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Biomedical subjects

V R Conti

Publications and source records attributed to V R Conti.

At least 19 recordsLinked to original sources
PubMed1992

Ischemic preconditioning attenuates acidosis and postischemic dysfunction in isolated rat heart.

The hypothesis that brief ischemia (preconditioning) protects the isolated heart from prolonged global ischemia was tested. Isovolumic rat hearts were preconditioned with either 5 min of ischemia followed by 5 min of perfusion (P1) or two 5-min episodes of ischemia separated by 5 min of perfusion (P2). Control hearts received no preconditioning. All hearts received 40 min of sustained ischemia and 30 min of reperfusion. Preconditioning (P1 or P2) significantly (P less than 0.0005) improved recovery of the rate-pressure product; percentage recoveries were 17.8 +/- 3.2 (n = 14), 59.9 +/- 5.5 (n = 6), and 46.4 +/- 4.7 (n = 8) for control, P1, and P2, respectively. Improved functional recovery of preconditioned hearts was associated with reduced end-diastolic pressure and improved myocardial perfusion. During the 40-min ischemic period, myocardial pH decreased from approximately 7.4 to 6.3 +/- 0.1 (n = 7) in the control hearts and to 6.7 +/- 0.1 (n = 7) in the preconditioned hearts (P less than 0.01). Also during the 40-min ischemic period, myocardial lactate (expressed as nmol/mg protein) increased to 146 +/- 11 (n = 7) and 101 +/- 12 (n = 8) in control and preconditioned hearts, respectively (P less than 0.02). The results demonstrate that a brief episode of ischemia can protect the isolated rat heart from a prolonged period of ischemia. This protection is associated with decreased tissue acidosis and anaerobic glycolysis during the sustained ischemic period.

Acidosis↗
PubMed1992

Postischemic recovery of mitochondrial adenine nucleotides in the heart.

BACKGROUND: Adenine nucleotides (AdNs) are lost from the mitochondrial fraction of the heart cell during ischemia. It is unknown whether this pool of AdNs can be replenished after reperfusion. The purpose of this study was to evaluate the postischemic recovery of the mitochondrial AdN pool. METHODS AND RESULTS: The left anterior descending coronary artery (LAD) of the canine heart was occluded for 30 minutes followed by either no reflow, 30-minute reflow, 1-day reflow, or 7-day reflow. Systolic shortening in the LAD-supplied region was absent during occlusion but recovered to approximately 30% of preocclusion values during early reperfusion. Mitochondrial and tissue AdNs (ATP, ADP, and AMP) were determined in the LAD-supplied and left circumflex-supplied (control) regions of the heart. The AdN content (expressed as percent of control values) of mitochondria from the LAD region was 55 +/- 10% (p less than 0.002), 64 +/- 7% (p less than 0.001), 81 +/- 6% (p less than 0.03), and 94 +/- 8% for the no-reflow, 30-minute-reflow, 1-day-reflow, and 7-day-reflow groups, respectively. The AdN content (expressed as percent of control values) of tissue samples from the LAD region was 52 +/- 9% (p less than 0.002), 48 +/- 12% (p less than 0.02), 68 +/- 5% (p less than 0.002), and 70 +/- 9% for the no-reflow, 30-minute-reflow, 1-day-reflow, and 7-day-reflow groups, respectively. There was a good correlation between mitochondrial and tissue AdN (r = 0.95). Using initial exchange rates, adenine nucleotide translocase activities of mitochondria from the LAD and control regions were not significantly different. State 3 respiration of LAD mitochondria was depressed (approximately 25%, p less than 0.05) only in the no-reflow group. Acceptor control ratios of the LAD mitochondria were not significantly different from control values in any group. CONCLUSIONS: After 30 minutes of regional ischemia, postischemic restoration of the mitochondrial AdN pool occurs between 1 and 7 days; this restoration is preceded by recovery of respiratory and adenine nucleotide translocase functions. Although the abnormally low levels of AdN persist in the mitochondrial compartment during the early reperfusion period, postischemic contractile dysfunction cannot be explained by depressed mitochondrial respiratory activity.

Adenine Nucleotides↗
PubMed1990

Oxygenator failure.

Explore the source record for details and available documents.

Cardiopulmonary Bypass↗
PubMed1990

Intermittent ischemia produces a cumulative depletion of mitochondrial adenine nucleotides in the isolated perfused rat heart.

