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Biomedical subjects

J A Lipp

Publications and source records attributed to J A Lipp.

17 recordsLinked to original sources
PubMed1979

Graded flow reductions and O2 consumption of small partially ischemic region of dog left ventricle.

The relationship of O2 supply and demand was studied in a small region of a normally functioning left ventricle in 11 pentobarbital anesthetized open chest dogs. A small myocardial vein was catheterized for flow and venous O2 content measurements. An electromagnetic flow probe and screw-type occluder were placed on the supply artery. Arterial flow reductions produced a lesser decrease in venous outflow. This indicated that collateral channels were functional even with relatively small reduction in arterial flow. Even with complete arterial blockage, venous flow never fell below 13.7% of control. Supply had to be reduced to 80.8% of control before we could predict with 95% confidence that O2 demand would fall. Using this technique, it would be possible to test antianginal agents' actions on the O2 supply and demand relation in a region of flow restricted myocardium.

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PubMed1978

Quantitative determination of regional oxygen consumption in the dog heart.

A micro-Fick method has been developed to measure the O2 consumption of different regions of an organ. The method was tested in isolated dog gracilis muscle and consisted of microspectrophotometric determination of arterial and venous O2 saturation in quick frozen tissue to determine O2 extraction and flow measured with 85Sr-labeled microspheres, with O2 consumption calculated from the product. This was compared to electromagnetically measured flow and O2 extraction determined by Van Slyke or CO-oximeter. The accuracy of the new measurement was at worst 8.7% for O2 consumption over the range tested in a single muscle. In the hearts of anesthetized open-chest dogs, right ventricular O2 consumption, 7.1 +/- 0.9 ml O2/min per 100 g, was significantly lower than left, 11.0 +/- 0.4. This gradient was related to a blood flow difference. Right ventricular base had a 51% lower O2 consumption than right ventricular apex. In the left ventricle, subepicardial O2 consumption, 9.5 +/- 0.7, was lower than that of the subenocardium, 12.1 +/- 0.7. This difference was related to a difference in O2 extraction.

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PubMed1978

Effect of atropine upon the cerebrovascular system during soman-induced respiratory depression.

The effect of soman-induced respiratory depression upon cerebral vascular physiology was studied in monkeys. There was a significant decrease in heart rate, mean arterial blood pressure, cerebral blood flow and cerebral perfusion pressure during the onset of respiratory depression, which terminated as apnea. Administration of atropine resulted in an immediate increase in all of the above mentioned parameters which coincided with improvement in respiration. It was concluded that soman impaired cerebral autoregulation, caused a decrease in cerebral blood flow and cerebral perfusion pressure. It was suggested that respiratory depression resulted, in part, from anoxia. Administration of atropine increased the cerebral blood flow and cerebral perfusion pressure, which in turn, possibly reversed the anoxic conditions resulting in the improvement of respiration.

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PubMed1976

Effect of atropine upon the cardiovascular system during soman-induced respiratory depression.

The effects of atropine, doxapram and isoproterenol upon soman-induced respiratory depression were investigated in the monkey. Administration of atropine resulted in an immediate increase in heart rate accompanied by a gradual increase in respiratory rate. The improvement in the EEG pattern coincided with improvement in respiratory function. Administration of either doxapram or isoproterenal during soman-induced apnea failed to significantly alter any of the physiological parameters. Clonazepam was used to control soman-induced seizure activity and convulsions.

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PubMed1976

Effect of alpha and beta adrenergic blockade on oxygen transport in rat skeletal muscle and brain.

The effects of phenoxybenzamine HCl and propranolol HCl, 2 mg/kg, on tissue oxygen tension (PO2), perfusion and small vessel blood content of the cerebral cortex and biceps brachii muscle of anesthetized rats were determined. Perfusion and PO2 were measured polarographically and small vessel blood content was measured with 59Fe-siderophilin-labeled blood. Under control conditions PO2, perfusion and small vessel blood content averaged 15.1 mm Hg., 15.6 ml/min/100 g and 0.91 ml/100 g in brain and 15.6 mm Hg, 13.1 ml/min/100 g and 1.63 ml/100 g in muscle. After phenoxybenzamine adminstration, there was a significant increase in muscle perfusion (17.4%) and decrease in cortical PO2 (9.2%). No other factors changed significantly. Propranolol caused no significant changes in any of the above factors. Arteriolar resistance in skeletal muscle decreased after phenoxybenzamine. Small vessel blood content measurements (an estimate of open capillary density) indicate no effects on precapillary sphincters with either agent. Since some changes in metabolism were indicated with these agents, regional oxygen consumption was calculated from this data.

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PubMedDate not supplied

Blood flow and relative tissue oxygenation of normal and partially ischaemic myocardium: effect of CO2.

1. Ischaemia of a portion of the myocardium in the dog heart was produced by tying off a small branch of a coronary artery: flow in the occluded region was reduced from 5 to 82% of the initial value. 2. The effect of inhalation of 5% CO2 in air on relative tissue PO2 and perfusion in normal and partially ischaemic myocardium was determined. 3. After 10 min inhalation of 5% CO2, there was an increase in tissue perfusion as measured by hydrogen desaturation; the increase was inversely proportional to the degree of flow reduction. 4. Relative intramyocardial PO2 measured polarographically, decreased with occlusion and increased after CO2 inhalation; the changes were inversely proportional to the degree of reduction in PO2. 5. The increase in flow after CO2 inhalation suggests that partially ischaemic myocardial tissue is capable of further vasodilation.

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