Mesenteric Blood Flow Velocity Research Articles

The effects of nutrition on mesenteric oxygenation among neonates with neonatal encephalopathy: a randomized clinical trial.

We aimed to evaluate the effects of minimal enteral nutrition (MEN) on mesenteric blood flow and oxygenation with Doppler USG and Near Infrared Spectroscopy (NIRS) during therapeutic hypothermia (TH) in babies with HIE. This prospective, randomized-controlled study was composed of infants receiving MEN (study group, n = 30) and infants who were not fed (control group, n = 30) during hypothermia. Infants were monitored continuously with NIRS and mesenteric blood flow velocities were measured with Doppler USG before and after feeding. The mean gestational age and birth weight for the study and control group were 38.73 ± 1.5-39.09 ± 1.02 weeks and 3076 ± 280.4-3295 ± 391 grams, respectively. Time to reach full enteral nutrition and hospital stay were significantly shorter in the study group (p = 0.049, p = 0.016). Infants in the study group experienced less feeding intolerance (p = 0.006). No infant developed necrotizing enterocolitis (NEC) in both groups. No difference was determined in pre- and post-feeding cerebral rSO2 measurements during TH and normothermia. Mesenteric rSO2, CSOR, and mesenteric blood flow measurements in the study group during normothermia were significantly increased, respectively (p = 0.03, p < 0.01, p < 0.01). In our study, we observed that MEN during TH does not lead to a significant change in cerebral and mesenteric oxygenation. Although we did not observe an increase in blood flow and oxygenation, the absence of NEC and a lower incidence of feeding intolerance in the study group may suggest that feeding during TH is safe and feasible. MEN during TH treatment does not lead to a significant change in cerebral and mesenteric oxygenation. This is the first study evaluating the effects of MEN on mesenteric oxygenation and blood flow velocities in infants with hypoxic-ischemic encephalopathy during TH with Doppler USG and NIRS, concomitantly. MEN during TH may be safe and feasible.

The association between NIRS and Doppler ultrasonography in preterm infants with patent ductus arteriosus

Objective: To determine if near-infrared spectroscopy (NIRS), which is easier to obtain than Doppler ultrasonography (USG), may be used in accordance with Doppler USG to provide additional data for assessment of organ blood flow velocities in preterm infants with hemodynamically significant PDA.Study design: Thirty-one infants who were treated with ibuprofen for closure of PDA were monitored continuously with NIRS. Cerebral, mesenteric, and renal arterial blood flow velocities were measured with Doppler USG before and after the treatment.Results: While cerebral, mesenteric, and renal fractional oxygen extraction (FTOE) measurements decreased significantly (p = .042, p < .001, p < .001, respectively), NIRS measurements (p = .016, p < .001, p < .001, respectively) and mean blood flow velocities (p = .003, p = .011, p = .002, respectively) increased significantly after the treatment. There was a significant correlation between pretreatment cerebral and mesenteric FTOE and resistive index (RI) values (r = 0.45, p = .01, and r = 0.46, p = .01, respectively). However, no correlation was observed between renal FTOE values and renal RI (r = 0.33, p = .06). Posttreatment cerebral, renal, and mesenteric FTOE values correlated positively with corresponding RI (r = 0.41, p = .02; r = 0.39, p = .02; r = 0.65, p < 01; respectively). Pretreatment and posttreatment cerebral, mesenteric, and renal FTOE values and arterial mean velocities were inversely correlated (pretreatment: r = 0.69, p < .01; r = 0.72, p < .01; r = 0.77, p < .01; posttreatment: r = 0.54, p = .01; r = 0.69, p < .01; r = 0.38, p = .01; respectively).Conclusion: As Doppler and NIRS measurements correlated significantly, we concluded that NIRS might be used in monitoring organ blood flow in preterm infants with PDA, which may provide additional data for management of this condition.

Blood transfusion in preterm infants improves intestinal tissue oxygenation without alteration in blood flow.

