Background:The development in the last decade of noninvasive, near infrared spectroscopy (NIRS) analysis of tissue hemoglobin saturation in vivo has provided a new and dramatic tool for the management of hemodynamics, allowing early detection and correction of imbalances in oxygen delivery to the brain and vital organs.Description:The theory and validation of NIRS and its clinical use are reviewed. Studies are cited documenting tissue penetration and response to various physiologic and pharmacologic mechanisms resulting in changes in oxygen delivery and blood flow to the organs and brain as reflected in the regional hemoglobin oxygen saturation (rSO2). The accuracy of rSO2 readings and the clinical use of NIRS in cardiac surgery and intensive care in adults, children and infants are discussed.Conclusions:Clinical studies have demonstrated that NIRS can improve outcome and enhance patient management, avoiding postoperative morbidities and potentially preventing catastrophic outcomes.

ABSTRACT:The developmentally regulated hemodynamic effects of vasoactive medications have not been well characterized. We used traditional and near-infrared spectroscopy monitoring technologies and investigated the changes in heart rate, blood pressure, common carotid artery (CCA) blood flow (BF), cerebral, renal, intestinal, and muscle regional tissue O 2 saturation, and acid-base and electrolyte status in response to escalating doses of vasoactive medications in normotensive anesthetized neonatal piglets. We used regional tissue O 2 saturation and CCA BF as surrogates of organ and systemic BF, respectively, and controlled minute ventilation and oxygenation. Low to medium doses of dopamine, epinephrine, dobutamine, and norepinephrine increased blood pressure and systemic and regional BF in a drug-specific manner, whereas milrinone exerted minimal effects. At higher doses, dopamine, epinephrine, and norepinephrine but not dobutamine decreased systemic, renal, intestinal, and muscle BF, while cerebral BF remained unchanged. Epinephrine induced significant increases in muscle BF and serum glucose and lactate concentrations. The findings reveal novel drug-and dose-specific differences in the hemodynamic response to escalating doses of vasoactive medications in the neonatal cardiovascular system and provide information for future clinical studies investigating the use of vasoactive medications for the treatment of neonatal cardiovascular compromise. (Pediatr Res 70: 473-479, 2011) C ardiovascular compromise is a frequently encountered condition in the critically ill preterm and term infant (1) resulting in inadequate tissue O 2 delivery, impaired cerebral blood flow (CBF) autoregulation, and, potentially, end-organ injury and death (1-3). Our limited ability to accurately monitor changes in neonatal hemodynamics curtails timely recognition, and thus treatment, of neonatal shock.Although vasopressor-inotropes, inotropes, and lusitropes have been used to manage neonatal cardiovascular compromise with an attempt to tailor the treatment to the suspected primary etiology (1), there is only limited information available on the safety and effectiveness of these medications (1,4) and little is known about their developmentally regulated dose-dependent hemodynamic actions (4,5). Recent advances in bedside hemodynamic monitoring techniques using, among others, near-infrared spectroscopy (NIRS) have made continuous, noninvasive monitoring of tissue O 2 delivery (6) possible. Accordingly, data on tissue O 2 delivery and utilization (7) and regional O 2 saturation in critically ill adults, children, and, more recently, neonates have become available (2,3,8 -10).To gain insight into the specific, drug-related changes in neonatal hemodynamics, we used traditional and NIRS hemodynamic monitoring technologies and investigated the changes in heart rate, blood pressure (BP), common carotid artery (CCA) blood flow (BF), cerebral regional tissue O 2 saturation (CrSO 2 ), renal (kidney) regional tissue O 2 saturation (KrSO 2 ), intestina...

Background:Changes in the arterial partial pressure of CO2 (PaCO2) has a direct though transient effect on the cerebral vasculature and cerebral circulation. Decreased PaCO2 levels lead to vasoconstriction and can result in dangerously low levels of cerebral perfusion that resolve in 4–6 h. It is currently believed that perfusion abnormalities contribute to intraventricular hemorrhage (IVH) and periventricular leukomalacia (PVL) in the neonate. PaCO2-induced vasoconstriction may contribute to the pathology of IVH and PVL.Methods:Near-infrared spectroscopy [NIRS; (INVOS cerebral/somatic oximeter; Somanetics Corporation, Troy, MI, USA)] was utilized to determine changes in regional oxygenation (rSO2) of the brain in response to changes in ventilation in isoflurane anesthetized newborn piglets.Results:Changes in cerebral rSO2 correlated significantly with end-tidal CO2 levels and to blood flow in the common carotid artery. This correlation was significant during baseline conditions, after periods of CO2 loading and during periods of hypothermia.Conclusions:The results of the study demonstrate the utility of NIRS to accurately reflect changes in cerebral oxygenation and flow to the brain in response to changes in CO2 levels in anesthetized, ventilated neonatal piglets. The use of NIRS may provide an early alert of low levels of cerebral blood flow and brain oxygenation, potentially helping in preventing the progression of IVH or PVL in the neonate.

Porcine ileal mucosa was homogenized and freeze-thawed in 0.05 M NH4HCO3 + 0.01 M EDTA + 1 mM benzamidine hydrochloride at pH 8.6. Subsequent stepwise precipitation with (NH4)2SO4 followed by fractionation on Sephadex G-50 medium and G-50 fine eluted with alkaline buffer and final fractionation on G-50 superfine in 1.0 M acetic acid yielded a pure protein of 13,000 daltons as determined by sodium dodecyl sulfate electrophoresis. The amino acid composition of the protein has been determined and it contains 126 residues with no tryptophan detectable. Tryptic peptide maps demonstrate that the protein does not contain glucagon and RIA of the peptide did not detect any immunoreactive glucagon or gastrin. The isoelectric point is 6.4. The intact protein is resistant to Edman degradation and the partial N-terminal sequences of two CNBr fragments are: Lys-Arg-Leu-Ala-Leu ...., Glu-Gly-Gly-Thr-Val-Val-Val-Asn-Ser.... The C-terminal residue, alanine was determined using carboxypeptidase Y. The isolated peptide, in the range of 10(-15)-10(-9) M stimulated oxyntic cell hydroxyl ion production in sections of guinea pig gastric fundus. The dose response was linear with biphasic peaks at 10(-14) and 10(-9) M and the maximal response to the peptide was equal to that observed with gastrin. The addition of either atropine (10(-5) M) or cimetidine (10(-5) M) with the peptide (10(-14) M) caused greater than 50% inhibition of oxyntic cell stimulation (P less than 0.005). This peptide is a potent stimulator of the oxyntic cell and its effect is inhibited by muscarinic cholinergic and H2 receptor blockers. Hence, it represents a significant component of the physiological enterooxyntin effect observed in response to intestinal meals.