The purpose of the present study was to determine if repetitive myocardial ischemia would result in the cumulative loss of mitochondrial adenine nucleotides. Isolated perfused rat hearts were subjected to continuous or intermittent ischemia. A single 5-minute period of continuous ischemia did not result in a significant decrease in the mitochondrial adenine nucleotide pool; a single 10-minute period of ischemia resulted in a decrease of approximately 17%. Next, the adenine nucleotide content of mitochondria from preischemic and 30-minute continuous ischemic hearts was compared with two groups of hearts undergoing intermittent ischemia (both groups receiving a total of 30 minutes of ischemia). One group received three 10-minute episodes of ischemia interrupted by 5-minute periods of reperfusion (3 x 10-minute intermittent ischemia); the other intermittent ischemic group received six 5-minute episodes of ischemia interrupted by 5-minute periods of perfusion (6 x 5-minute intermittent ischemia). The mitochondrial adenine nucleotide content (expressed as nanomoles per nanomole cytochrome a) for the preischemic and 30-minute continuous ischemic hearts was 14.7 +/- 0.6 and 8.0 +/- 0.4, respectively. The mitochondrial adenine nucleotide content of the 3 x 10-minute intermittent ischemia group (8.5 +/- 0.5) was not significantly different from the 30-minute continuous ischemic group. The mitochondrial adenine nucleotide content of the 6 x 5-minute intermittent ischemia group (11.0 +/- 0.6) was significantly larger than that of the 30-minute continuous and the 3 x 10-minute intermittent ischemia groups (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1990

Cardiac surgery for inmates in the Texas Department of Corrections.

All Texas prison inmates requiring hospitalization since 1983 have been transferred to a separate prison hospital adjacent to a tertiary care university hospital. We reviewed and analyzed the data regarding one major tertiary care service, namely cardiac surgery, to describe the rate of utilization of this service and its results. From January 1, 1984, to June 30, 1988, 73 inmates underwent 74 cardiac operations, 50 of which were coronary revascularizations. The age-adjusted rates of utilization for coronary artery bypass grafting were substantially higher for inmates over age 45 than for that described for the general population, whereas the utilization rates for valve surgery were comparable. There were no perioperative or late deaths, and 86% of the inmate patients are currently employed within the Texas Department of Corrections system or were employed at the time of their release. The utilization rates and the results of this representative tertiary medical care service for the state's prison population are comparable to those achieved in the private sector, and may have a substantial beneficial effect on inmate rehabilitation.

Adolescent↗
PubMed1989

Vascular sling with tracheomalacia: surgical management.

Surgical repair of pulmonary artery sling without concomitant correction of associated tracheal abnormalities has yielded poor results in the past. We combined vascular sling repair done during cardiopulmonary bypass through a median sternotomy incision with tracheopexy for severe associated tracheomalacia in 2 infants. Neither experienced substantial postoperative respiratory difficulties and both had patent vascular anastomoses at 1 year after repair, thus supporting this approach when this combination of lesions is present.

Cardiopulmonary Bypass↗
PubMed1989

Viable cryopreserved aortic homograft for aortic valve endocarditis and annular abscesses.

Six consecutive patients with active aortic valve endocarditis, including 2 with extensive subannular aortic root abscess, were successfully treated with viable cryopreserved homograft aortic valve replacement. Two patients required extensive aortic root reconstruction with an appropriately trimmed aortic homograft to cover large abscess cavities. All patients showed resolution of infection with no perioperative mortality or clinically significant morbidity. Three patients had a minor degree of aortic insufficiency on postoperative echo-Doppler study. On follow-up at 6 to 48 months, all patients were in New York Heart Association functional class I. The resistance of the unstented homograft to infection makes it an attractive choice for patients requiring aortic valve replacement for active endocarditis. The results of surgical intervention in patients with extensive aortic root involvement may be further improved by the flexibility afforded by the homograft to be "custom-fit" to the abnormal aortic root and the ability to achieve secure abnormal aortic root and the ability to achieve secure valve fixation without use of prosthetic material.

Abscess↗
PubMed1989

Blood conservation in coronary artery bypass surgery: prediction with assistance of a computer model.

A computer assisted model was created with the data from 514 consecutive coronary bypass patients in order to predict the potential need of a blood transfusion. During this time period strict management protocols were used. In this series 261 (55.9%) patients were never and 46 (9.9%) were only intraoperatively transfused. Intra- and postoperative transfusions were necessary for 160 (34.2%) patients. Preoperative hematocrit, age, sex, and weight were the statistically significant parameters in the development of the model.

Adult↗
PubMed1988

Life-threatening intrathoracic complications during treatment with extracorporeal membrane oxygenation.

