Root surface modifiers and subepithelial connective tissue graft for treatment of gingival recessions: a systematic review.

BACKGROUND AND OBJECTIVE: Many techniques and flap designs have been used to treat gingival recession by root coverage, but subepithelial connective tissue graft (SCTG) seems to be the gold standard procedure. In an attempt to improve the healing process and increase the success rate of root coverage, some authors have used root modifiers, including different root conditioners, lasers, EMD, recombinant human growth factors and platelet-rich plasma (PRP). The aim of this systematic review was to evaluate the effects of root biomodification in clinical outcomes of gingival recessions treated with SCTG. MATERIAL AND METHODS: Studies reporting SCTG associated with any form of root surface biomodification for root coverage of gingival recessions (Miller Class I and Class II) were considered as eligible for inclusion. Studies needed to have data of clinical outcomes in a follow up of at least 6 months. Screening of the articles, data extraction and quality assessment were conducted independently and in duplicate. RESULTS: None of the products evaluated (citric acid, EDTA, PRP, lasers and EMD) showed evident benefits in clinical outcomes. Test and control groups presented similar outcomes related to root coverage and periodontal parameters, with no statistical differences between them. The exception was root biomodification with the neodymium-doped yttrium aluminium garnet (Nd:YAG) laser, which impaired root coverage and had a detrimental effect on clinical outcomes. CONCLUSION: Based on the present clinical data, the use of root surface modifiers to improve clinical outcomes in gingival recessions treated with SCTG is not justified. More in vivo studies, and randomized clinical trials with larger sample sizes and extended follow up, are necessary.

Pharmacokinetic and pharmacodynamic analysis comparing diverse effects of detomidine, medetomidine, and dexmedetomidine in the horse: a population analysis.

The present study characterizes the pharmacokinetic (PK) and pharmacodynamic (PD) relationships of the α2-adrenergic receptor agonists detomidine (DET), medetomidine (MED) and dexmedetomidine (DEX) in parallel groups of horses from in vivo data after single bolus doses. Head height (HH), heart rate (HR), and blood glucose concentrations were measured over 6 h. Compartmental PK and minimal physiologically based PK (mPBPK) models were applied and incorporated into basic and extended indirect response models (IRM). Population PK/PD analysis was conducted using the Monolix software implementing the stochastic approximation expectation maximization algorithm. Marked reductions in HH and HR were found. The drug concentrations required to obtain inhibition at half-maximal effect (IC50 ) were approximately four times larger for DET than MED and DEX for both HH and HR. These effects were not gender dependent. Medetomidine had a greater influence on the increase in glucose concentration than DEX. The developed models demonstrate the use of mechanistic and mPBPK/PD models for the analysis of clinically obtainable in vivo data.

Pharmacokinetics and pharmacodynamics of intravenous dexmedetomidine in the horse.

The aim of the study was to describe the pharmacokinetics and selected pharmacodynamics of intravenous dexmedetomidine in horses. Eight adult horses received 5 µg/kg dexmedetomidine IV. Blood samples were collected before and for 10 h after drug administration to determine dexmedetomidine plasma concentrations. Pharmacokinetic parameters were calculated using noncompartmental analysis. Data from one outlier were excluded from the statistical summary. Behavioral and physiological responses were recorded before and for 6 h after dexmedetomidine administration. Dexmedetomidine concentrations decreased rapidly (elimination half-life of 8.03 ± 0.84 min). Time of last detection varied from 30 to 60 min. Bradycardia was noted at 4 and 10 min after drug administration (26 ± 8 and 29 ± 8 beats/min respectively). Head height decreased by 70% at 4 and 10 min and gradually returned to baseline. Ability to ambulate was decreased for 60 min following drug administration, and mechanical nociceptive threshold was increased during 30 min. Blood glucose peaked at 30 min (134 ± 24 mg/dL) and borborygmi were decreased for the first hour after dexmedetomidine administration. Dexmedetomidine was quickly eliminated as indicated by the rapid decrease in plasma concentrations. Physiological, behavioral, and analgesic effects observed after dexmedetomidine administration were of short duration.

Single- and multiple dose pharmacokinetics and multiple dose pharmacodynamics of oral ABT-116 (a TRPV1 antagonist) in dogs.

Six dogs were used to determine single and multiple oral dose pharmacokinetics of ABT-116. Blood was collected for subsequent analysis prior to and at 15, 30 min and 1, 2, 4, 6, 12, 18, and 24 h after administration of a single 30 mg/kg dose of ABT-116. Results showed a half-life of 6.9 h, k(el) of 0.1/h, AUC of 56.5 µg·h/mL, T(max) of 3.7 h, and C(max) of 3.8 µg/mL. Based on data from this initial phase, a dose of 10 mg/kg of ABT-116 (no placebo control) was selected and administered to the same six dogs once daily for five consecutive days. Behavioral observations, heart rate, respiratory rate, temperature, thermal and mechanical (proximal and distal limb) nociceptive thresholds, and blood collection were performed prior to and 4, 8, and 16 h after drug administration each day. The majority of plasma concentrations were above the efficacious concentration (0.23 µg/mL previously determined for rodents) for analgesia during the 24-h sampling period. Thermal and distal limb mechanical thresholds were increased at 4 and 8 h, and at 4, 8, and 16 h respectively, postdosing. Body temperature increased on the first day of dosing. Results suggest adequate exposure and antinociceptive effects of 10 mg/kg ABT-116 following oral delivery in dogs.