The objective of the study was to investigate the splanchnic blood flow velocity and oximetry response to blood transfusion in preterm infants according to postnatal age. Preterm infants receiving blood transfusion were recruited to three groups: 1-7 (group 1; n = 20), 8-28 (group 2; n = 21) and ≥29 days of life (group 3; n = 18). Superior mesenteric artery (SMA) peak systolic (PSV) and diastolic velocities were measured 30-60 min pre- and post-transfusion using Doppler ultrasound scan. Splanchnic tissue haemoglobin index (sTHI), tissue oxygenation index (sTOI) and fractional tissue oxygen extraction (sFTOE) were measured from 15-20 min before to post-transfusion using near-infrared spectroscopy. The mean pretransfusion Hb in group 1, 2 and 3 was 11, 10 and 9 g/dl, respectively. The mean (SD) pretransfusion SMA PSV in group 1, 2 and 3 was 0·63 (0·32), 0·81 (0·33) and 0·97 (0·40) m/s, respectively, and this did not change significantly following transfusion. The mean (SD) pretransfusion sTOI in group 1, 2 and 3 was 36·7 (19·3), 44·6 (10·4) and 41·3 (10·4)%, respectively. The sTHI and sTOI increased (P < 0·01), and sFTOE decreased (P < 0·01) following transfusion in all groups. On multivariate analysis, changes in SMA PSV and sTOI following blood transfusion were not associated with PDA, feeding, pretransfusion Hb and mean blood pressure. Pretransfusion baseline splanchnic tissue oximetry and blood flow velocity varied with postnatal age. Blood transfusion improved intestinal tissue oxygenation without altering mesenteric blood flow velocity irrespective of postnatal ages.

Splanchnic oxygenation patterns at first feed in stable preterm infants: Correlation with feeding intolerance development

Introduction and aim: Due to their gastro-intestinal immaturity, preterm infants aremore prone to develop feeding intolerance (FI), which frequently hampers the establishment of an adequate enteral nutrition. Previous Doppler studies showed an impaired mesenteric bloodflowvelocity after thefirst feed inpreterm infants developing FI. We aimed to evaluate splanchnic oxygenation patterns in response to the first enteral feed and possible correlations with subsequent FI development. Methods: Stable preterm infants (gestational age ≤34 weeks) underwent a 3-hourNear-Infrared Spectroscopymonitoring at first enteral feed administration. The enrolled infants were retrospectively allocated into 2 groups in relation to the development of FI during their hospital stay (food intolerance [FI] vs. food tolerance [FT]). Mann–Whitney U test was used to compare splanchnic oxygenation patterns between the two groups. Statistical significance was set at p<0.05. Results: Seventy-eight preterm infants were enrolled; 30 out of 78 developed FI during their hospital stay. Splanchnic oxygenation patterns in response to the first feed differed significantly between two groups, with lower values of splanchnic tissue oxygenation in the FI group during the first 35′ after the first feed and from 1h 30′ on (p<0.05). Conclusions: Splanchnic oxygenation in response to the first enteral feed is significantly lower in preterm infants developing FI. This finding could reflect an early impairment of mesenteric regional circulation with subsequent tissue hypoxia, which might possibly predispose to the development of FI.

Effects of a patent ductus arteriosus on postprandial mesenteric perfusion in premature baboons.

Superior mesenteric artery flow increases after a feeding to meet the intestines' increased metabolic demands. Although a patent ductus arteriosus can affect superior mesenteric artery perfusion in nonfeeding infants, there is no information about its effects on the hyperemic response that follows a feeding. Our goal was to study the effects of a patent ductus arteriosus on superior mesenteric artery perfusion in preterm baboons. Preterm baboons were delivered at 67% gestation and ventilated for 14 days. Enteral feedings were begun and advanced per protocol. Feeding studies were performed between days 10 and 14. Thirty-one studies were performed in animals with a closed ductus; 21 studies in those with a moderate patent ductus arteriosus shunt (pulmonary-to-systemic blood flow ratio>or=2:1). Two-dimensional echocardiographic and Doppler examinations were performed before and 10 and 30 minutes after a feeding. The groups were similar in birth weights, feeding volumes, and age at time of study. During the preprandial period, baboons with a moderate patent ductus arteriosus had significantly lower blood pressures and systemic blood flows than animals with a closed ductus. Preprandial superior mesenteric artery-blood flow velocities did not differ between the open and closed ductus groups. Animals with a closed ductus increased their superior mesenteric artery-velocities (diastolic and mean) and decreased their superior mesenteric artery relative-vascular-resistance (mean blood pressure/mean superior mesenteric artery-velocity) by 10 minutes after the feeding. By 30 minutes after the feeding, the values were returning to their preprandial values. In contrast, in baboons in the patent ductus arteriosus group, there were no significant changes in superior mesenteric artery-velocity or resistance after the feeding, and superior mesenteric artery-velocities were significantly lower than those in the closed ductus group. A moderate patent ductus arteriosus shunt limits the ability of the preterm newborn baboon to increase its postprandial mesenteric blood flow velocity. We speculate that this may interfere with its ability to meet increased intestinal metabolic demands and may contribute to feeding difficulties.

