Superior Mesenteric Artery Blood Flow Research Articles

Effect of caffeine on superior mesenteric artery blood flow velocities in preterm neonates

Objective: To investigate the effect of caffeine infusion on superior mesenteric artery (SMA) blood flow velocities (BFV) in preterm infants.Methods: Prospective observational study on 38 preterm neonates 28–33+6 weeks gestation, who developed apnea on their first day of life, and caffeine citrate infusion was initiated at a loading dose of 20 mg/kg, followed by a maintenance dose of 5–10 mg/kg/day. Duplex ultrasound measurements of SMA BFV were recorded: peak systolic velocity (PSV), end diastolic velocity (EDV) and resistive index (RI), at 15 min before, 1-, 2- and 6-h after caffeine loading dose, and 2 h after two maintenance doses.Results: There was a significant reduction in PSV 1-h (p = .008), a significant decrease in EDV 1- and 2-h (p = .000 and p = .005, respectively) and a significant increase in RI 1- and 2-h (p = .003 and p = .005, respectively) following caffeine loading dose, as compared to values before caffeine infusion. No significant effect of caffeine maintenance doses on SMA BFV was observed (p > .05).Conclusion: Blood flow in SMA is significantly reduced after caffeine citrate infusion at a loading dose of 20 mg/kg. This effect continues for at least 2 h. Meanwhile, SMA BFV seems not affected by maintenance doses.

Gastrointestinal Impedance Spectroscopy to Detect Hypoperfusion During Hemorrhage.

Changes in tissue impedance (Ω) have been proposed as early signs of impaired tissue perfusion. We hypothesized that hemorrhage may induce early changes in alimentary tract tissue impedance and that these can be detected by impedance spectroscopy. We evaluated impedance spectroscopy in an acute hemorrhage model in pigs. Twenty anesthetized pigs were randomized to stepwise hemorrhage to mean arterial blood pressure (MAP) targets of 60 mm Hg, 50 mm Hg, 45 mm Hg, and 40 mm Hg, followed by retransfusion in two steps, or control (n = 10 each). In the end, 500 mL of enteral nutrition was administered in both groups. Ω in four sites (sublingually, esophagus, stomach, proximal jejunum) and cardiac output (Qtot thermodilution), superior mesenteric artery blood flow (QSMA; Doppler ultrasound), and jejunal mucosal blood flow (LDF; laser Doppler) were measured. The bleeding (total volume 838 ± 185 mL; mean ± SD) resulted in progressive hypotension (actual MAP 65 ± 3 mm Hg, 59 ± 4 mm Hg, 55 ± 5 mm Hg, and 46 ± 6 mm Hg) and decrease in Qtot, QSMA, and mucosal LDF. Bleeding did not change Ω in any of the monitoring sites. Retransfusion restored the blood flows to at least baseline levels, again without change in Ω. Enteral nutrition did not alter Ω or any of the blood flows.Five animals (three in the hemorrhage group, two in the control group) had histologically proven acute gastric focal necrosis at the site of It transducer. Gastrointestinal impedance spectroscopy does not detect early changes in tissue perfusion during progressive hemorrhage or retransfusion. Ω spectroscopy is unlikely to provide any additional information of hypovolemia-induced early changes in gastrointestinal perfusion.

Duplex Doppler Sonographic Assessment of the Superior Mesenteric Artery in Patients With Mesenteric Panniculitis.

We aimed to determine how the hemodynamic parameters of the superior mesenteric artery are affected in mesenteric panniculitis. Twenty-one patients with a diagnosis of mesenteric panniculitis on computed tomography were evaluated with duplex Doppler sonography. The control group consisted 20 asymptomatic volunteers. The peak systolic velocity, end-diastolic velocity (EDV), resistive index (RI), pulsatility index (PI), blood flow volume, and body mass index were measured in the group of patients with mesenteric panniculitis, and the findings were compared with those of the control group. The mean blood flow volume and EDV were significantly higher in the patient group: The mean superior mesenteric artery blood flow volume ± SD was 917.86 ± 228.97 mL/min in the patient group versus 389.73 ± 92.72 mL/min in the control group (P < .001). The mean EDV was 31.56 ± 8.44 m/s in the patient group versus 19.27 ± 4.19 m/s in the control group (P < .001). The mean RI and PI were significantly lower in the patient group: The mean RI was 0.81 ± 0.04 in the patient group versus 0.85 ± 0.03 in the control group (P = .001). The mean PI was 2.69 ± 0.68 in the patient group versus 3.81 ± 1.13 in the control group (P = .001). the mean superior mesenteric artery diameter was 7.30 ± 0.67 mm in the patient group versus and 6.46 ± 0.66 mm in the control group (P < .001). The mean BMI was 27.95 ± 3.80 kg/m2 in the patient group versus 23.16 ± 3.47 kg/m2 in the control group (P < .001). In patients with mesenteric panniculitis, the Doppler spectrum of the superior mesenteric artery shows detectable changes, which are characterized by decreased vascular resistance and increased blood flow.

