[Classification of massive postburn scars on neck and the reconstruction strategy using pre-expanded perforator flaps from the back].

OBJECTIVE: To explore the classification of massive postburn scars on neck and the reconstruction strategy using pre-expanded perforator flaps from the back. METHODS: Thirty-seven patients with massive postburn scars on neck were admitted from January 2010 to December 2014 and treated by our treatment group. The massive postburn scars on neck were categorized into three types according to their size and location. Based on the principles of reconstructive ladder, matching in color and texture between donor site skin and neck skin, large size and thinner thickness of tissue of donor site skin, donor-recipient sites balance, and dominant supplying vessel, we proposed the following treatment strategy for choosing perforator flaps from the back. (1) In view of central cervical scar involving the central area (mainly in this area) and one side of peripheral zone, the free circumflex scapular artery perforator flap was chosen. (2) In view of peripheral cervical scar involving the central area and one side of peripheral zone (mainly in this area), the pedicled superficial cervical artery perforator flap was the first choice. In case the pedicled superficial cervical artery perforator flap was unavailable because of the absence of superficial cervical artery perforator or scarring within its vascular territory, the pedicled occipital artery perforator flap, pedicled dorsal scapular artery perforator flap, and free circumflex scapular artery perforator flap were chosen as alternative options considering specific condition. (3) In view of total cervical scar involving the central area and both sides of peripheral zone, the circumflex scapular artery perforator supercharged pedicled superficial cervical artery perforator flap was chosen. Tissue expansion was performed in the first stage for all the patients. In the second stage, after excision of the cervical scars, the flaps were transferred to cover the wounds. RESULTS: Among the 37 patients, 7 were with central cervical scar, 12 with total cervical scar, and 18 with peripheral cervical scar. Among patients with peripheral cervical scar, the pedicled superficial cervical artery perforator flaps were used in 11 cases, pedicled occipital artery perforator flaps in 2 cases, pedicled dorsal scapular artery perforator flap in 1 case, and free circumflex scapular artery perforator flaps in 4 cases. Tip necrosis occurred in 3 flaps of patients after surgery, which were healed by dressing change. The other flaps of patients grew well after surgery. Patients were followed up for 1 to 6 years, and all patients were able to extend neck beyond 110° with no sense of restricted neck flexion or rotation. No contracture of flap was observed. Thirty-five patients were satisfied with their appearance after surgery. CONCLUSIONS: Pre-expanded perforator flaps from the back are useful flaps for reconstruction of massive postburn scar on neck. Free circumflex scapular artery perforator flap is recommended for reconstruction of central cervical scar. Pedicled superficial cervical artery perforator flap is the first option for reconstruction of peripheral cervical scar, while the pedicled occipital artery perforator flap, pedicled dorsal scapular artery perforator flap and free circumflex scapular artery perforator flap are alternative options. For total cervical scar, the circumflex scapular artery perforator supercharged pedicled superficial cervical artery perforator flap is recommended.

Cloning and sequence analysis of the coding sequence of ß-actin cDNA from the Chinese alligator and suitable internal reference primers from the ß-actin gene.

ß-Actin is an essential component of the cytoskeleton and is stably expressed in various tissues of animals, thus, it is commonly used as an internal reference for gene expression studies. In this study, a 1731-bp fragment of ß-actin cDNA from Alligator sinensis was obtained using the homology cloning technique. Sequence analysis showed that this fragment contained the complete coding sequence of the ß-actin gene (1128 bp), encoding 375 amino acids. The amino acid sequence of ß-actin is highly conserved and its nucleotide sequence is slightly variable. Multiple alignment analyses showed that the nucleotide sequence of the ß-actin gene from A. sinensis is very similar to sequences from birds, with 94-95% identity. Ten pairs of primers with different product sizes and different annealing temperatures were screened by PCR amplification, agarose gel electrophoresis, and DNA sequencing, and could be used as internal reference primers in gene expression studies. This study expands our knowledge of ß-actin gene phylogenetic evolution and provides a basis for quantitative gene expression studies in A. sinensis.

[Influence of endothelin-1 on ventricular fibrillation threshold in acute myocardial ischemic rats].