Pharmacokinetic profile in relation to anaesthesia characteristics after a 5% micellar microemulsion of propofol in the horse.

BACKGROUND: To define the pharmacokinetic profile of propofol 5% microemulsion formulation in horses. METHODS: First, propofol was administered as bolus injection (2 mg kg(-1)) to six xylazine-sedated horses. Secondly, after sedation and bolus injection, propofol was maintained with continuous infusion for 3 h [8.1 (sd 3.2) mg kg(-1) h(-1)] to the same six horses. Thirdly, in two horses, a commercial propofol was used for comparison. Response to noxious stimulation was used to evaluate analgesia. Venous blood samples were obtained to measure propofol plasma concentration using liquid chromatography-mass spectrometry analysis. The plasma concentrations were related to the anaesthesia characteristics to determine the ED(50). RESULTS: The pharmacokinetic profile of propofol is best characterized by a non-compartmental model. The mean (confidence interval) for area under plasma concentration-time curve, elimination half-life, mean residence time, and clearance was 41 min microg ml(-1) (+/-7.7), 44.8 min (+/-21.3), 13.7 min (+/-3.2), and 45.8 ml min(-1) kg(-1) (+/-6.5), respectively. Linear regression analysis showed a correlation between plasma concentration and infusion rate (r(2)=0.47). Most propofol infusion rates did not inhibit the response to noxious stimulation and rates above 11.9 mg kg(-1) h(-1) caused involuntary muscle contractions. Better recoveries were associated with lower propofol plasma concentrations. Propofol plasma concentration frequently increased when horses woke from anaesthesia. CONCLUSIONS: Caution is warranted when propofol is used for continuous infusion due to variable kinetics, myoclonal activity, poor analgesia, and less desirable recovery quality.

Effects of nitrous oxide on minimum alveolar concentration of desflurane in dogs

Effects of nitrous oxide (N2O) on minimum alveolar concentration (MAC) of desflurane were studied. For that purpose, 30 dogs were randomly allocated into two groups: desflurane group (GD) and N2O and desflurane group (GDN). GD animals received propofol to intubation, and 11.5V percent of desflurane diluted in 100 percent O2. After 30 minutes, they received electric stimulus and if the animal did not react to stimulus, desflurane concentration was reduced by 1.5V percent. This protocol was repeated at each 15 minutes, and stimulus was interrupted when voluntary reaction was observed. GDN dogs were submitted to diluent flow 30 percent O2 and 70 percent N2O. Desflurane's MAC; heart (HR) and respiratory (RR) rates; systolic, diastolic and mean arterial pressures (SAP, DAP, and MAP, respectively); end tidal carbon dioxide (ETCO2); oxyhemoglobin saturation (SpO2) and body temperature (T) were evaluated. In both groups increase in HR and ETCO2, and decrease in RR and T were associated with administration of the highest dose of desflurane. Blood pressures decreased 30 minutes after desflurane administration in GDN, and after this measurement the values increased. Reduction in desflurane's MAC was observed as well. It is concluded that N2O associated with desflurane reduced desflurane's MAC by 16 percent with increase in HR and respiratory depression.

Estudaram-se os efeitos do óxido nitroso (N2O) sobre a concentração alveolar mínima (CAM) do desfluorano. Trinta cães foram distribuídos em dois grupos: desfluorano (GD) e N2O e desfluorano (GDN). Os do GD receberam propofol (8,9±1,65mg/kg) para intubação orotraqueal e após, 11,5V por cento de desfluorano em 100 por cento de O2. Após 30 minutos, os animais receberam estímulo elétrico e não havendo reação do animal, reduziu-se a concentração em 1,5V por cento. Repetiu-se o protocolo a cada 15 minutos, cessando-se os estímulos quando observada reação voluntária. Os GDN foram submetidos ao mesmo protocolo, substituindo-se o fluxo diluente por 30 por cento O2 e 70 por cento N2O. Mensuraram-se freqüências cardíaca (FC) e respiratória (FR), pressões arteriais sistólica, diastólica e média (PAS, PAD e PAM), concentração de dióxido de carbono ao final da expiração (ETCO2), saturação de oxihemoglobina (SpO2), temperatura corpórea (TC) e a CAM do desfluorano. Observou-se aumento da FC, ETCO2 e SpO2, e redução da FR e da TC concomitantemente à administração da maior dose de desfluorano, além de redução da CAM do desfluorano. As pressões arteriais diminuíram em M30 aumentando posteriormente. Concluiu-se que o N2O associado ao desfluorano reduz em 16 por cento a CAM do anestésico volátil. Além disso, essa associação promoveu aumento da FC e depressão respiratória.

