Effect of Repetitive Intracutaneous Injections with Local Anesthetics and Steroids for Acute Thoracic Herpes Zoster and Incidence of Postherpetic Neuralgia.

BACKGROUND: Treatment of established postherpetic neuralgia (PHN) is difficult and often disappointing. In this study, we assessed the efficacy of repetitive intracutaneous injections with local anesthetics and steroids in acute thoracic herpes zoster (HZ) pain, herpetic eruption, and incidence of PHN. METHODS: Ninety-three patients with acute thoracic HZ were randomly assigned to receive a standard treatment of antiviral medication with p.o. analgesics or the standard treatment with the addition of repetitive intracutaneous injections of a local anesthetic and steroid mixture. Patients were permitted to take tramadol when the visual analog scale (VAS) ≥ 4. Pain assessment using VAS was conducted at the initial visit, as well as 1, 2, 4, 12, and 24 weeks after the end of the treatments. RESULTS: In comparison with the standard treatment group, the VAS scores of the intracutaneous injection group were significantly lower during the study. The intracutaneous injection group also reported shorter duration of pain and skin eruption than the control group ( P = 0.005 vs P < 0.001, respectively). At 1 month post-therapy, 12.8% patients in the intracutaneous injection group reported zoster-associated pain, compared with 47.8% in the standard treatment group ( P < 0.001). At 3 and 6 months post-therapy, the incidence of PHN was still significantly lower in the intracutaneous injection group than the standard treatment group. EuroQol VAS scores were significantly higher in the intracutaneous injection group vs standard treatment group (P < 0.001). CONCLUSION: Repetitive intracutaneous injections with local anesthetics and steroids along with standard treatment significantly reduce the duration of pain and herpetic eruption and incidence of PHN.

Hydrogen sulfide postconditioning protects isolated rat hearts against ischemia and reperfusion injury mediated by the JAK2/STAT3 survival pathway

The JAK2/STAT3 signal pathway is an important component of survivor activating factor enhancement (SAFE) pathway. The objective of the present study was to determine whether the JAK2/STAT3 signaling pathway participates in hydrogen sulfide (H2S) postconditioning, protecting isolated rat hearts from ischemic-reperfusion injury. Male Sprague-Dawley rats (230-270 g) were divided into 6 groups (N = 14 per group): time-matched perfusion (Sham) group, ischemia/reperfusion (I/R) group, NaHS postconditioning group, NaHS with AG-490 group, AG-490 (5 µM) group, and dimethyl sulfoxide (DMSO; <0.2%) group. Langendorff-perfused rat hearts, with the exception of the Sham group, were subjected to 30 min of ischemia followed by 90 min of reperfusion after 20 min of equilibrium. Heart rate, left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), and the maximum rate of increase or decrease of left ventricular pressure (± dp/dt max) were recorded. Infarct size was determined using triphenyltetrazolium chloride (TTC) staining. Myocardial TUNEL staining was used as the in situ cell death detection method and the percentage of TUNEL-positive nuclei to all nuclei counted was used as the apoptotic index. The expression of STAT3, bcl-2 and bax was determined by Western blotting. After reperfusion, compared to the I/R group, H2S significantly improved functional recovery and decreased infarct size (23.3 ± 3.8 vs 41.2 ± 4.7%, P < 0.05) and apoptotic index (22.1 ± 3.6 vs 43.0 ± 4.8%, P < 0.05). However, H2S-mediated protection was abolished by AG-490, the JAK2 inhibitor. In conclusion, H2S postconditioning effectively protects isolated I/R rat hearts via activation of the JAK2/STAT3 signaling pathway.

Hydrogen sulfide postconditioning protects isolated rat hearts against ischemia and reperfusion injury mediated by the JAK2/STAT3 survival pathway.

The JAK2/STAT3 signal pathway is an important component of survivor activating factor enhancement (SAFE) pathway. The objective of the present study was to determine whether the JAK2/STAT3 signaling pathway participates in hydrogen sulfide (H2S) postconditioning, protecting isolated rat hearts from ischemic-reperfusion injury. Male Sprague-Dawley rats (230-270 g) were divided into 6 groups (N = 14 per group): time-matched perfusion (Sham) group, ischemia/reperfusion (I/R) group, NaHS postconditioning group, NaHS with AG-490 group, AG-490 (5 µM) group, and dimethyl sulfoxide (DMSO; <0.2%) group. Langendorff-perfused rat hearts, with the exception of the Sham group, were subjected to 30 min of ischemia followed by 90 min of reperfusion after 20 min of equilibrium. Heart rate, left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), and the maximum rate of increase or decrease of left ventricular pressure (± dp/dt(max)) were recorded. Infarct size was determined using triphenyltetrazolium chloride (TTC) staining. Myocardial TUNEL staining was used as the in situ cell death detection method and the percentage of TUNEL-positive nuclei to all nuclei counted was used as the apoptotic index. The expression of STAT3, bcl-2 and bax was determined by Western blotting. After reperfusion, compared to the I/R group, H2S significantly improved functional recovery and decreased infarct size (23.3 ± 3.8 vs 41.2 ± 4.7%, P < 0.05) and apoptotic index (22.1 ± 3.6 vs 43.0 ± 4.8%, P < 0.05). However, H2S-mediated protection was abolished by AG-490, the JAK2 inhibitor. In conclusion, H2S postconditioning effectively protects isolated I/R rat hearts via activation of the JAK2/STAT3 signaling pathway.