Timing of postexercise carbohydrate-protein supplementation: roles of gastrointestinal blood flow and mucosal cell damage on gastric emptying in humans.

It is well known that protein ingestion immediately after exercise greatly stimulates muscle protein synthesis during the postexercise recovery phase. However, immediately after strenuous exercise, the gastrointestinal (GI) mucosa is frequently injured by hypoperfusion in the organ/tissue, possibly resulting in impaired GI function (e.g., gastric emptying; GE). The aim of this study was to examine the effect of GI blood flow on the GE rate. Eight healthy young subjects performed an intermittent supramaximal cycling exercise for 30 min, which consisted of a 120% V̇o2peak for 20 s, followed by 20 W for 40 s. The subjects ingested 300 ml of a nutrient drink containing carbohydrate-protein at either 5 min postexercise in one trial (PE-5) or 30 min postexercise in another trial (PE-30). In the control trial (Con), the subjects ingested the same drink without exercise. The celiac artery blood flow (CABF) and superior mesenteric artery blood flow (SMABF) and GE rate were assessed by ultrasonography. Before drink ingestion in PE-5, CABF significantly decreased from baseline, whereas in PE-30, it returned to baseline. Following drink ingestion in PE-5, CABF did not change from baseline, but it significantly increased in PE-30 and Con. SMABF increased significantly later in PE-5 than in PE-30 and Con. The GE rate was consistently slower in PE-5 than in PE-30 and Con. In conclusion, the CABF response after exercise seems to modulate the subsequent GE rate and SMABF response.NEW & NOTEWORTHY A carbohydrate-protein drink was ingested at either 5 min (i.e., profoundly decreased celiac artery blood flow; CABF) or 30 min (i.e., already recovered CABF) postexercise. In the 5-min postexercise trial, the gastric emptying (GE) rate and superior mesenteric artery blood flow (SMABF) response were slower than those in the 30-min postexercise trial. The GE rate and SMABF response may be altered depending on the postexercise CABF response.

Assessment of developmental and radiological long-term outcomeof children with surgically treated midgut volvulus.

The aim is to evaluate the long-term outcome of asymptomatic patients who underwent surgical correction for midgut volvulus. Seven patients managed surgically for midgut volvulus in the last 3 years were included. Demographic features, symptoms at presentation, diagnoses, surgical procedures, and complications were recorded. Patients were then contacted for follow-up and evaluation of long-term outcomes. General physical conditions, anthropometric parameters, feeding habits, and defecation histories were evaluated. Laboratory examinations were performed. Color Doppler ultrasonography (CDUS) was performed to evaluate blood flow in the superior mesenteric artery (SMA). In total, seven patients were identified. The median age at admission was 3 days (0-90 days). Mean age at follow-up was 17 ± 2 months. Growth parameters were normal in all cases. Four patients had low levels of ferritin and transferrin saturation. One patient had microcytic anemia. Another patient had low serum zinc level. One patient who had ileal resection had a high level of steatorrhea in stool examination. In CDUS, SMA blood flow volume was low in all cases. Peak-systolic velocity and resistance index were low in all but one case. Despite uneventful postoperative courses, all patients operated on for midgut volvulus showed mild laboratory changes and decreased blood flow in the SMA in long-term follow-up.

Mesenteric vascular dysregulation and intestinal inflammation accompanies experimental spinal cord injury.

