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Objectives: Chronic mesenteric ischaemia (CMI) is an underdiagnosed but severe condition. Access to functional testing is often limited and the diagnosis is usually based primarily on symptoms and imaging. One of the functional tests available is measurement of the splanchnic blood flow (SBF). The purpose of the present investigation was to evaluate if changes in the splanchnic perfusion after revascularization can be detected by measuring the SBF and hepatic vein oxygenation. Materials and Methods: The SBF was measured in 10 patients before and after revascularization of the mesenteric arteries by either percutaneous transluminal angioplasty (n = 9) or open revascularization (n = 1). The SBF was measured indirectly using Fick's principle and using the tracer Tc‐99m Mebrofenin along with assessment of hepatic blood oxygenation, before and after a standard meal, following catheterization of a hepatic vein and the femoral artery. Results: Nine of 10 patients (90%) achieved a profound increase in SBF after revascularization (mean increase in postprandial response to meal stimulation from 71 ± 95 to 531 ± 295 ml/min, p = 0.001), and an increase in postprandial hepatic vein oxygen saturation (from 52 ± 14% to 59 ± 13%, p = 0.006). The symptoms of the patients diminished accordingly. One patient had no symptom relief, and no increase in postprandial SBF, but an angiographic result with no significant stenosis postrevascularization. Conclusions: Revascularization increased the SBF and hepatic vein oxygen saturation significantly concurrent with symptom relief and according with the angiographic successful result in the vast majority of patients. A satisfying angiographic result post vascular intervention does not rule out CMI. [ABSTRACT FROM AUTHOR]

Background: Chronic mesenteric ischaemia (CMI) is a vastly underdiagnosed condition that typically leads to postprandial abdominal pain and weight loss. The aim of the study was to explore the involvement of various mesenteric vessels in total splanchnic blood flow (SBF) and hepatic vein oxygenation. Methods: Single‐blinded comparative trial of 476 patients clinically suspected of CMI. Routine investigation included measurement of hepatic vein oxygen saturation, indirect measurement of the total splanchnic blood flow (SBF), using Fick's principle and the tracer [99mTc]Mebrofenin, before and after a meal, and digital subtraction angiography. Results: A total of 176 of the 476 patients (36%) had at least one angiographically significant stenosis (lumen reduction ≥70%). In patients with a significant one‐vessel disease, the percentage having CMI according to SBF was 10% for a celiac trunk stenosis (n = 60), 50% for a superior mesenteric stenosis (n = 24) and 6% for an inferior mesenteric artery stenosis (n = 34). In patients with a significant two‐vessel disease, the percentage with CMI according to SBF response was 92%, 18% and 79%, for no significant stenosis of the celiac trunk (n = 13), superior mesenteric artery (n = 17) and inferior mesenteric artery (n = 19), respectively. Conclusion: Patients with significant one‐ or two‐vessel stenosis involving the superior mesenteric artery have a higher likelihood of CMI according to flow criteria and a greater postprandial decrease in hepatic vein saturation on average than patients with no involvement of the superior mesenteric artery. [ABSTRACT FROM AUTHOR]

The stimulation-evoked 3H-overflow from rabbit isolated ear arteries preincubated with 3H-noradrenaline was studied. Three strips were derived from each central artery. The strips were incubated (30 min.) with 3H-noradrenaline (10-7M) and the spontaneous 3H-outflow and stimulation-evoked 3H-overflow were followed by fractional collection. After a wash-out period (75 min.), the strips were stimulated (225 mA; 150 monophasic pulses; 3 Hz; 0.5 msec.) several times. The initial stimulation-evoked 3H-overflow (S1) was about 5-fold higher than the subsequent five 3H-overflows (S2-S6) which remained almost constant. Bretylium (10-5M), tetrodotoxin (10-6M), and omission of Ca2+ from the physiological salt solution reduced the stimulation-evoked 3H-overflow by maximally 52%, 77% and 62%, respectively. An increase in stimulation current from 50 to 225 mA caused a continuous rise in stimulation-evoked 3H-overflow, which tended to be Ca2+-sensitive. The stimulation-evoked 3H-overflow was frequency-dependent: at 1-4 Hz, the 3H-overflows were the same; at 8 and 16 Hz, they increased. Cocaine (3 × 10-5M) plus corticosterone (4 ×10-5M) enhanced the stimulation-evoked 3H-overflow at 1-8 Hz, while it had no effect at 16 Hz. Propranolol (3 × 10-7M) did not antagonize this enhancement. An increase in number of pulses from 10 to 1000 in the stimulus caused a corresponding rise in the evoked 3H-overflow. This was also the case when cocaine plus corticosterone were present. Cocaine at low concentrations increased the stimulation-evoked 3H-overflow at two frequencies (3 and 16 Hz), while a high concentration of cocaine decreased the 3H-overflow at 16 Hz. The results suggest that the strip preparation of rabbit central ear artery is suitable for studying the release of 3H-noradrenaline evoked by electrical-field stimulation, and that this release is in part of extraneuronal origin. [ABSTRACT FROM AUTHOR]

The effect of chlorpromazine on the metabolism of 3H-noradrenaline (3H-NA) released spontaneously or by electrical-field stimulation was studied on the rabbit isolated aorta preloaded with 3H-NA. Chlorpromazine (10−6M) neither altered the spontaneous outflow of total tritium nor had any major effect on the distribution of the 3H-outflow on 3H-NA and its 3H-metabolites. Chlorpromazine (10−6M) altered the distribution in stimulation-evoked 3H-overflow. Thus, 3H-NA and 3H-NMN were increased, 3H-DOPEG was markedly decreased and 3H-DOMA and 3H-OMDA were unchanged. It is concluded that chlorpromazine is an inhibitor of uptake-1. [ABSTRACT FROM AUTHOR]