Kerr J C, Hobson R W, Seelig R F, Swan K G
Ann Surg. 1978 Feb;187(2):137-42. doi: 10.1097/00000658-197802000-00007.
BLOOD FLOWS THROUGH THE CANINE HEPATIC (HBF) AND SUPERIOR MESENTERIC ARTERIES (MBF) WERE MEASURED WITH ELECTROMAGNETIC FLOWMETERS, DURING INFUSIONS OF VASOPRESSIN, BY THREE ROUTES OF ADMINISTRATION: 1) intra-hepatic-arterially (IHA), 2) intra-portal-venously (IPV) and 3) intra-systemic-venously (IV). Mean control HBF was 148 +/- 17 (S.E.) ml min(-1); MBF was 243 +/- 27 ml min(-1); aortic pressure (AP) was 126 +/- 3 mm Hg; portal venous pressure (PVP) was 8.8 +/- 1.0 mm Hg. Infusions of vasopressin, at a rate of 5 x 10(-3) units kg(-1) min(-1), IHA, reduced HBF significantly (p < .001) to 121 +/- 21 ml min(-1), within one minute. Flow returned to control, despite continued drug infusion; and at the end of the fifth minute of infusion, the value (134 +/- 21 ml min(-1)) was not significantly (p > .05) different from control. During the same infusion, MBF fell to 129 +/- 28 ml min(-1) (p < .001), by the sixth minute of the infusion and remained at this level for the duration of the infusion. AP increased to 137 +/- 13 mm Hg, by the sixth minute of the infusion and was sustained at this level for the duration of the infusion. PVP decreased to 7.0 +/- 1.0 mm Hg, by the tenth minute of the infusion. The responses to IPV vasopressin were indistinguishable from those following IHA vasopressin, with the exception that HBF was reduced to only 147 +/- 22 ml min(-1) (from a preinfusion control of 160 +/- 23 ml min(-1)), at one minute. HBF returned to control, despite continuation of the infusion. IV vasopressin, at the same concentration, caused no change in HBF throughout the ten minute infusion. These observations indicate that the canine hepatic arterial circulation responds to vasopressin with vasoconstriction characterized by autoregulatory escape. By any of the three routes of administration, vasopressin causes a significant and sustained reduction in blood flow through the superior mesenteric artery. Autoregulatory escape, from vasopressin-induced mesenteric arterial constriction, is not observed. Based on these observations, significant changes in mesenteric arterial blood flow can be anticipated without associated significant changes in hepatic arterial blood flow, regardless of the route of administration of vasopressin.
通过电磁流量计测量了犬肝动脉(HBF)和肠系膜上动脉(MBF)的血流量,在通过三种给药途径输注加压素期间:1)肝动脉内(IHA),2)门静脉内(IPV)和3)全身静脉内(IV)。平均对照HBF为148±17(标准误)ml min⁻¹;MBF为243±27 ml min⁻¹;主动脉压(AP)为126±3 mmHg;门静脉压(PVP)为8.8±1.0 mmHg。以5×10⁻³单位kg⁻¹ min⁻¹的速率经IHA输注加压素,在1分钟内HBF显著降低(p <.001)至121±21 ml min⁻¹。尽管持续输注药物,血流量仍恢复至对照水平;在输注的第5分钟末,该值(134±21 ml min⁻¹)与对照无显著差异(p>.05)。在同一输注过程中,到输注的第6分钟时MBF降至129±28 ml min⁻¹(p <.001),并在输注期间维持在该水平。到输注的第6分钟时AP升至137±13 mmHg,并在输注期间维持在该水平。到输注的第10分钟时PVP降至7.0±1.0 mmHg。对IPV加压素的反应与IHA加压素后的反应无明显差异,不同之处在于1分钟时HBF仅降至147±22 ml min⁻¹(从输注前对照的160±23 ml min⁻¹)。尽管继续输注,HBF仍恢复至对照水平。相同浓度的IV加压素在整个10分钟输注过程中未引起HBF变化。这些观察结果表明,犬肝动脉循环对加压素的反应是血管收缩,其特征为自动调节逃逸。通过三种给药途径中的任何一种,加压素都会导致通过肠系膜上动脉的血流量显著且持续减少。未观察到从加压素诱导的肠系膜动脉收缩中的自动调节逃逸。基于这些观察结果,无论加压素的给药途径如何,预计肠系膜动脉血流量会发生显著变化,而肝动脉血流量无相关显著变化。