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Biomedical subjects

J A St Cyr

Publications and source records attributed to J A St Cyr.

At least 19 recordsLinked to original sources
PubMed2003

The benefits of ribose in cardiovascular disease.

Cardiovascular disease still ranks as the leading cause of death in men and women. Adults have tried to lower their risk of cardiovascular disease by improving their diet, quitting smoking, controlling blood pressure and exercising regularly. Additionally, many adults have turned to nutriceutical or natural products. Myocardial ischemia, produces a depression in myocardial tissue levels of high energy compounds, along with a compromise in myocardial function. Ribose, a naturally occurring sugar, has been extensively investigated, both in animal and clinical studies, as an agent to enhance the recovery of these depressed energy compounds. Results of these studies have been promising in enhancing the recovery of these energy molecules along with an improvement in myocardial function. Therefore, ribose should be considered as a potential agent in the treatment of ischemic cardiovascular disease.

Animals↗
PubMed1999

Effects on C3 and CH50 levels during and following extracorporeal whole body hyperthermia.

Cardiopulmonary bypass can affect inflammatory reactions and evoke the "postperfusion syndrome," manifested as multiple organ dysfunction in the recovery period. This syndrome is generated by the activation of complement, macrophages, neutrophils, and inflammatory cytokines. Following the use of hypothermia during cardiac procedures, active hyperthermic rewarming is used to reestablish body temperature. Complement levels and their interactions have been investigated during and following hypothermia. Hyperthermia is being used clinically; however, the effect of markedly elevated temperatures on complement is unknown and, therefore, needs to be investigated. A pilot canine study was designed to begin to explore what role hyperthermia may play on complement levels during and following extracorporeal whole body hyperthermia. Five dogs were heated to a core temperature of approximately 42 degrees C, held at this elevated temperature for 90 minutes, then cooled to normothermia. A decline in C3 levels at the end of warming with further declines through day 4 post treatment was observed. CH50 levels mimicked the C3 level decline; however, there was a trend for rebounding by day 4. The findings involving complement factors following hyperthermia signify that this increase in temperature causes a decrease in both C3 and CH50 levels.

Animals↗
PubMed1996

Impact of respiratory acid-base status in patients with pulmonary hypertension.

BACKGROUND: The perioperative management of patients undergoing mitral valve replacement (MVR) with pulmonary hypertension from mitral stenosis may be complicated by increased pulmonary vascular resistance. The purpose of this study was to examine the influence of respiratory acid-base status on the pulmonary hemodynamic indices of patients with pulmonary hypertension before and after MVR. METHODS: Ten patients with pulmonary hypertension from mitral stenosis (mean preoperative systolic pulmonary artery pressure, 73 +/- 8 mm Hg) undergoing MVR were studied in the operating room before and after MVR. Arterial partial pressure of carbon dioxide was manipulated by the addition of 5% carbon dioxide to the breathing circuit. Hemodynamic data were collected as the partial pressure of carbon dioxide rose from 30 mm Hg to 50 mm Hg and decreased back to 30 mm Hg. RESULTS: There were no differences in mean pulmonary artery pressure or pulmonary vascular resistance before and after MVR. Before MVR, mean pulmonary artery pressure increased from 32 +/- 1 mm Hg to 48 +/- 1 mm Hg as the partial pressure of carbon dioxide rose from 30 mm Hg to 50 mm Hg (p < 0.05), and pulmonary vascular resistance rose from 379 +/- 30 to 735 +/- 40 dynes.second.cm-5 (p < 0.05). These effects on mean pulmonary artery pressure and pulmonary vascular resistance were not different after MVR. CONCLUSION: Respiratory acid-base status has a profound impact upon pulmonary vascular resistance in patients with pulmonary hypertension from mitral stenosis undergoing MVR. This impact persists in the immediate postoperative period. We conclude that respiratory acidemia should be avoided in these patients, whereas respiratory alkalemia may be used to help minimize pulmonary vascular resistance.

Acid-Base Imbalance↗
PubMed1994

Protection of the patent internal mammary artery by-pass graft from subsequent sternotomy.

OBJECTIVE: We describe a technique to protect the patent internal mammary artery graft from injury by repeat sternotomy. INTERVENTIONS: The internal mammary artery is dissected as far proximally as possible. The left pleural space is opened widely thus allowing the left lung to protrude through the pleural defect once mechanical ventilation is resumed. The left lung is then interposed between the internal mammary graft and the sternum. The internal mammary artery is thereby protected from adherence to the sternum and injury upon resternotomy. RESULTS: In two patients in whom this technique was employed repeat sternotomy was easily performed without injury to the internal mammary artery. CONCLUSIONS: This simple technique effectively protects the patent internal mammary artery bypass graft from injury at subsequent sternotomy.

Humans↗
PubMed1993

Hemodynamic advantage of left atrial epinephrine administration after cardiac operations.