Blood Transfusion Alters the Superior Mesenteric Artery Blood Flow Velocity Response to Feeding in Premature Infants

Packed red blood cell transfusion may increase the risk of necrotizing enterocolitis in premature infants. We hypothesize that the postprandial increase in mesenteric blood flow velocity (MBFV) would not be altered by a blood transfusion in premature infants. Infants born at 25 to 32 weeks and feeding at least 60 mL/kg/d who required a transfusion were randomized within each of two weight strata to feed or not feed during the transfusion. Mean, peak systolic, and end diastolic Doppler MBFV was measured 30 minutes before and after feedings at baseline (anemic) and with the first feeding posttransfusion. Twenty-two infants (27.3 +/- 2.3 weeks' gestational age; hemoglobin [HgB] 9.3 +/- 1.3 g/dL) were studied on day of life 3 to 71 (mean 31.2 days) and a corrected gestational age of 31.8 +/- 2.9 weeks. In the entire cohort, the peak systolic ( P = 0.02) and the mean ( P = 0.01) MBFV increased in response to feeding in the anemic but not the transfused state. On subgroup analysis, only anemic infants > 1250 g ( N = 12, HgB 8.6 +/- 0.9 g/dL) had an increase in peak systolic ( P = 0.04) and mean ( P = 0.006) MBFV with feeding. In conclusion, the MBFV increases in response to feeding in anemic preterm infants > 1250 g. We speculate that the lack of response to feeding in the immediate posttransfusion state may contribute to the development of transfusion-associated necrotizing enterocolitis.

Cerebral and Splanchnic Hemodynamics after Duct Ligation in Very Low Birth Weight Infants

To describe mesenteric and cerebral blood flow velocities after surgical patent ductus arteriosus (PDA) closure in premature infants. We measured middle cerebral artery (MCA), celiac artery (CA), and superior mesenteric artery (SMA) Doppler ultrasound scanning blood flow velocity (BFV) preoperatively, 3 and 24 hours after ligation. We studied 32 infants, with a mean (+/- SD) birthweight of 762 +/- 170 g and gestational age of 25.6 +/- 1.4 weeks at a mean age of 34 +/- 13 days. Significant changes in end-diastolic (EDV), average velocity (AV), and vascular resistance were measured in all 3 vessels by 3 hours. AV increased significantly in the CA and SMA within 3 hours; however, no significant increase in MCA AV was found until 24 hours after surgery. PDA ligation significantly changes BFV in the MCA, CA, and SMA. In the MCA vascular tone is acutely modulated, with no change in AV at 3 hours. In the CA and SMA, AV increases acutely after ligation. These different patterns of change in BFV suggest region-specific adaptation to surgical PDA closure.

Intrauterine growth restriction, visceral blood flow velocity and exocrine pancreatic function

BackgroundAnimal models and observations in human neonates suggest fetal exocrine pancreas vulnerability to reduced maternofetal blood flow. We investigated the relationship between superior mesenteric artery blood flow velocity (sma bfv) and exocrine pancreatic function, in a cohort of very low birth weight (VLBW) babies.Group 1: 9 babies < 3rd percentile for birth weight. Antenatally, all had absent or reversed diastolic flow on Doppler ultrasound of the umbilical artery (UA).Group2: 18 babies > 10th percentile for birth weight.FindingsAll had Doppler ultrasound scan of the superior mesenteric artery (sma), by same operator (RMN), on day 1 of life before commencement of enteral feeding. Stool samples assayed for faecal chymotrypsin and weekly serum samples assayed for amylase and lipase (kinetic colorimetric assay) from days 1 to 14 of life.Growth restricted babies had significantly lower sma bfv values compared with appropriately grown preterm babies. Faecal chymotrypsin levels were also lower but this difference did not achieve statistical significance. Both groups had serum lipase levels detectable in adult concentrations. Serum amylase was undetectable in either group.ConclusionBabies with previous in-utero blood flow redistribution may exhibit altered gut ontogeny with re-setting of mesenteric blood flow velocities and altered exocrine pancreatic function.

