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Biomedical subjects

J R Van Camp

Publications and source records attributed to J R Van Camp.

8 recordsLinked to original sources
PubMed1997

Adjustable model of chronic left ventricular dysfunction.

BACKGROUND: As an adjunct to the development of skeletal muscle-powered left ventricular assist devices, an adjustable model of chronic left ventricular failure was developed. METHODS: Implantation of a left ventricular balloon to induce heart failure was accomplished via left thoracotomy. Upon recovery, left ventricular failure was simulated by manipulation of left ventricular balloon volume to chronically raise left atrial pressure. RESULTS: Left atrial pressure increased from a baseline of 9.3 +/- 0.7 mm Hg to 18.5 +/- 1.2 mm Hg, 20.2 +/- 1.8 mm Hg, and 26.0 +/- 1.2 mm Hg by the 2nd, 6th, and 10th postoperative week, respectively. Cardiac index declined from a baseline of 4.4 +/- 0.3 L x min(-1) x m(-2), reaching stability by the 8th postoperative week at 3.0 +/- 0.4 L x min(-1) x m(-2). Stroke volume index declined from 1.12 +/- 0.1 mL x kg(-1) x beat(-1) to 0.60 +/- 0.1 mL x kg(-1) x beat(-1) by the 10th postoperative week. Mean survival was 75 +/- 7 days. Causes of death included left ventricular failure, thromboembolism, and euthanasia. CONCLUSIONS: This method of simulating chronic left ventricular dysfunction proved to be stable and adjustable and has been useful in the development of ventricular assist systems.

Animals↗
PubMed1995

Functional recovery after ischemia: warm versus cold cardioplegia.

Warm continuous retrograde cardioplegia has been introduced for myocardial protection during cardiac operations, particularly in the setting of acute myocardial ischemia because of its theoretical advantage of producing arrest without ischemia. To investigate the ability of warm continuous retrograde cardioplegia to provide myocardial protection after acute global ischemia, versus the more commonly used cold intermittent antegrade cardioplegia, 12 dogs were subjected to 15 minutes of normothermic global myocardial ischemia on cardiopulmonary bypass followed by 75 minutes of protected cardioplegic arrest using either warm continuous retrograde cardioplegia or cold intermittent antegrade cardioplegia. Standard blood cardioplegia at clinically used volumes and flow rates was used. Warm continuous retrograde cardioplegia animals received 30 mL/kg antegrade to induce arrest followed by 1.5 to 1.8 mL.kg-1.min-1 retrograde at 37 degrees C, whereas cold intermittent antegrade cardioplegia animals received 30 mL/kg antegrade to induce arrest followed by 15 mL/kg antegrade every 15 minutes at 10 degrees C. Load-insensitive left ventricular systolic function, diastolic function, high energy nucleotides, and edema formation were assessed before and after ischemia. Results showed that myocardial preservation using clinically reported flow rates and volumes of warm continuous retrograde cardioplegia was significantly inferior to that provided by clinically used cold intermittent antegrade cardioplegia, as demonstrated by decreased preload recruitable stroke work slope (28 +/- 11 versus 71 +/- 6), increased alpha constant of the end diastolic stress-strain relationship (14.2 +/- 3.0 versus 3.6 +/- 1.0), decreased total nondiffusable nucleotides (40.7 +/- 2.3 versus 57.4 +/- 2.3 microM/g wet weight) and increased water content (82.2% +/- 0.4% versus 80.4% +/- 0.4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1994

Regulation of pulmonary vascular resistance by endogenous and exogenous nitric oxide.

Inhaled nitric oxide (NO) causes selective pulmonary vasodilation under conditions of hypoxia or pulmonary vascular dysfunction. We have observed that NO affects canine pulmonary vascular resistance minimally under normal conditions. We hypothesized that endogenous NO is partly responsible for pulmonary vasomotor regulation in normoxic and hypoxic states. Dogs were studied before and after pulmonary endothelial injury with monocrotaline and N-omega-nitro-L-arginine (LNNA). Systemic vascular resistance was unaffected by NO. Under normal conditions, exogenous NO had little effect on pulmonary vascular resistance. After monocrotaline administration, baseline pulmonary vascular resistance was unchanged but decreased further in response to NO. After LNNA administration, pulmonary vascular resistance increased and there was an exaggerated increase with hypoxia that was reduced by NO. The effect of monocrotaline on in vitro endothelial function was evaluated with isolated pulmonary arteries, which showed a decreased relaxation response to bradykinin (an endothelial-dependent vasodilator) and a normal response to nitroprusside (an endothelial-independent vasodilator). These results support the hypothesis that endogenous NO is an important regulator of pulmonary vasomotor tone and is of even greater importance during hypoxia.

Animals↗
PubMed1989

Photosensitization of single-strand breaks in pBR322 DNA by rose bengal.

Rose bengal photosensitized the formation of frank single-strand breaks (SSBs) in double-stranded, supercoiled pBR322 DNA as measured by neutral agarose electrophoresis. The yield of SSBs followed first order kinetics with respect to light fluence and dye concentration. The efficiency of cleavage was more than 20 times greater in an argon atmosphere than in an oxygen atmosphere. The quantum yield in an air atmosphere was 1.7 (+/- 0.3) X 10(-8). Sodium azide quenched the cleavage more efficiently in an oxygen atmosphere than when the oxygen concentration was reduced. Isopropanol and mannitol were poor quenchers; ribose-5-phosphate and guanosine-5'-monophosphate did not quench the cleavage. Substituting D2O for H2O increased the yield of SSBs in both oxygen and oxygen-depleted atmospheres. The results are consistent with initiation of cleavage by reaction of the triplet state of rose bengal (or a radical derived from it) with DNA. In the presence of oxygen, an additional mechanism is introduced.

DNA Damage↗