Cardiac surgical patients frequently require catecholamines, typically administered via the central venous circulation. Potential disadvantages of this route of administration include catecholamine metabolism by the pulmonary vascular bed before gaining access to the heart and pulmonary vasoconstriction producing increased pulmonary vascular resistance. We therefore prospectively compared administration of epinephrine via the left atrium versus central venous administration of epinephrine with particular interest in cardiac output, mean pulmonary artery pressure, and pulmonary vascular resistance. Fifteen consecutive aortocoronary bypass patients were studied after cardiopulmonary bypass. Epinephrine (mean dose, 0.07 +/- 0.02 micrograms.kg-1.min-1) was administered via the central venous route, then via the left atrium, then via the central venous route again. Hemodynamic data were collected 10 minutes after changing the route of administration. Left atrial administration of epinephrine produced a 35% greater cardiac output, 25% lower pulmonary artery pressure, and 32% lower pulmonary vascular resistance when compared with central venous administration (all significant; p < 0.05). Left atrial epinephrine administration may offer hemodynamic advantage in cardiac surgical patients in whom central venous administration does not produce an adequate cardiac output or in patients with pulmonary hypertension to avoid any further increase in pulmonary vascular resistance.

Aged↗
PubMed1993

Repair of multiple mycotic aortic aneurysms in a newborn.

Thoracoabdominal aortic and common and internal iliac artery mycotic aneurysms resulted from an umbilical arterial catheter in a 3 1/2-week-old boy. He underwent staged repair including an 8-mm Gore-tax tube graft, primary repair of the common iliac artery aneurysm, and resection of the internal iliac aneurysm. His operative and postoperative course was uneventful. He was asymptomatic at 17 months' follow-up, with equal blood pressure in the upper and lower extremities. Magnetic resonance imaging showed no stenoses or recurrent aneurysms at the anastomotic sites of the Gore-tex tube graft. Blood supply to his left leg came from collaterals, principally a large crossing vessel from the right iliac artery. This case represents the first successful aortic replacement in a 5 week old with extensive involvement of the thoracoabdominal aorta and its branch vessels.

Aneurysm, Infected↗
PubMed1993

The influence of respiratory acid-base status on adult pulmonary vascular resistance before and after cardiopulmonary bypass.

Respiratory acid-base status has recently been shown to affect pulmonary vascular resistance (PVR) in adults following cardiac surgery. The purpose of this study was to examine what influence cardiopulmonary bypass has on the pulmonary vascular response to changes in respiratory acid-base status. Fifteen consecutive patients undergoing aortocoronary bypass were studied under general anesthesia both before and after cardiopulmonary bypass. Arterial PCO2 was manipulated by the addition of 5 percent carbon dioxide to the breathing circuit. Both before and after bypass, PVR increased significantly as PCO2 rose from 30 mm Hg to 50 mm Hg (p < 0.05). The PVR returned to baseline as PCO2 was returned to 30 mm Hg. These data suggest that increased PVR induced by hypercarbic acidemia is not simply a result of the effects of cardiopulmonary bypass on the pulmonary circulation. Instead, we conclude that respiratory acid-base status is an important determinant of adult PVR. We believe these data may be helpful in the treatment of mechanically ventilated patients, since patients are at particular risk of having abnormalities develop in respiratory acid-base status.

Acid-Base Equilibrium↗
PubMed1993

Influence of hydrogen ion concentration versus carbon dioxide tension on pulmonary vascular resistance after cardiac operation.

Disturbances of respiratory acid-base status are common in patients supported with mechanical ventilation of the lungs after cardiac operations. This study was conducted with two protocols. The purpose was to determine whether respiratory acid-base status influences pulmonary vascular resistance in adults after cardiac operations and whether the influence is mediated by hydrogen ion concentration or carbon dioxide tension. Patients were studied while under general anesthesia immediately after aorta-coronary bypass. In the first protocol, with seven patients, arterial carbon dioxide tension was manipulated by the addition of 5% carbon dioxide to the breathing circuit. Pulmonary vascular resistance index was determined as arterial carbon dioxide tension rose from 30 mm Hg to 50 mm Hg and back to 30 mm Hg. In the second protocol, with 10 different patients, hydrogen ion concentration was manipulated by the addition of 0.2N hydrochloric acid, sodium bicarbonate, or both as arterial carbon dioxide tension was held constant. We used analysis of variance for statistical data. The results of the first protocol showed that pulmonary vascular resistance index rose by 44% (p < 0.05) as arterial carbon dioxide tension rose from 30 to 50 mm Hg. The results of the second protocol showed that changes in pulmonary vascular resistance index were parallel to changes in hydrogen ion concentration as arterial carbon dioxide tension was held constant (p < 0.05). These data demonstrate that respiratory acid-base status is an important determinant of pulmonary vascular resistance in the adult after cardiac operations. Furthermore, these data suggest the effect is mediated by hydrogen ion concentration, not carbon dioxide tension.

Acid-Base Equilibrium↗
PubMed1992

Cryopreserved allograft repair of aortic hypoplasia and interrupted aortic arch.