Effects of nociceptin/orphanin FQ (N/OFQ) and the N/OFQ antagonist [Nphe1,Arg 14,Lys15]N/OFQ‐NH2 on rat mesenteric blood flow in vivo

Nociceptin (N/OFQ) is the endogenous ligand for the nociceptin receptor (NOP). Our previous studies have demonstrated that N/OFQ is dilator within the rat mesenteric microcirculation in vivo, and this response is inhibited by the novel N/OFQ antagonist [Nphe1,Arg14,Lys15]N/OFQ-NH2 (UFP101). However, its effects on microvascular blood flow are uncertain. Male Wistar rats (220–300g) were anesthestized with thiopental (30mg/kg bolus, 40–90 mg/kg/hr infusion, i.v). The jugular vein was cannulated for administration of 1μm fluorescent microspheres (0.1mL/100g), N/OFQ (0.6, 3, 15 and 60ng/kg) and UFP101 (60,150nmol/kg). Mesenteric blood flow velocity and blood flow were measured in arterioles and venules using intravital microscopy. Compared to baseline (BL) N/OFQ caused a decrease in velocity (arterioles/venules, BL: 2932 ±27 /1230 ±370μm/s, 15nmol/kg N/OFQ: 2089±180/755 ± 250 μm/s) (P<0.05), responses that were abolished by 150nmol/kg UFP101. N-OFQ only induced a slight decrease in blood flow (NS) in arterioles and venules (BL: 0.05 ± 0.00/0.02 ± 0.02mL/min, 15nmol/kg N/OFQ: 0.04 ± 0.01/0.04 ± 0.01 mL/min). UFP101 alone had no effect on either velocity or blood flow. In conclusion, blood flow to the mesentery is maintained in response to N/OFQ.

Mesenteric blood flow velocities in the newborn with single-ventricle physiology: Modified Blalock-Taussig shunt versus right ventricle-pulmonary artery conduit

Neonates with ductal-dependent single-ventricle congenital heart disease palliated with a modified Blalock-Taussig shunt (mBTS) commonly have retrograde diastolic flow in the aorta, which may place them at increased risk of mesenteric ischemia. Recently, palliation with a right ventricle-to-pulmonary artery conduit, known as the Sano procedure, has been shown to eliminate retrograde diastolic flow, theoretically leading to better systemic perfusion. To compare the changes in superior mesenteric artery (SMA) and celiac artery velocities and flow after a bolus enteral feed in patients with single-ventricle congenital heart disease palliated with an mBTS vs. those palliated with the right ventricle-to-pulmonary artery conduit. Prospective clinical study. Cardiothoracic intensive care unit and pediatric ward of a tertiary care children's hospital. A total of 27 patients with single-ventricle congenital heart disease (15 with mBTS, 12 with Sano) after stage-1 palliation. Doppler ultrasound of the SMA and celiac artery was performed 30 mins before and after a bolus enteral feed. SMA and celiac artery peak systolic flow velocity, mean flow velocity, and time-velocity integral were measured. After a bolus enteral feed, 8 of 15 infants palliated with an mBTS had retrograde diastolic flow through the SMA yet demonstrated significant increases in all variables of both the SMA and celiac artery flow velocities (SMA peak systolic flow velocity: 0.96 +/- 0.33 vs. 1.2 +/- 0.4 m/sec, p = .01). Those palliated with the Sano procedure did not demonstrate SMA retrograde diastolic flow but also did not have any significant changes in their mesenteric flow variables (SMA peak systolic flow velocity: 0.79 +/- 0.16 vs. 0.89 +/- 0.26 m/sec, p = .2). Postprandial retrograde diastolic flow was observed in the majority of patients palliated with an mBTS vs. none of the patients in the Sano group. However, contrary to expectations, postprandial mesenteric blood flow velocities in those palliated with an mBTS are significantly higher than in Sano patients, although the increase is not as high as that historically seen in normal neonates. This may place this population at risk for mesenteric ischemia and feeding intolerance in the postoperative period, and the risk may be even greater for those neonates palliated with a right ventricle-to-pulmonary artery conduit.