The influence of endothelin-1 on ventricular fibrillation threshold was studied in acute myocardial ischemic rats. Endothelin-1 (1.5-3.0 micrograms.kg-1 i.v.) given 5 min before ischemia reduced the ventricular fibrillation threshold in a dose- and time-dependent manner. Its effect lasted at least 60 min. A marked increase of spontaneous ventricular tachycardia and myocardial infarct size was seen and the arterial blood pressure was at a higher level (18.5-20.1/14.4-15.8 kPa) after 3.0 micrograms.kg-1. Diltiazem prevented partially from reduction of ventricular fibrillation threshold, eliminated completely the vasopressor response and limited the extension of myocardial necrosis induced by endothelin-1.

[Effects of stimulation and cauterization of hypothalamic paraventricular nucleus on acupuncture analgesia].

The role of hypothalamic paraventricular nucleus (PVH) in acupuncture analgesia was investigated by local brain stimulation and cauterization. The results showed that electrical or L-glutamate sodium stimulation of PVH could enhance the effect of analgesia of Zusanli acupuncture, both in a dose dependent manner. Electrical cauterization of PVH decreased the effect of acupuncture analgesia, while removal of pituitary had no effect on the enhancing effect by L-glutamate sodium injection.

[Effect of intraventricular injection of anti-beta-endorphin serum on shock after burn in rats].

Intraventricular injections of anti-beta-endorphin serum (8 microliters) at 0, 1, 2, 3 h after burn shock (20% body surface area, 100 degrees C, 20 s) in different group rats prolonged the survival time, delayed the decrease of mean arterial pressure (MAP) and heart rate, and postponed the abnormal changes of ECG. The effect was most prominent at 1 h and little at 3 h after burn.

Comparison of selective arginine vasopressin V1 and V2 receptor antagonists on burn shock in the rat.

STUDY OBJECTIVE: Two selective V1 and V2 receptor antagonists of arginine vasopressin, d(CH2)5Tyr(Me)AVP and d(CH2)5[D-Ile2, Ile4, Ala9-NH2]AVP, were given intravenously in burn shocked rats to investigate the respective effects of V1 and V2 receptor blockade on the haemodynamic variables in burn shock. DESIGN: Computer assisted on line real time measurements of mean arterial blood pressure, diastolic blood pressure, left ventricular systolic pressure, dP/dtmax, and heart rate were used to study the effects of the receptor antagonists during burn shock. In addition, the radioactive microsphere method was used to measure the changes of cardiac output and regional blood flows to heart, kidney, and liver in response to the antagonists during burn shock. Third degree burns extending over 30% of body surface area were made by dipping the rat's shaved back into water at 100 degrees C for 20 s. EXPERIMENTAL MATERIAL: Male Sprague-Dawley rats (250-300 g) were used in groups of 6-9 per experiment. MEASUREMENTS AND MAIN RESULTS: Mean and diastolic arterial blood pressures, left ventricular systolic pressure, dP/dtmax and heart rate were measured for 8 h after burns. Cardiac output and regional blood flow were measured at 3 h and 8 h postburn. Results showed that blockade of V1 receptor lowered mean and diastolic arterial blood pressures throughout the 8 h period, and raised left ventricular systolic pressure and dP/dtmax only during the early phase of shock. Cardiac output and blood flows to heart, kidney, and liver were increased by the V1 antagonist at 3 h but not at 8 h postburn. The V2 receptor antagonist increased mean and diastolic arterial blood pressures, left ventricular systolic pressure, and dP/dtmax both during the early and during the late phases of burn shock. It also improved cardiac output and blood flows to the heart, kidney, and liver during the early and late phases of burn shock. However, heart rate was not affected by V1 and V2 receptor antagonists. CONCLUSIONS: The V2 like receptor may be the dominating receptor mediating vasopressin's inhibitory effect on the heart. V1 receptor mediated coronary vasoconstriction contributes to the myocardial depression possibly only at the compensatory phase of shock. In addition V1 receptor mediated vasoconstriction is important in maintaining blood pressure during burn shock.

Effect of peripheral injection of arginine vasopressin and its receptor antagonist on burn shock in the rat.