Mortality for interruption of the aortic arch approaches 100% within the first year of life if untreated. Prostaglandin E1 can stabilize the patient's condition in anticipation of surgical palliation, but total repair is required for long-term survival. Successful complete repair of type B interrupted aortic arch, hypoplasia of the left ventricular outflow tract, and ventricular septal defect was possible using a cryopreserved allograft in a child who previously had undergone unusual palliation.

Aorta, Thoracic↗
PubMed1992

Cardiac 5'-nucleotidase activity increases with age and inversely relates to recovery from ischemia.

The metabolic basis for the enhanced tolerance of immature hearts to ischemia remains to be elucidated. Loss of high-energy phosphate nucleotides occurs during ischemia/reperfusion in mature (adult) hearts through the breakdown of adenosine triphosphate, diphosphate, and monophosphate (nondiffusible) to adenosine (freely diffusible). However, previous work has shown that after ischemia nondiffusible nucleotides are better retained by immature (neonatal) hearts than by mature hearts. The enzyme responsible for the conversion of adenosine monophosphate to adenosine is 5'-nucleotidase. We therefore hypothesized lower activity of this enzyme in neonatal than in adult myocardium. The purposes of this study were (1) to document 5'-nucleotidase activities in neonatal and adult rabbit myocardium and (2) to correlate differences of 5'-nucleotidase activity with functional recovery from ischemia. Neonatal (5- to 10-day-old) and adult (4- to 6-month-old) rabbit hearts were isolated and perfused (retrograde Langendorff). A left ventricular balloon measured functional parameters. Hearts were subjected to 20 minutes of global 37 degrees C ischemia and 10 minutes of reperfusion followed by freeze clamping. Tissue homogenates were assayed for 5'-nucleotidase by the linked formation of nicotinamide-adenine dinucleotide at 340 nm (Arkesteijn method). Postischemic recovery of developed pressure was 86% +/- 3% in neonates (n = 5) versus 38% +/- 3% in adults (n = 8) (mean +/- standard deviation) (p less than 0.01). 5'-Nucleotidase activity was 4400 +/- 1208 nmol/min/gm in neonates (n = 5) versus 13,938 +/- 830 nmol/min/gm in adults (n = 8) (mean +/- standard deviation) (p less than 0.01). We conclude that (1) 5'-nucleotidase activity is 68% lower in neonatal than in adult myocardium and (2) functional recovery after ischemia inversely relates to 5'-nucleotidase activity.

5'-Nucleotidase↗
PubMed1991

Bezold-Jarisch reflex in postoperative pediatric cardiac surgical patients.

The Bezold-Jarisch reflex is an inhibitory reflex that originates from the heart, is mediated by the vagus nerve, and is manifested by hypotension and bradycardia. We present 4 pediatric cardiac surgical patients, aged 1 day to 9 months, who exhibited cardiovascular collapse in their early postoperative course. In each patient, cardiovascular deterioration was marked by an insidious decrease in arterial blood pressure without an associated change in heart rate, central venous pressure, or airway pressure. Bradycardia followed the decrease in blood pressure. The Bezold-Jarisch reflex was suspected and atropine was administered, first as a bolus injection at 0.01 mg/kg, and later, as a continuous infusion at 0.01 mg.kg-1.h-1. Atropine prevented recurrent episodes of hypotension and bradycardia. We believe the Bezold-Jarisch reflex is more prevalent than previously suspected in postoperative pediatric cardiac surgical patients.

Atropine↗
PubMed1990

Unilateral pulmonary hypertension as a result of chronic high flow to one lung.

The patient presented is a 27-month-old male with complex congenital heart disease consisting of severe left ventricular outflow tract obstruction and ventricular septal defect who had undergone a pulmonary trunk-to-aorta graft and a pulmonary artery banding procedure as a neonate. Sometime after this repair, but at least 15 months prior to presentation to this institution for placement of an aortic homograft, the pulmonary trunk band apparently slipped and migrated over the right pulmonary artery, severely limiting blood flow to the right lung and increasing flow to the left. Severe pulmonary hypertension developed, with a main pulmonary artery pressure of 94/53 mm Hg. We present clinical and radiographic evidence that the resulting chronic high blood flow and pressure in the left lung ultimately resulted in hypoperfusion of that lung, presumably secondary to chronic vascular changes with greatly increased vascular resistance. Upon surgical repair and removal of the constrictive band from the previously banded right PA, blood flow was increased to the low resistance right lung causing right-sided unilateral pulmonary edema, ventilation/perfusion mismatching, and severe hypoxemia. Perfusion studies documented that less than 10% of blood was directed to the left lung, with greater than 90% to the right. Perfusion studies 9 months postoperatively continued to demonstrate minimal blood flow to the left lung. Discussion focuses on the effects of mechanical forces and the interaction with hypoxia in causing pulmonary vascular remodeling.

Child, Preschool↗