花生四烯酸、二十碳五烯酸及二十二碳六烯酸对兔主动脉条张力的影响

外源性AA引起兔动脉条收缩,呈剂量依赖性;EPA抑制AA收缩血管亦呈浓度依赖性;DHA对AA收缩血管作用无明显影响。破坏血管内皮后AA收缩血管作用大为减弱,EPA抑制AA收缩血管作用也几乎消失。吲哚美辛能阻断AA收缩兔主动脉条的作用。兔主动脉6-keto-PGF_1α、TXB₂及其比值随AA浓度升高而增加,低剂量EPA对前列腺素类代谢无明显影响,较大剂量时则降低上述指标。     

Effect of helium-neon and infrared laser irradiation on wound healing in rabbits

We examined the biostimulating effects of helium-neon laser radiation (HeNe; 632.8 nm), pulsed infrared laser radiation (IR; 904 nm), and the two combined on skin wound healing in New Zealand white rabbits. Seventy-two rabbits received either 1) no exposure, 2) 1.65 J/cm2 HeNe, 3) 8.25 J/cm2 pulsed IR, or 4) both HeNe and IR together to one of two dorsal full-thickness skin wounds, daily, for 21 days. Wound areas were measured photographically at periodic intervals. Tissue samples were analyzed for tensile strength, and histology was done to measure epidermal thickness and cross-sectional collagen area. Significant differences were found in the tensile strength of all laser-treated groups (both the irradiated and nonirradiated lesion) compared to group 1. No differences were found in the rate of wound healing or collagen area. Epidermal growth was greater in the HeNe-lased area compared to unexposed tissue, but the difference was not significant. Thus, laser irradiation at 632.8 nm and 904 nm alone or in combination increased tensile strength during wound healing and may have released tissue factors into the systemic circulation that increased tensile strength on the opposite side as well.     

Enflurane anesthesia for surgical removal of pheochromocytoma

Four cases describing the use of enflurane as the main anesthetic during surgical removal of pheochromocytoma (PCC) are presented and the preoperative preparation and intraoperative management of the patients are discussed. Serum levels of epinephrine and norepinephrine were measured in 3 of the reported cases. Intraoperative values were extremely elevated during tumor manipulation, but there was only 1 minor episode of arrhythmias. Criteria for choosing anesthetic agents for surgical removal of PCC are outlined. The authors conclude from their experience and that of others that enflurane is as safe and effective an anesthetic as any now available for PCC excision.     

4α-phorbol 12,13-didecanoate activates cultured mouse dorsal root ganglia neurons independently of TRPV4

Background and Purpose

The Ca²⁺-permeable cation channel TRPV4 is activated by mechanical disturbance of the cell membrane and is implicated in mechanical hyperalgesia. Nerve growth factor (NGF) is increased during inflammation and causes mechanical hyperalgesia. 4α-phorbol 12,13-didecanoate (4αPDD) has been described as a selective TRPV4 agonist. We investigated NGF-induced hyperalgesia in TRPV4 wild-type (+/+) and knockout (–/–) mice, and the increases in [Ca²⁺]_i produced by 4αPDD in cultured mouse dorsal root ganglia neurons following exposure to NGF.

Experimental Approach

Withdrawal thresholds to heat, von Frey hairs and pressure were measured in mice before and after systemic administration of NGF. Changes in intracellular Ca²⁺ concentration were measured by ratiometric imaging with Fura-2 in cultured DRG and trigeminal ganglia (TG) neurons during perfusion of TRPV4 agonists.

Key Results

Administration of NGF caused a significant sensitization to heat and von Frey stimuli in TRPV4 +/+ and –/– mice, but only TRPV4 +/+ mice showed sensitization to noxious pressure. 4αPDD stimulated a dose-dependent increase in [Ca²⁺]_i in neurons from +/+ and –/– mice, with the proportion of responding neurons and magnitude of increase unaffected by the genotype. In contrast, the selective TRPV4 agonist GSK1016790A failed to stimulate an increase in intracellular Ca²⁺ in cultured neurons. Responses to 4αPDD were unaffected by pretreatment with NGF.

Conclusions and Implications

TRPV4 contributes to mechanosensation in vivo, but there is little evidence for functional TRPV4 in cultured DRG and TG neurons. We conclude that 4αPDD activates these neurons independently of TRPV4, so it is not appropriate to refer to 4αPDD as a selective TRPV4 agonist.