Cervical and high thoracic spinal cord injury (SCI) drastically impairs autonomic nervous system function. Individuals with SCI at thoracic spinal level 5 (T5) or higher often present cardiovascular disorders that include resting systemic arterial hypotension. Gastrointestinal (GI) tissues are critically dependent upon adequate blood flow and even brief periods of visceral hypoxia triggers GI dysmotility. The aim of this study was to test the hypothesis that T3-SCI induces visceral hypoperfusion, diminished postprandial vascular reflexes, and concomitant visceral inflammation. We measured in vivo systemic arterial blood pressure and superior mesenteric artery (SMA) and duodenal blood flow in anesthetized T3-SCI rats at 3 days and 3 wk postinjury either fasted or following enteral feeding of a liquid mixed-nutrient meal (Ensure). In separate cohorts of fasted T3-SCI rats, markers of intestinal inflammation were assayed by qRT-PCR. Our results show that T3-SCI rats displayed significantly reduced SMA blood flow under all experimental conditions (P < 0.05). Specifically, the anticipated elevation of SMA blood flow in response to duodenal nutrient infusion (postprandial hyperemia) was either delayed or absent after T3-SCI. The dysregulated SMA blood flow in acutely injured T3-SCI rats coincides with abnormal intestinal morphology and elevation of inflammatory markers, all of which resolve after 3 wk. Specifically, Icam1, Ccl2 (MCP-1), and Ccl3 (MIP-1α) were acutely elevated following T3-SCI. Our data suggest that arterial hypotension diminishes mesenteric blood flow necessary to meet mucosal demands at rest and during digestion. The resulting GI ischemia and low-grade inflammation may be an underlying pathology leading to GI dysfunction seen following acute T3-SCI.

The investigation of therapeutic effect and its mechanism of acarbose on postprandial hypotension with concomitant abnormal glucose metabolism in elderly patients

Objective To explore the of therapeutic effect and its mechanism of acarbose on postprandial hypotension(PPH)with concomitant abnormal glucose metabolism in elderly patients. Methods The 43 elderly patients(>80 years)with PPH and concomitant abnormal glucose metabolism were randomly divided into two groups: acarbose group(n=21)and control group(n=22). Before and two weeks after treatment, the blood pressure, blood glucose level, and the superior mesenteric artery blood flow of the two groups were monitored. Results The decrement of postprandial systolic blood pressures was lower in acarbose group than in control group〔(22.3±6.9)vs.(30.7±8.4)mmHg, 1 mmHg=0.133 kPa, P=0.000〕. The increment of postprandial blood glucose was lower in acarbose group than in control group〔(2.3±1.6)vs.(3.5±0.9)mmol/L, P=0.002〕. The decrement of postprandial diastolic blood pressure had no significant difference between two groups〔(11.3±5.3)vs.(10.8±5.6)mmHg, P=0.058〕. The incidence rate of PPH before versus after treatment was 100%(21/21 cases)vs.47.6%(10/21 cases)(P=0.002)in acarbose treatment group and 100%(21/21 cases)vs.100%(21/21 cases)in control group(P>0.05). Acarbose treatment showed no significant side effects. Conclusions The abnormal increase in postprandial splanchnic perfusion is one of the reasons for PPH.Acarbose may exert its role in PPH treatment by reducing superior mesenteric artery blood flow.Giving acarbose to treat PPH with concomitant abnormal glucose metabolism is effective and safe in very old patients. Key words: Hypotension; Postprandial period; Mesenteric arteries

A computer model simulating human glucose absorption and metabolism in health and metabolic disease states

A computer model designed to simulate integrated glucose-dependent changes in splanchnic blood flow with small intestinal glucose absorption, hormonal and incretin circulation and hepatic and systemic metabolism in health and metabolic diseases e.g. non-alcoholic fatty liver disease, (NAFLD), non-alcoholic steatohepatitis, (NASH) and type 2 diabetes mellitus, (T2DM) demonstrates how when glucagon-like peptide-1, (GLP-1) is synchronously released into the splanchnic blood during intestinal glucose absorption, it stimulates superior mesenteric arterial (SMA) blood flow and by increasing passive intestinal glucose absorption, harmonizes absorption with its distribution and metabolism. GLP-1 also synergises insulin-dependent net hepatic glucose uptake (NHGU). When GLP-1 secretion is deficient post-prandial SMA blood flow is not increased and as NHGU is also reduced, hyperglycaemia follows. Portal venous glucose concentration is also raised, thereby retarding the passive component of intestinal glucose absorption. Increased pre-hepatic sinusoidal resistance combined with portal hypertension leading to opening of intrahepatic portosystemic collateral vessels are NASH-related mechanical defects that alter the balance between splanchnic and systemic distributions of glucose, hormones and incretins.The model reveals the latent contribution of portosystemic shunting in development of metabolic disease. This diverts splanchnic blood content away from the hepatic sinuses to the systemic circulation, particularly during the glucose absorptive phase of digestion, resulting in inappropriate increases in insulin-dependent systemic glucose metabolism. This hastens onset of hypoglycaemia and thence hyperglucagonaemia. The model reveals that low rates of GLP-1 secretion, frequently associated with T2DM and NASH, may be also be caused by splanchnic hypoglycaemia, rather than to intrinsic loss of incretin secretory capacity. These findings may have therapeutic implications on GLP-1 agonist or glucagon antagonist usage.