Mesenteric blood flow response to feeding after systemic-to-pulmonary arterial shunt palliation

Background We hypothesized that the splanchnic circulation protects against diastolic steal through a systemic-to-pulmonary arterial shunt by reducing its resistance. To test the hypothesis we compared the basal and postprandial mesenteric blood flow velocities and vascular resistance in infants after shunt palliation for their underlying cyanotic heart disease with those in nonshunted infants. Methods The basal and postprandial superior mesenteric arterial (SMA) time-average flow velocity (TAMV), end-diastolic flow velocity (EDFV), and relative resistance were assessed in 23 infants with congenital heart disease. The findings in the 9 shunted infants (group I) were compared with those in 14 nonshunted ones (group II). Results In group II, TAMV (0.25 ± 0.07 versus 0.33 ± 0.09 m/s, p < 0.001) and EDFV (0.08 ± 0.04 versus 0.11 ± 0.04 m/s, p = 0.003) increased, while SMA relative resistance decreased (297 ± 121 versus 198 ± 73 mm Hg/ms −1, p < 0.001) postprandially. Similarly, in group I, TAMV (0.35 ± 0.13 versus 0.48 ± 0.19 m/s, p = 0.008) increased, while SMA relative resistance decreased (182 ± 61 versus 116 ± 38 mm Hg/ms −1, p = 0.005) after feeding. However, whereas basal and postprandial diastolic flow was antegrade in group II, absent or retrograde diastolic flow was characteristic of group I (preprandial, −0.10 ± 0.07 m/s; postprandial, −0.13 ± 0.06 m/s). Furthermore, group I had significantly lower SMA relative resistance both before ( p = 0.02) and after ( p = 0.006) feeding. Conclusions Profound disturbance of splanchnic perfusion occurs in infants palliated with a systemic-to-pulmonary arterial shunt. Their basal and postprandial SMA diastolic blood flow is either absent or reversed. The lowering of basal and postprandial resistance of the splanchnic circulation probably represents an adaptive mechanism to counteract such diastolic steal.

Hypotension in the Neonate

After completing this article, readers should be able to: 1. Describe the relationship between blood pressure and birthweight, gestational age, and postnatal age. 2. Delineate potential negative consequences of treating hypotension in the neonate. 3. Characterize the evaluation of a neonate prior to treating suspected hypotension. 4. Describe current and potential future therapeutic options for treatment of neonatal hypotension. Deciding which neonates require treatment for a low arterial blood pressure (BP) often is difficult. To some extent, this has been due to a lack of normative BP data, particularly among preterm neonates. However, we now have reliable data relating birthweight, gestational age, and postnatal age to BP in term and preterm neonates. Nevertheless, the management of suspected hypotension in various neonatal intensive care units differs. Although there are good studies comparing various modes of therapy, prospective trials relating long-term outcome to treatment versus no treatment at various BP values have not been performed. Concern about the deleterious effects of hypotension is greater for preterm neonates primarily because of the relative inability to regulate cerebral blood flow in preterm neonates compared with infants who are born at term. ### Preterm Neonates Clearly, the primary issue surrounding possible hypotension in preterm neonates is the concern that these infants may experience impaired central nervous system perfusion, leading to ischemic damage. Low arterial BP has been associated with a decrease in cerebral blood flow, and the apparent impairment of autoregulation of cerebral blood flow in distressed infants emphasizes the importance of preventing both hypotension and rapid increases in BP in preterm neonates. Impaired autoregulation, demonstrated by near-infrared spectroscopy, and BP have been shown to be predictive of germinal matrix-intraventricular hemorrhage, periventricular leukomalacia, or both. When mean blood pressure (MBP) was measured continuously in neonates at gestational ages 26 to 30 weeks, a highly significant relationship was demonstrated between MBP less than …

Frequency modulation of mesenteric and renal vascular resistance.