Evaluation of intraocular pressure in association with cardiovascular parameters in normocapnic dogs anesthetized with sevoflurane and desflurane.

The objective of this study was to determine intraocular pressure (IOP) and cardiac changes in normocapnic dogs maintained under controlled ventilation and anesthetized using sevoflurane or desflurane. Sixteen healthy adult mixed-breed dogs, seven males and nine females, weighing 10-15 kg were used. The dogs were randomly assigned to one of two groups composed of eight animals anesthetized with sevoflurane (SEVO) or desflurane (DESF). In both groups, anesthesia was induced with propofol (10 mg/kg), and neuromuscular blockade was achieved with rocuronium (0.6 mg/kg/h i.v.). No premedication was given. Ventilation was adjusted to maintain end-tidal carbon dioxide partial pressure at 35 mmHg. Anesthesia was maintained with 1.5 minimum alveolar concentration (MAC) of sevoflurane or desflurane. In both groups IOP was measured by applanation tonometry (Tono-Pen) before induction of anesthesia. IOP, mean arterial pressure (MAP), heart rate (HR), cardiac index (CI) and central venous pressure (CVP) were also measured 45 min after the beginning of inhalant anesthesia and then every 20 min for 60 min. A one-way repeated measures anova was used to compare data within the same group and Student's t-test was used to assess differences between groups. P < 0.05 was considered statistically significant. Measurements showed normal IOP values in both groups, even though IOP increased significantly from baseline during the use of desflurane. IOP did not differ between groups. CI in the desflurane group was significantly greater than in the sevoflurane group. Sevoflurane and desflurane have no clinically significant effects on IOP, MAP, HR, CI or VCP in the dog.

Effects of desflurane, sevoflurane and isoflurane on pulmonary shunt in dogs during spontaneous ventilation

The aim of this study was to compare the effects of desflurane, sevoflurane and isoflurane on pulmonary shunt in dogs during spontaneous ventilation. General anesthesia was induced in 30 healthy, adult, mongrel dogs by intravenous administration of propofol. The animals were separated into three groups of 10 dogs each and submitted to general inhalation anesthesia with 1.5 MAC of desflurane (G1), sevoflurane (G2) and isoflurane (G3). Arterial blood was collected by puncture of the right femoral artery, and mixed blood was collected by introducing a Swan-Ganz catheter into the pulmonary artery. These samples were used to determine the parameters employed for calculation of the intrapulmonary shunt. Measurements began at 20min after orotracheal intubation and were repeated every 20min, totaling six measurements. Means were compared by the Student t-test (P£ 0.05). Desflurane led to a higher shunt than sevoflurane and isoflurane at 40 and 60min. At 80min, the mean values obtained for desflurane were higher than those obtained for isoflurane, while at 100min the values observed for dogs anesthetized with desflurane were higher than those obtained with sevoflurane. Desflurane caused respiratory depression by reducing PaO2, and a higher percentage of intrapulmonary shunt than isoflurane and sevoflurane

Alteraçöes eletrocardiográficas em cäes pré-medicados com levomepromazina e submetidos à anestesia por propofol e sevoflurano / Electrocardiographic changes in dogs under propofol-sevoflurane anesthesia after pre-medication with levomepromazine

Avaliaram-se as variáveis eletrocardiográficas em cäes submetidos à anestesia pelo sevoflurano. Foram empregados 16 cäes clinicamente sadios, adultos, machos ou fêmeas, com peso médio de 15±3,5kg. Administrou-se levomepromazina (1,0 mg/kg) seguida pela administraçäo de propofol (5,0 mg/kg), ambos pela via endovenosa. Os animais foram intubados e submetidos à anestesia inalatória com sevoflurano diluído em oxigênio, através de circuito semi-fechado na concentraçäo de 3,5V por cento. As aferiçöes das freqüências cardíaca e respiratória, oximetria, capnometria, pressöes arteriais sistólica, diastólica e média e das variáveis eletrocardiográficas foram realizadas imediatamente antes da administraçäo da levomepromazina, 15 minutos após e imediatamente antes da administraçäo do propofol, após 15 minutos da administraçäo do agente inalatório e consecutivamente a cada 20 minutos. Após administraçäo de levomepromazina, propofol e sevoflurano observou-se decréscimo das pressöes arteriais sistólica e média. A levomepromazina ocasionou prolongamento do intervalo QT. O sevoflurano promoveu prolongamento da onda P e aumento de sua amplitude aos 70 e 130 minutos de anestesia, respectivamente, além de prolongamento do intervalo QT. Concluiu-se que a anestesia por sevoflurano, nas condiçöes deste experimento, promoveu prolongamento do intervalo QT, sem no entanto incorrer em arritmias