics, target points and signalling cascade mediators of these pathways. Drugs targeted against these pathways may provide new therapies for treatment of ABCB1/Pgp-mediated MDR.

Effects of m-nisoldipine on delayed afterdepolarization of canine Purkinje fibers.

Effects of m-nisoldipine (m-Nis) on delayed after depolarization (DAD) and triggered activity (TA) were studied using standard microelectrode technique. The development of DAD and TA were markedly inhibited by pre-treatment with m-Nis (1-4 mumol.L-1) as well as m-Nis treatment after DAD and TA had been elicited. The amplitude of DAD was reduced from 15.3 +/- 2.7 to 2.3 +/- 2.0 mV, and the duration from 980 +/- 45 to 130 +/- 27 ms. The occurrence of TA was also reduced or prevented by m-Nis. These effects of m-Nis might be attributed to its blocking effects on voltage-dependent calcium channel and the resultant alleviation of intracellular calcium overload.

Effects of m-nisoldipine on transmembrane currents of guinea pig papillary muscles.

Effects of m-Nis on the transmembrane currents were studied using single sucrose gap voltage clamp technique. The amplitude of slow inward current (I(si)) was 10.6 +/- 4.1 microA. Maximal inward current was induced at a membrane potential range between -20 to -25 mV. The amplitude of I(si) were significantly decreased by m-Nis (0.2 mumol.L-1) with a reduction of 47.3%. The transient inward current (I(ti)) induced by ouabain was also greatly depressed or prevented by m-Nis, resulting in the inhibition of DAD.

Electrophysiologic effects of agmatine on pacemaker cells in sinoatrial node of rabbits.

AIM: To study the electrophysiologic effects of agmatine (Agm) on pacemaker cells in sinoatrial (SA) node. METHODS: Parameters of action potential (AP) in SA node were recorded using intracellular microelectrode technique. RESULTS: Agm not only slowed down the amplitude of action potential (APA), maximal rate of depolarization (Vmax), velocity of diastolic (phase 4) depolarization (VDD), and rate of pacemaker firing (RPF), but also prolonged 90% duration of action potential (APD90) in a concentration-dependent manner. The effects of Agm (10 mmol.L-1) could be blocked completely by pretreatment with idazoxan (0.15 mmol.L-1), an alpha 2-adrenergic receptor (alpha 2-AR) and imidazoline receptor (IR) antagonist. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 1 mmol.L-1), an NOS inhibitor, did not affect the electrophysiologic effects of Agm on pacemaker cells in SA node. Elevation of Ca2+ concentration (5 mmol.L-1) in perfusate antagonized the effects of Agm (10 mmol.L-1). Lemakalim (Lem, 30 mumol.L-1), an opener of ATP-sensitive potassium channels, partially inhibited the prolonging effect of Agm on repolarization. CONCLUSION: The electrophysiologic effects of Agm on pacemaker cells in SA node were likely attributed to the reduction in calcium influx and potassium efflux and mediated by alpha 2-AR and IR.

17 beta-Estradiol inhibits carotid sinus baroreceptor activity in anesthetized male rats.

AIM: To study the effect of 17beta-estradiol (E2) on carotid baroreceptor activity (CBA). METHODS: The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus. RESULTS: E2 3, 10, and 30 micromol/L shifted FCCB to the right and downward, with a marked decrease in peak slope (PS) and peak integral value of carotid sinus nerve discharge (PIV) in a concentration-dependent manner, indicating the inhibitory effect of E2 on CBA. Pretreatment with tamoxifen (TAM) 10 micromol/L, an inhibitor of estrogen receptor, did not block the effect of E2 on CBA. Preperfusion with L-NAME 100 micromol/L, an inhibitor of NO synthase, could completely abolish the effect of E2 on CBA. NO donor SIN-1 10 micromol/L could potentiate the inhibitory effect of E2. CONCLUSION: E2 inhibits CBA via endothelial NO release.

[An automatic system controlled by microcontroller for carotid sinus perfusion].

AIM: To establish a new method for controlling automatically the carotid perfusion pressure. METHODS: A cheap practical automatic perfusion unit based on AT89C2051 micro controller was designed. The unit, LDB-M perfusion pump and the carotid sinus of an animal constituted an automatic perfusion system. RESULTS AND CONCLUSIONS: This system was able to provide ramp and stepwise updown perfusion pattern and has been used in the research of baroreflex. It can insure the precision and reproducibility of perfusion pressure curve, and improve the technical level in corresponding medical field.