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Biomedical subjects

C P Rose

Publications and source records attributed to C P Rose.

At least 37 records · Page 2Linked to original sources
PubMed1985

Reflex sympathetic effects on liver vascular space and liver perfusion in dogs.

The effects of sympathetic fiber activation on liver vascular volume and on the perfusion of the liver were ascertained in dogs by use of the multiple indicator-dilution technique. Portal vein-hepatic vein dilution patterns were obtained following injection of a mixture containing 51Cr-labeled red blood cells (a vascular reference), 14C-labeled sucrose (an interstitial reference), and 3H-labeled water (a cellular reference). Liver vascular, interstitial, and cellular water spaces were measured from the dilution data under control conditions and following activation of the sympathetic system by bilateral occlusion of carotid arteries. Carotid occlusion significantly increased plasma norepinephrine values without changing plasma epinephrine concentration, indicating that the resulting reflex sympathetic activation was selective for peripheral fibers. Although average blood flow did not change, liver vascular volume decreased by 40% during the sympathetic activation, and sucrose interstitial space and accessible cellular water space were unchanged. These findings indicate that there were no areas of no flow in the liver during the sympathetic activation, despite the observed large diminution in vascular blood content.

Animals↗
PubMed1985

Limitations of tracer oxygen uptake in the canine coronary circulation.

Theoretical models of oxygen transport in the myocardium have failed to account for low average tissue pO2 relative to to coronary sinus pO2, measured with pO2 electrodes and myoglobin saturation, and for hypoxic contractile failure at relatively high coronary sinus pO2 levels. These findings could be explained by either arteriovenous diffusional shunting or a limiting rate of transfer of oxygen from blood to tissue, or both. To gain new insights, we performed multiple indicator dilution tracer experiments across the coronary circulation in the dog, with 18O2 as the oxygen tracer and 51Cr-labeled red cells as the reference tracer for oxygen. 125I-Albumin and 22Na+ were included to provide the relative plasma flow rate. The tracer oxygen outflow curve consisted of a large early peak related to its reference red cell curve. No tracer emerged before the labeled red cells. The downslope, which contains the returning component of the tracer curve, decreased less steeply when oxygen consumption was reduced by propranolol. Fitting the tracer oxygen outflow curve with a distributed model including irreversible sequestration behind a resistance gave a transfer rate constant which was relatively small, and a relatively large rate constant for sequestration. Relative oxygen consumption (estimated from the arteriovenous difference) correlated closely with the rate constant for sequestration. Estimated average tissue oxygen concentrations were of the order of one-third blood concentration. Dimensional analysis indicates that the low transfer rate constant derives from hemoglobin-oxygen binding; this decreases fractional tracer oxygen transfer in proportion to the ratio of plasma:red cell oxygen pools.

Animals↗
PubMed1985

Tracer norepinephrine kinetics in coronary circulation of patients with heart failure secondary to chronic pressure and volume overload.

Controversy exists over the nature of the abnormality in cardiac sympathetic nerves in heart failure. In the cardiomyopathy of the Syrian hamster, reduction in tissue stores and increased turnover of norepinephrine is clearly associated with excessive sympathetic stimulation but in animal models and humans with heart failure secondary to mechanical overload there is evidence for depression of neuronal uptake. Because norepinephrine is both released and taken up by sympathetic fibers it is impossible to assess norepinephrine kinetics in an intact heart without separating these two functions. A technique for doing so has recently been developed in normal dogs and we therefore acquired similar data in humans with heart failure secondary to chronic pressure and volume overload. The technique involves the combination of transient norepinephrine tracer coronary sinus outflow in relation to intravascular and interstitial references after simultaneous injection into the left coronary artery and the measurement of endogenous norepinephrine concentrations in artery and coronary sinus. We found a marked reduction in cardiac norepinephrine release and uptake in a group of patients with clinical left ventricular failure secondary to mechanical overload, relative to a group of patients with no failure. Norepinephrine balance and overflow across the heart were not significantly different. We conclude that there is hypofunction of the cardiac sympathetic nerves in heart failure secondary to mechanical overload and that traditional methods are inadequate in assessing cardiac norepinephrine kinetics when there are simultaneous changes in neuronal uptake and release.

