Neurokinin A and B are putative inflammatory mediators. We assessed their ability to alter prenodal lymphatic resistance. Intralymphatic neurokinin A (3.0 × 10−6, 3.0 × 10−5 and 3.0 × 10−4 mol l−1) significantly constricted lymphatics at the two highest doses. Preliminary experiments suggested that neurokinin B might dilate lymphatics. To test this, lymphatic pressure was increased by norepinephrine (3.1 × 10−6 mol l−1). Neurokinin B (2.7 × 10−4 mol l−1) was then infused intralymphatically during norepinephrine infusion. Norepinephrine increased perfusion pressure from 5.6 ± 0.6 mmHg to 12.1 ± 1.4 mmHg. Subsequent infusion of neurokinin B significantly decreased lymphatic perfusion pressure from 11.9 ± 1.3 mmHg to 9.9 ± 1.1 mmHg. These data indicate that neurokinin A and B can alter lymphatic resistance and are consistent with the hypothesis that lymph vessel function may be subject to modulation by neurokinins.
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机译：神经激肽A和B是假定的炎症介质。我们评估了它们改变结前淋巴抵抗的能力。淋巴内神经激肽A（3.0×10 -6 ，3.0×10 -5 和3.0×10 -4 mol l -1 < / sup>）在两个最高剂量时显着收缩淋巴管。初步实验表明神经激肽B可能会扩张淋巴管。为了测试这一点，去甲肾上腺素提高了淋巴压力（3.1×10 -6 mol l -1 ）。然后在去甲肾上腺素输注期间淋巴内注射神经激肽B（2.7×10 −4 mol l -1 ）。去甲肾上腺素将灌注压力从5.6±0.6 mmHg增加到12.1±1.4 mmHg。随后输注神经激肽B可使淋巴灌注压力从11.9±1.3 mmHg降低至9.9±1.1 mmHg。这些数据表明神经激肽A和B可以改变淋巴抵抗，并且与淋巴管功能可能受到神经激肽调节的假设相一致。
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