A computer model simulating human glucose absorption and metabolism in health and metabolic disease states.

A computer model designed to simulate integrated glucose-dependent changes in splanchnic blood flow with small intestinal glucose absorption, hormonal and incretin circulation and hepatic and systemic metabolism in health and metabolic diseases e.g. non-alcoholic fatty liver disease, (NAFLD), non-alcoholic steatohepatitis, (NASH) and type 2 diabetes mellitus, (T2DM) demonstrates how when glucagon-like peptide-1, (GLP-1) is synchronously released into the splanchnic blood during intestinal glucose absorption, it stimulates superior mesenteric arterial (SMA) blood flow and by increasing passive intestinal glucose absorption, harmonizes absorption with its distribution and metabolism. GLP-1 also synergises insulin-dependent net hepatic glucose uptake (NHGU). When GLP-1 secretion is deficient post-prandial SMA blood flow is not increased and as NHGU is also reduced, hyperglycaemia follows. Portal venous glucose concentration is also raised, thereby retarding the passive component of intestinal glucose absorption. Increased pre-hepatic sinusoidal resistance combined with portal hypertension leading to opening of intrahepatic portosystemic collateral vessels are NASH-related mechanical defects that alter the balance between splanchnic and systemic distributions of glucose, hormones and incretins.The model reveals the latent contribution of portosystemic shunting in development of metabolic disease. This diverts splanchnic blood content away from the hepatic sinuses to the systemic circulation, particularly during the glucose absorptive phase of digestion, resulting in inappropriate increases in insulin-dependent systemic glucose metabolism. This hastens onset of hypoglycaemia and thence hyperglucagonaemia. The model reveals that low rates of GLP-1 secretion, frequently associated with T2DM and NASH, may be also be caused by splanchnic hypoglycaemia, rather than to intrinsic loss of incretin secretory capacity. These findings may have therapeutic implications on GLP-1 agonist or glucagon antagonist usage.

Effects of Bolus and Continuous Nasogastric Feeding on Gastric Emptying, Small Bowel Water Content, Superior Mesenteric Artery Blood Flow, and Plasma Hormone Concentrations in Healthy Adults

Objective:We aimed to demonstrate the effect of continuous or bolus nasogastric feeding on gastric emptying, small bowel water content, and splanchnic blood flow measured by magnetic resonance imaging (MRI) in the context of changes in plasma gastrointestinal hormone secretion.Background:Nasogastric/nasoenteral tube feeding is often complicated by diarrhea but the contribution of feeding strategy to the etiology is unclear.Methods:Twelve healthy adult male participants who underwent nasogastric intubation before a baseline MRI scan, received 400 mL of Resource Energy (Nestle) as a bolus over 5 minutes or continuously over 4 hours via pump in this randomized crossover study. Changes in gastric volume, small bowel water content, and superior mesenteric artery blood flow and velocity were measured over 4 hours using MRI and blood glucose and plasma concentrations of insulin, peptide YY, and ghrelin were assayed every 30 minutes.Results:Bolus nasogastric feeding led to significant elevations in gastric volume (P < 0.0001), superior mesenteric artery blood flow (P < 0.0001), and velocity (P = 0.0011) compared with continuous feeding. Both types of feeding reduced small bowel water content, although there was an increase in small bowel water content with bolus feeding after 90 minutes (P < 0.0068). Similarly, both types of feeding led to a fall in plasma ghrelin concentration although this fall was greater with bolus feeding (P < 0.0001). Bolus feeding also led to an increase in concentrations of insulin (P = 0.0024) and peptide YY (P < 0.0001), not seen with continuous feeding.Conclusion:Continuous nasogastric feeding does not increase small bowel water content, thus fluid flux within the small bowel is not a major contributor to the etiology of tube feeding-related diarrhea.