To investigate the effect of arginine vasopressin (AVP) in the peripheral circulation on burn shock in the rat, AVP and its nonselective V1/V2 receptor antagonist d(CH2)5Tyr (Et)VAVP were administered intravenously in burn shocked rats. Cardiovascular parameters were recorded including left ventricular systolic pressure (LVSP), +/- dP/dt max, total area of the cardiac force loop (Lo), mean arterial blood pressure (MAP), heart rate (HR) and electrocardiogram (ECG). Our results showed that AVP failed to increase MAP in burned rats whereas it elicited a greater fall in LVSP, +/- dP/dt max and Lo and MAP than seen in control burned rats and hastened the onset of the decompensatory phase of burn shock resulting in the early death of burn shocked animals. The receptor antagonist d(CH2)5Tyr(Et)VAVP elevated LVSP, +/- dp/dt max and Lo for the eight hour observation period, and allowed MAP to recover from the initial profound fall following burn injury. Furthermore, it prolonged the survival time of the burned rats. AVP treated rats also displayed earlier abnormal changes such as elevation of S-T segment, inversion of T wave and ventricular fibrillation in ECG. The onset of these changes was much delayed in antagonist treated rats.

Ventromedial hypothalamic somatostatin may affect gastric somatostatin concentration in rats.

Changes in the somatostatin-like immunoreactivity (SLI) concentrations in gastric antral mucosa were detected by RIA following microinjections of synthetic somatostatin (SS) or cysteamine (CSH) into the ventromedial nucleus of the hypothalamus (VMH). SLI concentrations in the antral mucosa were increased by 60.8% (p less than 0.001) and 42.3% (p less than 0.05), respectively, one and four hours after microinjection of somatostatin (0.5 microgram/0.5 microliter) into the VMH, and decreased by 32.6% (p less than 0.05) four hours after microinjection of cysteamine (15 microgram/0.5 microliter) into the VMH. Moreover, microinjection of somatostatin (0.5 microgram/0.5 microliter) into the VMH could only elicit an increase of 16.0% (p less than 0.05) in the SLI concentration in the antral mucosa one hour after bilateral subdiaphragmatic vagotomies, but still produced an increase of 120.0% (p less than 0.05) following celiac ganglionectomies. In conclusion, somatostatin (exogenous and endogenous) in the VMH seems to affect the gastric somatostatin levels via the vagal nerves.

[The role of central oxytocin in electroacupuncture analgesia].

The effects of intraventricular injection (ICV) of oxytocin (OT) and antioxytocin serum (AOTS) on the pain threshold and electroacupuncture (EA) analgesia in rats were investigated in this study. The potassium iontophoresis induced tailflick was used to measure the pain threshold. An increase of 20-38% in the pain threshold was observed within 80 min after OT injection (50 ng), while the OT administration (50 ng) in combination with EA produced a dramatic increase of 139-234% in the pain threshold, which was much higher than that in the saline-EA group (P less than 0.05 or 0.01). The OT effect was dose-related in the range between 25-100 ng. Although ICV of AOTS did not change the pain threshold, the EA analgesia became weakened significantly. After injection of AOTS, EA only produced an increase of 47-61% in the pain threshold, while following ICV injection of normal rabbit serum instead of AOTS the EA could cause a rise of 104-123% in the pain threshold. There was a significantly statistical difference between the above two groups (P less than 0.05-0.01). The data indicate that ICV of OT not only elevates the pain threshold, but also enhances the EA effect, and that AOTS attenuates the EA analgesia. These results suggest that endogenous oxytocin in the central nervous system may play a role in the electroacupuncture analgesia.

Possible involvement of beta-endorphin in the deteriorating effect of arginine vasopressin on burn shock in rats.

The effect of intracerebroventricular injections of arginine vasopressin (AVP) on burn shock in the rat and its possible mechanism were explored in this study. AVP was administered intraventricularly at 30 min intervals (50 ng) in the burned rats. The arterial pressure and electrocardiogram (ECG) were recorded with a multipurpose polygraph before and after burn. Compared with the control, the MAP of the rats in the AVP group was elevated at the initial stage and fell dramatically at the late stage of burn shock with a higher mortality. The ECG of the rats in the AVP group also displayed earlier changes such as elevation of S-T segment, inversion of T wave, and ventricular fibrillation. These findings suggest an unfavorable role of AVP in burn shock. The plasma, hypothalamic, and anterior and posterior pituitary levels of beta-endorphin 3 hr after burn were measured by radioimmunoassay. The increased level of beta-endorphin in the plasma after AVP treatment indicates the possible involvement of beta-endorphin in the deteriorating effect of AVP on burn shock.