The mechanisms of splenic control in the Antarctic fish, Pagothenia borchgrevinki, were investigated using isolated spleen and mesenteric artery strips in vitro and perfused spleen preparations in situ. Splenosomatic index (SSI) [100 x (spleen wt/body wt)] and hematocrit were determined in animals treated with atropine and phentolamine. Atropine injection increased the SSI from 0.60 +/- 0.06 to 0.89 +/- 0.04, whereas phentolamine decreased SSI to 0.45 +/- 0.03. In atropine-injected fish, hematocrit was 18.6 +/- 1.4 before and 6.6 +/- 0.8% 3 h after injection. Electrical stimulation of the splenic nerves produced biphasic flow responses. In 11 of 12 tested preparations, atropine (3 x 10(-7) to 10(-6) NI) abolished the response, suggesting a major cholinergic component in the splenic innervation. Isolated spleen strip prepara tions contracted in response to carbachol, a response that was antagonized by atropine. The response to acetylcholine was markedly enhanced by the specific cholinesterase inhibitor BW-284c51. Catecholamine effects were somewhat irregular, and maximal contraction force with epinephrine and norepinephrine was 41 and 56%, respectively, of the carbachol response. The results suggest a mainly, if not solely, cholinergic autonomic control of the borch spleen, and a major function of the cholinergic innervation in the control of hematocrit in this species.

Central venous blood pressure (P-ven) increases in response to hypoxia in rainbow trout ( Oncorhynchus mykiss), but details on the control mechanisms of the venous vasculature during hypoxia have not been studied in fish. Basic cardiovascular variables including Pven, dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (PwO(2) = similar to 9 kPa), where PwO(2) is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80-100, 90-110, and 100-120% of total blood volume by transiently (8 s) occluding the ventral aorta and measure Pven during circulatory arrest to estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance. MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by alpha-adrenoceptor blockade with prazosin (1 mg/kg body mass). MCFP still increased during hypoxia after pretreatment with the adrenergic nerve-blocking agent bretylium (10 mg/kg body mass), but the decrease in USBV only persisted at 80-100% blood volume, whereas vascular capacitance decreased significantly at 90-110% blood volume. In all treatments, hypoxia typically reduced heart rate while cardiac output was maintained through a compensatory increase in stroke volume. Despite the markedly reduced response in venous capacitance after adrenergic blockade, Pven always increased in response to hypoxia. This study reveals that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an alpha-adrenergic mechanism with both humoral and neural components.