Extracorporeal membrane oxygenation (ECMO) has been successful (greater than 80% survival) in 35 centers in greater than 900 newborns with severe respiratory failure having an estimated mortality of greater than 80% on conventional management. During the last 3 years we have treated 79 newborns with 74 survivors (94%). Their diagnoses included meconium aspiration, persistent fetal circulation, respiratory distress syndrome, congenital diaphragmatic hernia, and sepsis. Seven patients (9%) had life-threatening intrathoracic complications requiring emergent intervention while on ECMO: tension hemothorax (3), tension pneumothorax (2), and pericardial tamponade (2). Pericardial tamponade and tension hemothorax and pneumothorax show a similar pathophysiology of increasing intrapericardial pressure and decreasing venous return. Perfusion is initially maintained by the nonpulsatile flow of the ECMO circuit before further decrease in venous return results in decreasing ECMO flow and progressive hemodynamic deterioration. Each of the seven patients demonstrated a clinical triad that includes increasing PaO2 and decreasing peripheral perfusion (as evidenced by decreasing pulse pressure and decreasing SvO2) followed by decreasing ECMO flow with progressive deterioration. The diagnoses were confirmed by transillumination, chest x-ray, or cardiac echocardiogram. Initial emergent placement of a percutaneous drainage catheter was temporizing in all seven cases. However, four patients required emergent thoracotomy for definitive treatment while still on ECMO. All seven patients were weaned from ECMO and are short-term survivors (6 months to 3.5 years). As use of ECMO for newborn severe respiratory failure increases, responsible physicians must be familiar with life-threatening intrathoracic complications and appropriate treatment strategies.

Cardiac Tamponade↗
PubMed1988

Aortic arch thrombosis in the neonate.

Thrombotic occlusion of the aortic arch in the neonate is a rare lesion for which successful operative repair with survival beyond the immediate postoperative period has not been previously reported. We report a case in which surgical repair of this lesion with survival was achieved and discuss the diagnostic and technical aspects of management of aortic arch thrombosis in the neonate.

Aorta, Thoracic↗
PubMed1987

Hemodynamic action of calcitonin gene-related peptide in the isolated rat heart.

The effects of calcitonin gene-related peptide (CGRP) on heart rate, coronary flow, pressure development, and time to ischemic contracture were studied in the isolated, perfused rat heart. A bolus of CGRP (2640 pmols) caused significant increases in heart rate and coronary flow; these effects were sustained for at least five minutes after injection. The increase in coronary flow was independent of heart rate, since CGRP caused an increase in coronary flow in non-beating (potassium-arrested) hearts. The dose-response of CGRP was studied using five doses (65, 218, 658, 1320 and 2640 pmols) given as bolus injections. Although the increase in heart rate was apparently dose-dependent, significant increases above baseline were observed only with the two highest doses. In contrast, coronary flow increased significantly above baseline with the injection of all but the lowest dose of CGRP. Ten minutes after injection of CGRP, all hearts were made ischemic. The time to onset of ischemic contracture was approximately 11 minutes for those hearts that received 65 pmols of CGRP; however, for those hearts receiving all other doses of CGRP, the time to onset of contracture was approximately 8 minutes. We conclude that CGRP significantly decreases the resistance of the coronary vascular bed, and that it may be an important regulator of regional blood flow in the heart.

Animals↗
PubMed1987

Effect of increasing volume of cardioplegic solution on postischemic myocardial recovery.

Multidose cardioplegia has been reported to be superior to single-dose cardioplegia in protecting the heart during ischemia. However, large volumes of cardioplegic solution may be detrimental because of washout of adenine nucleotide degradation products that accumulate during ischemia, which limits recovery of adenosine triphosphate. We designed an experiment to test the effects of increasing the volume of cardioplegic solution on postischemic myocardial recovery. Four groups were studied: Group 1, initial 2 minute single dose of cardioplegic solution; Group 2, infusion of cardioplegic solution every 30 minutes for 1 minute; Group 3, infusion of cardioplegic solution every 20 minutes for 1 minute; and Group 4, infusion of cardioplegic solution every 20 minutes for 2 minutes. All groups were ischemic for 2 hours at 20 degrees C. Although washout of nucleotide degradation products during the ischemic interval increased with higher volumes of cardioplegic infusion, the total washout (infusion plus initial 5 minutes of reperfusion) was not different among all groups. The multidose groups recovered function better and had significantly higher levels of total tissue purines after 30 minutes of reperfusion. There was no difference in adenosine triphosphate levels among all groups after reperfusion. We conclude that increasing the volume of cardioplegic solution, within a clinically relevant range is not associated with increasing loss of adenine nucleotides from the cell or with impaired functional recovery of the heart.

Adenosine Triphosphate↗
PubMed1986

Indications for replacement of the Beall 103 and 104 disc valves.

