Biphasic vasomotor reflex responses of the hand skin following intradermal injection of melittin into the forearm skin.

Melittin is the main toxin of honeybee venom. Previously, we have reported that intradermal injection of melittin into the volar aspect of forearm in humans produces a temporary pain and a subsequent sustained increase in the skin temperature due to axon reflex. To clarify the interaction between nociceptive inputs and vascular changes, we studied the influence of noxious stimulation by intradermal melittin on the vasomotor control of the distal extremities in human volunteers. Temperature changes of the bilateral palmar surface were recorded by means of a computer-assisted infrared thermography. Unexpectedly, we found a biphasic response of skin temperature. The skin temperature of both fingers and hands decreased immediately after the melittin injection and then increased well above the control level, prior to the injection. There was a considerable individual variation in the baseline skin temperature, prior to melittin. The skin temperature in a finger/hand with lower preinjection value increased more markedly in the second phase. Consequently, the individual variation in the peak temperature of the second phase was less pronounced. The initial decrease was interpreted as sympathetic vasoconstrictor reflex induced by noxious stimulation and the later increase as release of sympathetic vasomotor tone.     

Diadenosine Polyphosphates’ Action on Calcium and Vessel Contraction

The effects of the endogenous, platelet-derived vasoactive compounds, diadenosine tetraphosphate (AP₄A), diadenosine pentaphosphate (AP₅A), and diadenosine hexaphosphate (AP₆A) on the vasoconstriction of isolated rat renal resistance vessels and rat aortic strips were measured using a vessel myograph. In addition, the effects of AP₄A, AP₅A, and AP₆A on the cytosolic free calcium concentration ([Ca²⁺]_i) were evaluated in cultured rat vascular smooth muscle cells (VSMC) using the fluorescent dye technique. Diadenosine polyphosphates dose-dependently increased the force of renal resistance vessels and isolated aortic strips. The administration of 10 μmol/L AP₄A, AP₅A, or AP₆A significantly increased the force of isolated renal resistance vessels by 3.48 ± 0.43 mN (n = 8), 2.14 ± 0.40 mN (n = 12), or 2.70 ± 0.31 mN (n = 11, each P < .01 compared with resting tension), respectively. The administration of 10 μmol/L AP₄A, AP₅A, or AP₆A significantly increased the force of isolated aortic strips by 2.45 ± 0.97 mNewton (n = 10), 2.70 ± 0.30 mN (n = 6), or 1.48 ± 0.20 mN (each P < .01 compared with resting tension), respectively. The administration of 10 μmol/L AP₄A, AP₅A, or AP₆A significantly increased [Ca²⁺]_i in VSMC to a peak concentration of 314 ± 60 nmol/L (n = 6), 247 ± 25 nmol/L (n = 15), or 332 ± 100 nmol/L (n = 5), respectively (each P < .01 compared with resting value). Both the diadenosine polyphosphate-induced vasoconstriction and [Ca²⁺]_i increase was significantly reduced in the absence of extracellular calcium or after administration of a specific inhibitor of P2 purinoceptors. It is concluded that diadenosine polyphosphates increase [Ca²⁺]_i and hence cause vessel constriction.     

急性低氧大鼠肺动脉平滑肌内质网钙信号的变化及意义

目的：观察急性低氧大鼠肺动脉平滑肌内质网钙信号的变化及意义。方法:细胞水平：钙荧光探针(Fura-2/AM)负载大鼠肺动脉平滑肌细胞（PASMCs），荧光分光光度法，细胞外液无Ca2+及含Ca2+，在常氧（37 ℃、5% CO2、21 %O2、74 %N2 ）和急性低氧(37 ℃、5% CO2、2% O2、93 %N2)时，检测理阿诺碱（RD）和环匹阿尼酸（CPA）等对细胞浆内游离钙离子浓度（［Ca2+］i）的影响；离体血管环水平：相同条件，离体血管灌流方法检测肺动脉环张力变化。结果:(1)急性低氧时［Ca2+］i升高：常氧组［Ca2+］i为（96.99±7.16） nmol/L，低氧组为(257.06±32.48) nmol/L (P<0.01)。(2)与低氧组比较，预先用RD或普鲁卡因(procain)抑制内质网理阿诺碱受体敏感钙库，随后再给予低氧刺激时［Ca2+］i不升高，为（100.91±11.21） nmol/L (P<0.01)；而用CPA或thapsigargin（TG）抑制内质网摄取Ca2+，再给低氧刺激时［Ca2+］i呈升高状态(P>0.05)，而在细胞外液含钙及低氧下CPA及TG引起［Ca2+］i进一步升高(P<0.05)。(3)低氧引起肺动脉环收缩：常氧对基础张力无影响，低氧引起肺动脉环收缩，最大收缩张力达（49.28±8.64） g/g,P<0.01。(4)与低氧组比较，预先用RD或procain抑制内质网理阿诺碱受体敏感钙库，再给予低氧刺激，肺动脉环不收缩，最大收缩张力（3.75±1.14） g/g, P<0.01；而用CPA或TG后，再给予低氧刺激，肺动脉环呈收缩状态(P>0.05)，而在细胞外液含钙及低氧下CPA及TG引起肺动脉环进一步收缩(P<0.05)。结论:急性低氧可以引起内质网释放Ca2+，至少来自理阿诺碱受体敏感钙库的Ca2+释放参与了低氧肺血管收缩的发病机制；这可能是PASMCs自身具有的，既不依赖细胞外Ca2+内流，也不依赖血管内皮。     

Pulmonary Artery Vasoconstriction Due to Bronchial Obstruction

Pulmonary artery (PA) vasoconstriction resulting from pulmonary ventilation/perfusion imbalance is infrequently detected with computed tomography (CT). An 85-year-old woman presented to the emergency room with dyspnea and desaturation, despite oxygen supply. A CT pulmonary angiography (CTPA) revealed massive central bronchial mucoid impaction in all but the right upper bronchus. Only the right upper pulmonary veins were opacified, which we speculate was linked to the central bronchial obstruction, with identical distributions, through vasoconstriction of the corresponding PAs.Teaching Point: This case demonstrates the unusual imagery-physiology correlation of pulmonary artery vasoconstriction that cannot normally be detected by CTPA.