Acarbose, the α-glucosidase inhibitor, attenuates the blood pressure and splanchnic blood flow responses to meal in elderly patients with postprandial hypotension concomitant with abnormal glucose metabolism.

Postprandial hypotension (PPH) is a unique clinical phenomenon in the elderly, but its underlying pathogenesis has not been completely elucidated, and drug treatment is still in clinical exploratory stage. The aim of the study was to evaluate the relationship between the fall in postprandial blood pressure and splanchnic blood flow, and to provide a theoretical basis for the treatment of PPH by taking acarbose. The study included 20 elderly inpatients diagnosed with PPH concomitant with abnormal glucose metabolism at stable condition. They were treated with 50 mg acarbose with their meal to observe the changes in blood pressure, heart rate, and blood glucose level, and to monitor the hemodynamics of the superior mesenteric artery (SMA) before and after treatment. Without acarbose treatment, patients after a meal had significantly decreased systolic and diastolic blood pressure, faster postprandial heart rate, higher postprandial glucose level at each period, and increased postprandial SMA blood flow compared with that at fasting state (P<0.05). Acarbose treatment significantly attenuated the decrease of postprandial systolic blood pressures from 35.50±12.66 to 22.25±6.90 mmHg (P=0.000), the increase of heart rate from 9.67±5.94 to 5.33±3.20 beats/min (P=0.016), the increase of postprandial blood glucose from 3.55±1.69 to 2.28±1.61 mmol/l (P=0.000), the increase of postprandial SMA blood flow from 496.80±147.15 to 374.55±97.89 ml/min (P=0.031), and the incidence of PPH, syncope, falls, dizziness, weakness, and angina pectoris (P<0.05). The maximal decrease of postprandial systolic blood pressure was positively associated with the maximal increase in postprandial SMA blood flow (r=0.351, P=0.026). Acarbose treatment showed no significant side effects. The increase in postprandial splanchnic perfusion is one of the reasons for PPH formation. Acarbose may exert its role in PPH treatment by reducing postprandial gastrointestinal blood perfusion. Giving 50 mg acarbose with a meal to treat PPH concomitant with abnormal glucose metabolism is effective and safe in very old patients.

Thalidomide Improves the Intestinal Mucosal Injury and Suppresses Mesenteric Angiogenesis and Vasodilatation by Down-Regulating Inflammasomes-Related Cascades in Cirrhotic Rats.

Background and AimsBy blocking TNFα-related effects, thalidomide not only inhibits hepatic fibrogenesis but improves peripheral vasodilatation and portal hypertension in cirrhotic rats. Nonetheless, the investigation of thalidomide's effects on splanchnic and collateral microcirculation has been limited. Our study explored the roles of intestinal and mesenteric TNFα along with inflammasome-related pathway in relation to cirrhosis and the splanchnic/collateral microcirculation.MethodsUsing in vivo and in vitro approaches, mechanisms of the effects of thalidomide on intestinal and mesenteric inflammatory, vasodilatory and angiogenic cascades-related abnormalities were explored in cirrhotic rats that had received 1-month thalidomide (C-T) treatment.ResultsIn cirrhotic rats, high tumor necrosis factor (TNF)α, vascular endothelial growth factor (VEGF) and nitric oxide (NO)x levels were associated with the NOD-like receptors protein 3 (NLRP3), IL-1β and caspase-1 inflammasome over-expression in splenorenal shunt and mesenteric tissues. The thalidomide-related inhibition of mesenteric and splenorenal shunt inflammasome expression was accompanied by a significantly decreased intestinal mucosal injury and inflammasome immunohistochemical staining expression. Suppression of various angiogenic cascades, namely VEGF-NOS-NO, was paralleled by a decrease in mesenteric angiogenesis as detected by CD31 immunofluorescence staining and by reduced portosystemic shunting (PSS) in C-T rats. The down-regulation of the mesenteric and collateral vasodilatory VEGF-NOS-NO cascades resulted in a correction of vasoconstrictive hypo-responsiveness and in an attenuation of vasodilatory hyper-responsiveness when analyzed by in situ perfusion of the superior mesenteric arterial (SMA) and portosystemic collaterals. There was also a decrease in SMA blood flow and an increase in SMA resistance in the C-T rats. Additionally, acute incubation with thalidomide abolished TNFα-augmented VEGF-mediated migration of and tube formation of human umbilical vein endothelial cells, which was accompanied by corresponding changes in inflammatory and angiogenic substances release.ConclusionsThe suppression of inflammasome over-expression by chronic thalidomide treatment ameliorates inflammatory, angiogenic and vasodilatory cascades-related pathogenic changes in the splanchnic and collateral microcirculation of cirrhotic rats. Thalidomide seems to be a promising agent that might bring about beneficial changes to the disarrangements of peripheral, hepatic, splanchnic and collateral systems in cirrhosis.