Adult↗
PubMed1984

Effect of beta-adrenergic blockade on in vivo norepinephrine release in canine heart.

The beta-adrenergic blockade-induced reduction in myocardial norepinephrine overflow during sympathetic stimulation was examined by use of the multiple indicator-dilution technique. A kinetic model incorporating the effects of flow, capillary permeability surface product for norepinephrine, the interstitial uptake rate constant for neurotransmitter, and plasma norepinephrine input and output values was used to estimate the rate of local release of norepinephrine into the interstitial space. The model was tested by first examining the effects of two drugs that increase myocardial norepinephrine overflow during sympathetic stimulation by differing mechanisms: desmethylimipramine, a norepinephrine uptake inhibitor, and phentolamine, an alpha-adrenergic blocker. The uptake inhibitor was demonstrated to reduce interstitial uptake and the alpha-blocker to increase local neurotransmitter release, without change in blood flow. The beta-adrenergic blocker, in contrast, reduced coronary blood flow and decreased the capillary norepinephrine permeability surface product but did not change the rate of local release. The decreased norepinephrine overflow after beta-blockade was deduced to result from the decrease in transcapillary flux and secondary increase in interstitial uptake.

Adrenergic beta-Antagonists↗
PubMed1983

Effects of saturating metabolic uptake on space profiles and tracer kinetics.

Vascular and steady-state lengthwise concentrations evolving in tissue as a consequence of saturable uptake processes are explored when there is no effective barrier between blood and tissue, when there is one effective barrier (the liver), and when barriers are present at both capillary and cell membrane. Falling exponential profiles develop at low-input concentrations and grade over into much smaller linear decreases at high concentrations. Uptake behind an effective barrier produces a step-down in concentration. With no effective barriers, a tracer impulse propagates to the outflow in a delayed fashion, reversible binding to the enzymic removal mechanism increasing its space of distribution and delaying it further and irreversible uptake diminishing its area. As bulk concentration is increased, proportional tracer uptake diminishes and ultimately approaches zero. With barriers in the system, tracer output consists of an impulse damped by cell entry, followed by outflow recovery of material that has escaped cell uptake. Increase in bulk concentration is found to saturate the uptake mechanism, with a proportionate increase in the returning material.

Animals↗
PubMed1983

Blood flow and norepinephrine effects on liver vascular and extravascular volumes.

The relative effects of changes in hepatic blood flow and in levels of sympathetic activity on liver volumes were ascertained by use of multiple-indicator dilution studies. Portal vein-hepatic vein dilution patterns were obtained following injection of a mixture containing 51Cr-labeled red blood cells (a vascular reference) and 14C-labeled sucrose (a reference extracellular substance). Hepatic blood volume was calculated as the product of liver blood flow and red cell transit times, and interstitial space as the product of plasma flow and the difference between labeled sucrose and red cell transit times. Concentrations of norepinephrine and epinephrine were measured in aorta, portal vein, and hepatic vein. Hepatic blood volume and interstitial space increased with increased blood flow; and elevated plasma norepinephrine levels, especially in portal vein (following either exogenous infusion or activation of peripheral sympathetic fibers) selectively reduced the distending effect of hepatic inflow on the vascular volume. The data provide a description of the in vivo variation in canine liver vascular and interstitial volumes with blood flow and sympathetic activation.

Animals↗
PubMed1983

Reduced aortocoronary sinus extraction of epinephrine in patients with left ventricular failure secondary to long-term pressure or volume overload.