The hypothesis was tested that low-frequency vasomotions in individual vascular beds are integrated by the cardiovascular system, such that new fluctuations at additional frequencies occur in arterial blood pressure. In anesthetized rats (n = 8), the sympathetic splanchnic and renal nerves were simultaneously stimulated at combinations of frequencies ranging from 0.075 to 0.8 Hz. Blood pressure was recorded together with mesenteric and renal blood flow velocities. Dual nerve stimulation at low frequencies (<0.6 Hz) caused corresponding oscillations in vascular resistance and blood pressure, whereas higher stimulation frequencies increased the mean levels. Blood pressure oscillations were only detected at the individual stimulation frequencies and their harmonics. The strongest periodic responses in vascular resistance were found at 0.40 +/- 0.02 Hz in the mesenteric and at 0.32 +/- 0.03 Hz (P < 0.05) in the renal vascular bed. Thus frequency modulation of low-frequency vasomotions in individual vascular beds does not cause significant blood pressure oscillations at additional frequencies. Furthermore, our data suggest that sympathetic modulation of mesenteric vascular resistance can initiate blood pressure oscillations at slightly higher frequencies than sympathetic modulation of renal vascular resistance.

Changes in cerebral, renal and mesenteric blood flow velocity during continuous and bolus infusion of indomethacin

Vasoconstriction induced by bolus injection of indomethacin reduces organ perfusion and has been related to the well‐known side effects of indomethacin given for closure of the patent ductus arteriosus (PDA). The aim of the study was to compare the changes in cerebral, renal and mesenteric blood flow velocities after continuous infusion versus bolus injection of indomethacin for closure of the PDA. Thirty‐two preterm infants (range 26–35 wk gestational age) with PDA were randomly assigned to receive the same amount of indomethacin either as three bolus injections (n= 14) or as a continuous infusion (n= 18) over 36 h. Blood flow velocities were measured in the internal carotid, right renal and superior mesenteric arteries at baseline and serially at 10, 30, 60 and 120 min and 12, 24, 36 and 48 h after the start of indomethacin treatment. There were no differences in blood flow velocities between both groups at baseline. During continuous infusion of indomethacin there was no significant change in the cerebral, renal and mesenteric blood flow velocities, whereas the flow velocities in the infants receiving bolus injections decreased significantly during the first 2 h after indomethacin administration in all arteries measured. There was a transient, but significant reduction in urine output after bolus injection of indomethacin. Conclusion: In contrast to bolus injections, decrease of organ blood flow and impairment of urine output do not accompany continuous infusion of indomethacin over 36 h.

Effects of electrical stimulation of the dorsal skin on systemic and mesenteric microvascular hemodynamics in anesthetized rats.

The effects of electrical stimulation of the dorsal skin area on the mesenteric arterioles were investigated in anesthetized rats by the use of an intravital microscope-television system. Changes in the diameter of the mesenteric precapillary arterioles (10-40 microm in diameter) were measured with an image processor. Blood flow velocity in the mesenteric precapillary arterioles was monitored by the dual sensor method developed by the authors. Electrical stimulation was performed through two platinum electrodes placed at the right dorsal Th5-12 level skin area by the use of an electrical stimulator (0.2 ms, 20 Hz). Continuous stimulation lasting for 30 s (1-10 mA) and intermittent stimulation lasting for 10 min (3 mA) were applied. The pressor response following the depressor response was induced by a stimulus current above 8 mA. The decrease in mesenteric blood flow velocity was induced by stimulus current above 10 mA. These responses were abolished by lidocaine injection into the subcutaneous area where the electrodes were attached. No significant change in arteriolar diameter or heart rate were induced by the stimulation for 30 s. Electrical stimulation of the skin for 10 min evoked a decrease in the diameter of arterioles (-3.4 +/- 2%, p < 0.01, n = 12). In the adrenalectomized group, electrical stimulation of the skin for 10 min elicited a slight increase in the diameter (1.1 +/- 0.5%, n = 6). It is therefore suggested that electrical stimulation of the skin for 30 s reflexly evoked decreases in MAP and in blood flow velocity, and that the constriction of the mesenteric precapillary arterioles induced by the stimulation for 10 min was mediated by humoral adrenaline and noradrenaline released by somato-adrenal medullary reflex.