Feasibility of measuring superior mesenteric artery blood flow during cardiac surgery under hypothermic cardiopulmonary bypass using transesophageal echocardiography: An observational study.

Background:Abdominal complications being rare but results in high mortality, commonly due to splanchnic organ hypoperfusion during the perioperative period of cardiac surgery. There are no feasible methods to monitor intraoperative superior mesenteric artery blood flow (SMABF). Hence, the aim of this study was to evaluate the feasibility and to measure SMABF using transesophageal echocardiography (TEE) during cardiac surgery under hypothermic cardiopulmonary bypass (CPB).Methodology:Thirty-five patients undergoing elective cardiac surgery under CPB were enrolled. Heart rate, mean arterial pressure (MAP), cardiac output (CO), SMABF, superior mesenteric artery (SMA) diameter, superior mesentric artery blood flow over cardiac output (SMA/CO) ratio and arterial blood lactates were recorded at three time intervals. T0: before sternotomy, T1: 30 min after initiation of CPB and T2: after sternal closure.Results:SMA was demonstrated in 32 patients. SMABF, SMA diameter, SMA/CO, MAP and CO decreased significantly (P < 0.0001) between T0 and T1, increased significantly (P ≤ 0.001) between T0 and T2. Lactates increased progressively from T0 to T2.Conclusion:Study shows that there is decrease in SMABF during CPB and returns to baseline after CPB. Hence, it is feasible to measure SMABF using TEE in patients undergoing cardiac surgery under hypothermic CPB. TEE can be a promising tool in detecting and preventing splanchnic hypoperfusion during perioperative period.

Gastric emptying, postprandial blood pressure, glycaemia and splanchnic flow in Parkinson's disease.

To determine gastric emptying, blood pressure, mesenteric artery blood flow, and blood glucose responses to oral glucose in Parkinson's disease. Twenty-one subjects (13 M, 8 F; age 64.2 ± 1.6 years) with mild to moderate Parkinson's disease (Hoehn and Yahr score 1.4 ± 0.1, duration of known disease 6.3 ± 0.9 years) consumed a 75 g glucose drink, labelled with 20 MBq (99m)Tc-calcium phytate. Gastric emptying was quantified with scintigraphy, blood pressure and heart rate with an automated device, superior mesenteric artery blood flow by Doppler ultrasonography and blood glucose by glucometer for 180 min. Autonomic nerve function was evaluated with cardiovascular reflex tests and upper gastrointestinal symptoms by questionnaire. The mean gastric half-emptying time was 106 ± 9.1 min, gastric emptying was abnormally delayed in 3 subjects (14%). Systolic and diastolic blood pressure fell (P < 0.001) and mesenteric blood flow and blood glucose (P < 0.001 for both) increased, following the drink. Three subjects (14%) had definite autonomic neuropathy and 8 (38%) had postprandial hypotension. There were no significant relationships between changes in blood pressure, heart rate or mesenteric artery blood flow with gastric emptying. Gastric emptying was related to the score for autonomic nerve function (R = 0.55, P < 0.01). There was an inverse relationship between the blood glucose at t = 30 min (R = -0.52, P < 0.05), while the blood glucose at t = 180 min was related directly (R = 0.49, P < 0.05), with gastric emptying. In mild to moderate Parkinson's disease, gastric emptying is related to autonomic dysfunction and a determinant of the glycaemic response to oral glucose.