Because of the unpredictable risk of failure of the Beall 103 and 104 valves, 29 patients who had such a valve implanted between 1969 and 1975 were identified in 1979 and studied to determine clinical status, degree of hemolysis, and valve function by cinefluoroscopy and echocardiography. Seven had valve replacement early after initial study because of cardiac symptoms or severe hemolysis or both. Of the 22 patients followed from January, 1980 to August, 1985, 13 experienced new symptoms or hemolysis, and had valve replacement. Serial observations over a mean of 2.8 years in patients with an isolated Beall valve eventually requiring operation for severe valve wear showed increasing hemolysis frequently concomitant with onset of cardiac symptoms. There were no perioperative deaths in 20 Beall valve replacements, which included 9 multiple valve operations. The mean interval to replacement for all patients was 8.5 years. When the only prosthetic valve was the Beall mitral valve, severe valve wear was associated with higher levels of lactate dehydrogenase (LDH) (1,117 +/- 67 IU [+/- standard error]) than those with mild or moderate valve wear at reoperation (LDH, 565 +/- 68 IU; p less than 0.01). Cinefluoroscopy identified abnormal disc motion in 3 patients, all with clinical deterioration; all patients with disc to cage ratios of 0.90 or less had severe valve wear, but more patients with severe wear had normal ratios. Cardiac catheterization frequently did not show major abnormalities. The onset of new cardiac symptoms or evidence of increasing hemolysis from serial serum LDH determinations or evidence of abnormal disc size or motion by cinefluoroscopy indicate a high probability of severe Beall valve wear.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Paraganglioma of the heart. The value of magnetic resonance imaging in the preoperative evaluation.

Although the 131I-metaiodobenzylguanidine scan has proven reliable in identifying mediastinal paragangliomas, further localization has usually required dynamic computerized tomographic scanning which requires rapid bolus injection of contrast material. In the case presented herein, magnetic resonance imaging provided accurate preoperative localization and added important anatomic detail that was not appreciated with dynamic computerized tomograms or with other studies. Magnetic resonance imaging can accurately localize cardiac paragangliomas without injection of contrast material and may provide more detailed information for better guidance for surgical excision.

3-Iodobenzylguanidine↗
PubMed1985

Release of AMP and adenosine from rat heart mitochondria.

Release of AMP and adenosine from rat heart mitochondria was studied. The rate of appearance of extramitochondrial adenosine was independent of the extramitochondrial phosphate concentration between 5 and 20 mM. In the absence of exogenous, respiratory substrates or in the presence of glutamate/malate plus rotenone, the rate of appearance of adenosine was relatively low when phosphate was not added. The appearance of extramitochondrial AMP + adenosine was found to be directly proportional to the extra-mitochondrial phosphate concentration. Zn2+ (10 mM) decreased the rate of adenosine appearance by 90% and increased the rate of AMP appearance 6-fold. The mitochondrial preparations dephosphorylated exogenous AMP; this activity was inhibited by 10 mM Zn2+. We conclude that the adenosine appearing in the extramitochondrial space was not due to a direct release from the matrix, but instead was due to adenine nucleotide release with subsequent conversion to adenosine in the extramitochondrial space.

5'-Nucleotidase↗
PubMed1985

Phosphate-induced efflux of adenine nucleotides from heart mitochondria.

Adenine nucleotide efflux from isolated rat heart mitochondria was studied. Inorganic phosphate induced efflux of adenine nucleotides from the mitochondria. This efflux was inhibited by carboxyatractyloside and atractyloside. The rate of efflux showed saturation kinetics with respect to extramitochondrial phosphate (Km, 9.5 mM). Lowering the pH from 7.4 to 6.8 had little or no effect on the rate of efflux. Deenergizing the mitochondria enhanced carboxyatractyloside-insensitive efflux, but it did not affect carboxyatractyloside-sensitive efflux. Extramitochondrial ATP (200 microM) or AMP (200 microM) prevented efflux when the phosphate concentration was 10 mM. AMP (200 microM) did not inhibit efflux when the phosphate concentration was 40 mM. Atractyloside inhibited efflux noncompetitively with respect to inorganic phosphate. Mersalyl (10 nmol/mg protein) did not inhibit efflux. Phenylsuccinate (20 mM) totally inhibited phosphate-induced efflux. The results of this study indicate that under conditions found in the ischemic heart cell (low ATP, high phosphate), adenine nucleotides may be lost from the mitochondria via the adenine nucleotide translocase. Phosphate does not induce this efflux by interacting with the translocase or the phosphate-hydroxyl carrier. The site of action of phosphate may be the dicarboxylate carrier.

Adenine Nucleotides↗