Somatosensory nociceptive mechanical stimulation modulates systemic and mesenteric microvascular hemodynamics in anesthetized rats

The effects of somatosensory nociceptive pinch stimulation of the hindpaw on mesenteric microvascular hemodynamics and systemic circulatory parameters were investigated in anesthetized rats using an intravital microscope–television system. Blood flow velocity in the terminal (18–40 μm in diameter) or precapillary (10–20 μm in diameter) arterioles of the mesentery was monitored by the dual sensor method developed by the authors. In the proximal terminal arterioles, blood flow velocity decreased substantially along with arteriolar constriction induced by pinching of the hindpaw for 30 s. In the distal terminal arterioles and precapillary arterioles, blood flow velocity increased after pinching. In the proximal terminal arterioles, the decrease of velocity in response to reflex vasoconstriction was abolished by intravenous injection of an α-blocker (phentolamine, 10 mg/kg). The increase in mesenteric precapillary arteriolar blood flow velocity (43±9%, p<0.01) associated with the increase in mean arterial pressure (MAP) (22±1%, p<0.01) was observed within a few seconds after the onset of the stimulation, and then the response in blood flow velocity returned to the baseline ahead of MAP response recovery after the end of the stimulus. These responses were diminished by α-adrenergic receptor blockade. The heart rate (HR) increase (4±1%, p<0.01) induced by pinching was abolished by β-adrenergic receptor blockade (propranolol, 3 mg/kg, i.v.). There was a strong correlation between the increase in MAP and the decrease in renal blood flow measured by laser Doppler flowmeter ( r=0.87–0.98). Pinch stimulation of the rat hindpaw evoked changes in mesenteric arteriolar blood flow velocity that were mediated via the somato-sympathetic reflex vasoconstriction and the pressor response.

Effects of indomethacin and ibuprofen on mesenteric and renal blood flow in preterm infants with patent ductus arteriosus

Objective: To evaluate the effect of intravenous ibuprofen and indomethacin for treatment of patent ductus arteriosus (PDA) on mesenteric and renal blood flow velocity in preterm infants. Study design: Seventeen mechanically ventilated preterm infants (<33 weeks’ gestation) with PDA received either 0.2 mg/kg indomethacin (n = 8) or 10 mg/kg ibuprofen (n = 9), infused over 15 minutes. Mesenteric and renal blood flow velocity were measured by using Doppler ultrasonography. Results: Indomethacin caused a significant reduction in mesenteric and renal blood flow velocity 30 minutes after drug administration; mesenteric and renal blood flow velocity did not return to the pretreatment values by 120 minutes. Ibuprofen did not alter blood flow 30 minutes after treatment, and blood flow increased 120 minutes after treatment. Mesenteric and renal blood flow velocity changes were significantly different between the 2 treatment groups. Conclusions: Compared with indomethacin, ibuprofen did not significantly reduce mesenteric and renal blood flow velocity.(J Pediatr 1999;135:733-8)

Effects of prophylactic low-dose indomethacin on hemodynamics in very low birth weight infants

Indomethacin decreases cerebral and mesenteric blood flow velocities in premature infants with symptomatic patent ductus arteriosus. Low-dose indomethacin is recommended for the prevention of intraventricular hemorrhage in very low birth weight infants. The hemodynamic effects of prophylactic indomethacin have not been previously examined. We hypothesized that prophylactic indomethacin does not change cerebral and mesenteric blood flow velocities and cardiac function in very low birth weight infants. Twenty-one infants (775 to 1245 gm, 24 to 31 weeks' gestation) were studied before and after indomethacin (0.1 mg/kg) administration at 6, 30, and 54 hours of life. Mean and end-diastolic cerebral and mesenteric blood flow velocities decreased (ANOVA, p < 0.05) after prophylactic indomethacin. The 38% increase in cerebral relative vascular resistance was significantly greater than the 18% increase in mesenteric relative vascular resistance (ANOVA, p < 0.05). In five infants who were fed 1 hour after the third indomethacin dose, the postprandial mesenteric blood flow velocity was significantly greater than the mesenteric blood flow velocity before both indomethacin and feeding (ANOVA, p < 0.05). Cardiac output, stroke volume, fractional shortening, and blood pressure did not change after prophylactic indomethacin administration. We conclude that prophylactic indomethacin (1) reduces cerebral and mesenteric blood flow velocity without affecting cardiac function, (2) increases cerebral more than mesenteric relative vascular resistance, and (3) does not prevent postprandial increases in mesenteric blood flow velocity. We speculate that the increase in cerebral relative vascular resistance is a beneficial effect that contributes to protection against intraventricular hemorrhage. (J Pediatr 1998;132:28-34)