Relationship between postprandial hypotension and superior mesenteric artery blood flow in elderly patients aged 80 years and over

Objective To explore the relationship between the fall of postprandial blood pressure and superior mesenteric artery (SMA) blood flow in elderly patients aged 80 years and over. Methods The study included 25 inpatients aged 80 years and over with postprandial hypotension (PPH group) and 27 age-matched cases without PPH (control group). The changes in blood pressure and the hemodynamics of SMA at fasting stage and 2 hour after meal were observed. The differences between the two groups were compared. Results The incidence of abnormal glucose metabolism (including diabetes and impaired glucose tolerance) was significantly higher in PPH group than in control group〔92.0% (23 cases) vs. 40.7% (11 cases), P 0.05). The blood pressure in two groups at different time points was decreased after meal significantly as compared with that at fasting stage (all P>0.05). The maximal fall of postprandial systolic blood pressure and diastolic blood pressure was significantly increased in PPH group as compared with in control group〔(31.3±14.8) mmHg (1 mmHg=0.133 kPa) vs. (6.9±16.5) mmHg, (13.1±6.6) mmHg vs. (9.0±3.9) mmHg, both P 0.05). The maximal increase of postprandial SMA blood flow was larger in PPH group than in control group〔(550.5±149.5) ml/min vs. (312.8±241.4) ml/min, P<0.05〕. The maximal fall of postprandial systolic blood pressure was positively associated with the maximal increase of postprandial SMA blood flow (r=0.352, P=0.025). Conclusions The fall of postprandial blood pressure is associated with the increase of the SMA blood flow. Postprandial increase in splanchnic perfusion is one of the mechanisms for the formation of PPH. Key words: Hypotension; Postprandial poriod; Mesenteric artery

Splanchnic Hemodynamics and Intestinal Vascularity in Crohn's Disease: An In Vivo Evaluation Using Doppler and Contrast-Enhanced Ultrasound and Biochemical Parameters

Crohn's disease (CD) is characterized by inflammation and angiogenesis of affected bowel. We evaluated the correlation among vascularity of intestinal wall in CD, splanchnic hemodynamics, clinical activity and biochemical parameters of inflammation and angiogenesis. Sixteen patients with ileal CD and 10 healthy controls were investigated by means of Doppler ultrasound of the superior mesenteric artery and color Doppler and contrast-enhanced ultrasound of the ileal wall. In parallel, serum levels of vascular endothelial growth factor, tumor necrosis factor-α (TNF-α) and nitric oxide, before and 30 min after a standard meal, were evaluated. In CD patients, there was a significant post-prandial reduction in the resistance index and pulsatility index of the superior mesenteric artery, associated with increased levels of nitric oxide and decreased amounts of TNF-α. A correlation was observed between vascular endothelial growth factor and contrast-enhanced ultrasound parameters of intestinal wall vascularity (r = 0.63–0.71, p < 0.05) and between these parameters and superior mesenteric artery blood flow after fasting (resistance and pulsatility indexes: r = −0.64 and −0.72, p < 0.05). Our results revealed a post-prandial increase in nitric oxide and decrease in TNF-α in CD patients in vivo. They also confirm the role of vascular endothelial growth factor in angiogenesis and in pathologic vascular remodeling of CD and its effect on splanchnic blood flow.

Intestinal blood flow by Doppler ultrasound: the impact of clarithromycin treatment for feeding intolerance in preterm neonates

Objective: To compare the blood flow velocities of superior mesenteric artery (SMA) before versus after clarithromycin treatment for feeding intolerance in very low-birth weight infants.Methods: A prospective study was conducted in a group of infant <1500 g with feeding intolerance who received clarithromycin 7.5 mg/kg/dose bid. Before and at the third day of the clarithromycin therapy, SMA blood flow velocity was measured with Doppler ultrasound.Results: SMA peak systolic velocity (PSV) and mean systolic velocity (MV) on the third day of the treatment was found significantly higher than the initial measurement (p = 0.013 and p = 0.027, respectively). End diastolic velocity of the SMA did not change with clarithromycin therapy (p = 0.113). There were no significant changes about pulsatility and resistive index of SMA with regard to clarithromycin therapy.Conclusion: Clarithromycin effects the splanchnic circulation. The rise in PSV and MV in SMA is remarkable. These results suggest that the splanchnic blood flow increases significantly after clarithromycin usage.

Effects of norepinephrine on tissue perfusion in a sheep model of intra-abdominal hypertension.

