Heme oxygenase/carbon monoxide system affects the placenta and preeclampsia.

Preeclampsia affects 2% to 8% of pregnancies worldwide and results in significantly high maternal and perinatal morbidity and mortality, with delivery being the only definitive treatment. It is not a single disorder, but rather a manifestation of an insult(s) to the uteroplacental unit -whether maternal, fetal, and/or placental. Multiple etiologies have been implicated, including uteroplacental ischemia, maternal infection and/or inflammation, maternal obesity, sleep disorders, hydatidiform mole, maternal intestinal dysbiosis, autoimmune disorders, fetal diseases, breakdown of maternal-fetal immune tolerance, placental aging, and endocrine disorders.

Heme oxygenase/carbon monoxide system and development of the heart.

Progressive differentiation controlled by intercellular signaling between pharyngeal mesoderm, foregut endoderm, and neural crest-derived mesenchyme is required for normal embryonic and fetal development. Gasotransmitters (criteria: 1) a small gas molecule; 2) freely permeable across membranes; 3) endogenously and enzymatically produced and its production regulated; 4) well-defined and specific functions at physiologically relevant concentrations; 5) functions can be mimicked by exogenously applied counterpart; and 6) cellular effects may or may not be second messenger-mediated, but should have specific cellular and molecular targets) are integral to gametogenesis and subsequent embryogenesis, fetal development, and normal heart maturation. Important for in utero development, the heme oxygenase/carbon monoxide system is expressed during gametogenesis, by the placenta, during embryonic development, and by the fetus.

Effects of lactate and carbon monoxide interactions on neuroprotection and neuropreservation.

Lactate, historically considered a waste product of anerobic metabolism, is a metabolite in whole-body metabolism needed for normal central nervous system (CNS) functions and a potent signaling molecule and hormone in the CNS. Neuronal activity signals normally induce its formation primarily in astrocytes and production is dependent on anerobic and aerobic metabolisms. Functions are dependent on normal dynamic, expansive, and evolving CNS functions.

Cardiac function dependence on carbon monoxide.

Nitric oxide, studied to evaluate its role in cardiovascular physiology, has cardioprotective and therapeutic effects in cellular signaling, mitochondrial function, and in regulating inflammatory processes. Heme oxygenase (major role in catabolism of heme into biliverdin, carbon monoxide (CO), and iron) has similar effects as well. CO has been suggested as the molecule that is responsible for many of the above mentioned cytoprotective and therapeutic pathways as CO is a signaling molecule in the control of physiological functions.

Neurointegrity and neurophysiology: astrocyte, glutamate, and carbon monoxide interactions.

Astrocyte contributions to brain function and prevention of neuropathologies are as extensive as that of neurons. Astroglial regulation of glutamate, a primary neurotransmitter, is through uptake, release through vesicular and non-vesicular pathways, and catabolism to intermediates. Homeostasis by astrocytes is considered to be of primary importance in determining normal central nervous system health and central nervous system physiology - glutamate is central to dynamic physiologic changes and central nervous system stability.

The internal mammary artery as a shunt in a noncyanotic infant with hemitruncus: surgical and anesthetic management.

The internal mammary artery (IMA) has been used as a systemic-to-pulmonary artery shunt in selected patients with congenital heart disease. Growth and development of hypoplastic pulmonary arteries have been described. We discuss the surgical and anesthetic management of an infant with an atretic-thrombosed right pulmonary artery originating from the ascending aorta in whom the IMA was used to create a systemic-to-pulmonary artery shunt after failure of a previous shunt and later successful pulmonary artery reconstruction.

Neuroprotective, neurotherapeutic, and neurometabolic effects of carbon monoxide.

Studies in animal models show that the primary mechanism by which heme-oxygenases impart beneficial effects is due to the gaseous molecule carbon monoxide (CO). Produced in humans mainly by the catabolism of heme by heme-oxygenase, CO is a neurotransmitter important for multiple neurologic functions and affects several intracellular pathways as a regulatory molecule. Exogenous administration of inhaled CO or carbon monoxide releasing molecules (CORM's) impart similar neurophysiological responses as the endogenous gas.

Inhaled carbon monoxide provides cerebral cytoprotection in pigs.

Carbon monoxide (CO) at low concentrations imparts protective effects in numerous preclinical small animal models of brain injury. Evidence of protection in large animal models of cerebral injury, however, has not been tested. Neurologic deficits following open heart surgery are likely related in part to ischemia reperfusion injury that occurs during cardiopulmonary bypass surgery.

Ultrasonic biophysical measurements in the normal human fetus for optimal design of the monolithic fetal pacemaker.

Ultrasound measurements, including xiphoid-to-pericardial distance and deployment angle, were made on human fetuses as a function of gestational age for the purpose of assessing the likelihood of 3 failure modes of a monolithic fetal pacemaker, including primary positioning failure due to device length and secondary dislodgement failure due to somatic growth. The small variation of the measurements over the gestational age range relevant to device implantation for the major indications of the device (for complete heart block complicated by hydrops and for bradycardia risk after fetal surgery or intrauterine intervention) predicts a small likelihood of these failure modes.

Does antegrade cerebral perfusion protect the brain during deep hypothermic circulatory arrest?

Purpose: This study compares cerebral protection using no cerebroplegia and using antegrade cerebroplegia with variable flow rates during deep hypothermic circulatory arrest (DHCA).

Methods: Twenty healthy neonatal piglets (2.5-3.