Antenatal Steroids and Hemodynamic Maturation of Very Low Birth Weight (VLBW) Infants † 1114

Antenatal glucocorticoids (AG) for the prevention of respiratory distress syndrome in VLBW infants reduce the incidence of patent ductus arteriosus, intraventricular hemorrhage and necrotizing enterocolitis. In preterm fetal lambs, AG increase postnatal cardiac output (CO), heart rate (HR) and blood pressure (BP). We hypothesized that AG improve hemodynamic maturation in preterm infants. Twenty infants (750-1250 g; 24-31 wk) were enrolled in a prospective observational study. We measured middle cerebral (C) and superior mesenteric (M) artery Doppler blood flow velocities (BFV) and cardiac function at 6, 30, 54 and 168 hr of life. Infants were divided into three groups: non-treated controls (n=6), one dose (n=4), and two or more doses (n=10) of AG. Mean and end-diastolic CBFV increased (ANOVA, p<0.0001) by 83 and 230%, respectively, from 6 to 168 hr of age. Cerebral relative vascular resistance(RVR) decreased (ANOVA, p<0.05) by 27%. Mean MBFV and MRVR did not change, but end-diastolic MBFV increased (ANOVA, p<0.05) by 47%. HR, BP, and CO (fig.) increased (ANOVA, p<0.001) by 7, 35, and 60%, respectively. Contractility did not change. Mean and end-diastolic CBFV, mean and end-diastolic MBFV, CRVR, MRVR, HR, BP, CO and contractility did not differ among groups. We conclude that AG do not alter Doppler ultrasound indices of postnatal hemodynamic maturation in VLBW infants. Funded by Wyeth Pediatrics.

Mesenteric blood flow velocity and its relation to transitional circulatory adaptation in appropriate for gestational age preterm infants.

We investigated the early postnatal changes of the mesenteric circulation and its relation to the systemic circulation in 15 preterm infants. The infants were studied before the first feeding on d 1 and pre- and postprandially on d 3, 4, 5, and 7. Blood flow velocity was measured by ultrasound Doppler in the superior mesenteric artery, middle cerebral artery, and the aortic orifice for cardiac output calculations. Blood pressure and heart rate were monitored. From d 1 to d 3, the preprandial stroke volume decreased [1.5 +/- 0.3 to 1.3 +/- 0.2 mL/kg (mean +/- SD), p < 0.05], whereas blood pressure (36 +/- 3 to 50 +/- 7 mm Hg, p < 0.001), superior mesenteric artery mean velocity (Vmean) (0.17 +/- 0.08 to 0.30 +/- 0.11 m/s, p < 0.05), and middle cerebral artery Vmean increased (0.15 +/- 0.05 to 0.22 +/- 0.03 m/s, p < 0.001). From d 3 through d 7, the preterm infants demonstrated higher preprandial end diastolic flow velocity in the superior mesenteric artery than we previously reported in term infants (0.15 +/- 0.05 versus 0.12 +/- 0.04, p < 0.05). Like the term infants, preterm infants increased their superior mesenteric artery Vmean by 83% postprandially and maintained a stable cerebral circulation with feeding. Unlike the term infants, feeding in the preterm infants induced a blood pressure decrease (51 +/- 6 to 48 +/- 6 mm Hg, p < 0.01) and a cardiac output increase (176 +/- 30 to 188 +/- 32 mL/kg/min, p < 0.001). These findings suggest that, in contrast to term infants, healthy preterm infants require compensatory systemic hemodynamic changes in response to feeding.