BackgroundThe aim of the study was to describe the effects of intra-abdominal hypertension (IAH) on regional and microcirculatory intestinal blood flow, renal blood flow, and urine output, as well as their response to increases in blood pressure induced by norepinephrine.MethodsThis was a pilot, controlled study, performed in an animal research laboratory. Twenty-four anesthetized and mechanically ventilated sheep were studied. We measured systemic hemodynamics, superior mesenteric and renal blood flow, villi microcirculation, intramucosal-arterial PCO2, urine output, and intra-abdominal pressure. IAH (20 mm Hg) was generated by intraperitoneal instillation of warmed saline. After 1 h of IAH, sheep were randomized to IAH control (n = 8) or IAH norepinephrine (n = 8) groups, for 1 h. In this last group, mean arterial pressure was increased about 20 mm Hg with norepinephrine. A sham group (n = 8) was also studied. Fluids were administered to prevent decreases in cardiac output. Differences between groups were analyzed with two-way repeated measures of analysis of variance (ANOVA).ResultsAfter 2 h of IAH, abdominal perfusion pressure decreased in IAH control group compared to IAH norepinephrine and sham groups (49 ± 11, 73 ± 11, and 86 ± 15 mm Hg, P < 0.0001). There were no differences in superior mesenteric artery blood flow, intramucosal-arterial PCO2, and villi microcirculation among groups. Renal blood flow (49 ± 30, 32 ± 24, and 102 ± 45 mL.min−1.kg−1, P < 0.0001) and urinary output (0.3 ± 0.1, 0.2 ± 0.2, and 1.0 ± 0.6 mL.h−1.kg−1, P < 0.0001) were decreased in IAH control and IAH norepinephrine groups, compared to the sham group.ConclusionsIn this experimental model of IAH, the gut and the kidney had contrasting responses: While intestinal blood flow and villi microcirculation remained unchanged, renal perfusion and urine output were severely compromised.Electronic supplementary materialThe online version of this article (doi:10.1186/s40635-015-0046-1) contains supplementary material, which is available to authorized users.

Effects of antenatal magnesium exposure on intestinal blood flow and outcome in preterm neonates.

This study aims to investigate the effects of antenatal magnesium sulfate on intestinal blood flow in preterm neonates. In this prospective case-match study, 25 preterm neonates exposed to magnesium sulfate antenatally were included (study group). Overall, 25 gestational age-matched neonates who had no exposure to magnesium constituted the control group. Serial daily Doppler flow measurements of superior mesenteric artery (SMA) were performed. The time to reach full feeds, first meconium passage were assessed. Presence of feeding intolerance or necrotizing enterocolitis was recorded. Blood flow velocities of SMA were not different between the groups during the first five postnatal days. However, SMA blood flow showed an increasing trend in the control group unlike the study group (control group, p < 0.001; study group, p = 0.29). There was no significant difference between the two groups regarding the time to reach full feeds or first meconium passage and presence of feeding intolerance. No case of necrotizing enterocolitis was seen. Antenatal magnesium does not significantly affect intestinal blood flow, but it seems to attenuate the increasing trend of the intestinal blood flow in the early postnatal days. However, this study failed to show any impact of this finding on clinical outcomes.

A Doppler velocimetry evaluation of intestinal blood flow characteristics in neonates receiving intravenous immunoglobulin therapy: a prospective observational study.

To evaluate intestinal blood flow changes after intravenous immunoglobulin (IVIg) infusion among neonates with Rh isoimmunization and alloimmune thrombocytopenia. This prospective observational study was conducted in level III NICU from July 2011 through August 2012. Thirty three consecutive instances (30 neonates) of IVIg treatment (1g/kg) were studied. Celiac (CA) and superior mesenteric artery (SMA) doppler evaluations were performed immediately prior (baseline), immediately after and 12 to18h following IVIg infusion. Peak systolic velocity, end diastolic velocity, time-averaged mean velocity, pulsatility index, resistive index and systolic/diastolic ratio were measured. The doppler indices measured immediately after and 12 to 18h after IVIg infusion were compared with the baseline values. The mean gestation and birth weight of the cohort were 36 ± 2wk and 2597 ± 563g respectively. Doppler flow variables measured immediately after and 12 to 18h after IVIg were comparable to baseline values, in both the arteries. However, systolic/diastolic ratio in SMA immediately post-IVIg was lower than baseline, [median (IQR): 5 (3, 9) vs. 7 (4, 14), respectively; p=0.02]. None of the study infants developed feed intolerance or necrotizing enterocolitis (NEC). There was no significant change in the celiac and SMA blood flows following IVIg therapy in neonates with Rh isoimmunization and alloimmune thrombocytopenia.