title: Vascular perfusion limits mesenteric lymph flow during anaphylactic hypotension in rats.
abstract: To determine fluid extravasation in the splanchnic vascular bed during anaphylactic hypotension, the mesenteric lymph flow (Q(lym)) was measured in anesthetized rats sensitized with ovalbumin, along with the systemic arterial pressure (P(sa)) and portal venous pressure (P(pv)). When the antigen was injected into the sensitized rats (n = 10), P(sa) decreased from 125 ± 4 to 37 ± 2 mmHg at 10 min with a gradual recovery, whereas P(pv) increased by 16 mmHg at 2 min and returned to the baseline at 10 min. Q(lym) increased 3.3-fold from the baseline of 0.023 ± 0.002 g/min to the peak levels of 0.075 ± 0.009 g/min at 2 min and returned to the baseline within 12 min. The lymph protein concentrations increased after antigen, a finding indicating increased vascular permeability. To determine the role of the P(pv) increase in the antigen-induced increase in Q(lym), P(pv) of the nonsensitized rats (n = 10) was mechanically elevated in a manner similar to that of the sensitized rats by compressing the portal vein near the hepatic hilus. Unexpectedly, P(pv) elevation alone produced a similar increase in Q(lym), with the peak comparable to that of the sensitized rats. This finding aroused a question why the antigen-induced increase in Q(lym) was limited despite the presence of increased vascular permeability. Thus the changes in splanchnic vascular surface area were assessed by measuring the mesenteric arterial flow. The mesenteric arterial flow was decreased much more in the sensitized rats (75%; n = 5) than the nonsensitized P(pv) elevated rats (50%; n = 5). In conclusion, mesenteric lymph flow increases transiently after antigen presumably due to increased capillary pressure of the splanchnic vascular bed via downstream P(pv) elevation and perfusion and increased vascular permeability in anesthetized rats. However, this increased extravasation is subsequently limited by decreases in vascular surface area and filtration pressure.
authors.affiliation: Department of Physiology II, Kanazawa Medical University, Uchinada, Japan.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Toshishige
authors.initials: T
authors.lastname: Shibamoto
authors.forename: Yuhichi
authors.initials: Y
authors.lastname: Kuda
authors.forename: Yasutaka
authors.initials: Y
authors.lastname: Kurata
authors.forename: Shohei
authors.initials: S
authors.lastname: Shinomiya
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kida
authors.forename: Hideaki
authors.initials: H
authors.lastname: Tsuchida
mesh_terms: D000707:Anaphylaxis / Q000503:physiopathology*; D000818:Animals; D000941:Antigens / Q000494:pharmacology; D002199:Capillary Permeability / Q000187:drug effects / Q000502:physiology; D007022:Hypotension / Q000503:physiopathology*; D008196:Lymph / Q000502:physiology*; D042601:Lymphatic Vessels / Q000503:physiopathology*; D008297:Male; D008638:Mesenteric Arteries / Q000503:physiopathology*; D023421:Models, Animal; D010047:Ovalbumin / Q000494:pharmacology; D017082:Portal Pressure / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology*; D013152:Splanchnic Circulation / Q000187:drug effects / Q000502:physiology
chemical_list: D000941:Antigens; D010047:Ovalbumin