Heart failure is associated with a reduction in tissue norepinephrine concentration, catecholamine fluorescence, and tyrosine hydroxylase activity. We hypothesized that this attrition of sympathetic nerve function might also be associated with a reduction in the ability of the neuronal membrane to sequester catecholamines. Since the heart does not release epinephrine, the cardiac extraction of epinephrine should be an index of the membrane uptake system. In 12 patients with documented left ventricular failure (pulmonary edema) secondary to mechanical overload and in 10 patients with no history of heart failure, we measured simultaneous plasma catecholamine concentrations in the aorta, coronary sinus, and femoral vein. The aortocoronary sinus extraction of epinephrine was 43 +/- 17% in the group with no evidence of heart failure but 0 +/- 14% in the group with failure. Net norepinephrine outflow (release minus extraction) was significantly higher in the group with failure, possibly because of reduced extraction. There was neither a reduction in the ability of the lower limb to extract epinephrine nor an increased norepinephrine outflow from the limb. These findings suggest that the sympathetic neuronal membrane uptake system is also depressed in the failing heart and that if the mechanism of catecholamine sequestration in the heart is related to that in the lower limb, the ablation of sympathetic nerve function is specific to the heart and is not a result of a generalized depression of the peripheral sympathetic nervous system.

Aorta↗
PubMed1983

Changes in cardiac transcapillary exchange with metabolic coronary vasodilation in the intact dog.

The effects of metabolic coronary vasodilation on transcapillary exchange in the heart were examined in anesthetized dogs by use of the multiple indicator dilution technique. Animals were studied under basal conditions and during coronary sinus pacing. To obviate adrenal medullary stimulation, catheters were placed in coronary artery and coronary sinus in a closed chest preparation. Plasma catecholamine concentrations were determined to provide an index of the level of sympathetic tone. Labeled albumin and sucrose were injected into the coronary artery, and outflow dilution curves were secured. Analysis of these, with a model incorporating throughput and returning components, and heterogeneity of capillary transit times, provided parameters reflecting flow, permeability-surface product for sucrose, and capillary heterogeneity. Coronary sinus pacing increased both heart rate and plasma norepinephrine values; in response, myocardial oxygen consumption increased, metabolic vasodilation occurred, and coronary flow increased. The capillary permeability-surface product for sucrose increased with the flow but tended to plateau at higher values, showing a saturation phenomenon. Capillary heterogeneity, present in control animals with low sympathetic tone, was grossly decreased during cardiac metabolic activation. The Crone-Renkin approximation formula for the permeability-surface product yielded values that were too low at low flows and values approaching those from the complete model at high flows. The findings indicate an integrated pattern of circulatory response to cardiac metabolic activation characterized by decreased resistance, increased flow, increased permeability-surface product, and reduced heterogeneity. The last two effects amplify the capacity of increased flow to deliver substrates to heart muscle cells.

Animals↗
PubMed1983

Selective right ventricular dysfunction after coronary artery bypass grafting.

Preoperative and postoperative right (RVEF) and left ventricular ejection fractions (LVEF) were studied by means of radionuclide techniques in 15 patients undergoing coronary bypass operations. Three of them, all with right coronary artery lesions, had postoperative depression of RVEF without concomitant decrease in LVEF. In contrast to those with left ventricular dysfunction, the patients with selective RVEF depression did not have significant elevation of myocardial injury index calculated from creatine kinase isoenzyme (CK-MB) curves.

Cardiac Output↗
PubMed1982

Anterior femoral erosion and patello-femoral osteoarthritis.

The relationship between classical signs of osteoarthritis, anterior femoral erosion, and patellar tendon lengths was determined in 130 patients derived from a sports medicine clinic and a general hospital. A method for detecting and measuring anterior lower femoral erosion is described. A significant relationship was found between anterior femoral erosions and osteoarthritis, but no significant relationship was found between patellar tendon length and osteoarthritis. The results bring into question previously described explanations for femoral erosions. It is suggested that this erosion is due to pressure transmitted from the supra-patellar bursa in active patients with joint effusions.

Adolescent↗
PubMed1981

Inaccuracy of radiographic measurements of colon polyps.

Polyp size is one of the main determinants of the surgical management of polyps in areas without colonoscopy services. We reviewed 47 patients with 59 polyps at two hospitals. Polyp dimensions were measured directly from air contrast barium enema radiographs, and again after resection and fixation. In over 95% of polyps the radiographic size exceeded the pathologic size by 10 to 100%. Since surgery may be decided on the basis of polyp size, an inaccurate measurement may result in unnecessary colonoscopy or laparotomy. We therefore recommend a correction factor derived from measuring a rectal tube of known diameter.

Colonic Neoplasms↗