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R L Clancy

Publications and source records attributed to R L Clancy.

At least 181 records · Page 10Linked to original sources

Inotropic and intracellular acid-base changes during metabolic acidosis.

Experiments in isolated, Ringer-perfused isovolumic rabbit hearts showed that metabolic acidosis resulted in a decrease in peak left ventricular pressure and dP/dt. Concomitantly, the decrease in extracellular pH from 7.28 plus or minus 0.02 to 6.82 plus or minus 0.02 at constant PaCO2 was associated with a negative av HCO3- difference that lasted throughout the duration of acidosis. This negative av HCO3- difference indicated that either HCO3- moved into the intravascular space or H+ moved in the opposite direction during acidosis. During perfusion with normal pH solution av HCO3- was not significantly different from zero. Washout of the extracellular space with the acid solution can account for only 32 percent of the total amount of HCO3-recovered in the venous perfusate during the 30 min of acidosis. The remaining 68 percent (10.7 plus or minus 3.1 mmol times kg-1 of cardiac tissue) must then have originated in the cellular fluid. When intracellular fluid volume is taken into account, it can be calculated that 21.3 plus or minus 6.1 mmol of HCO3- moved into the vascular space per liter of intracellular water. The magnitude of this HCO3- flux suggests that significant myocardial cellular acid-base changes are associated with metabolic acidosis.

Acidosis↗

Effect of norepinephrine on myocardial intracellular hydrogen ion concentration.

The effect of norepinephrine (NE) on the intracellular hydrogen ion concentration [H+]i of isolated rat hearts perfused with a modified Krebs-Henseleit solution (SHS) was determined. The [H+]i was calculated with the [14C]-dimethyloxazolidinedione method. Respiratory or metabolic acidosis was produced by equilibrating the KHS with 20% C02 or decreasing the [HC03-] of the KHS, respectively. Three types of experiments were carried out: 1) beta blockade--MJ 1999 (Sotalol) was added to the KHS; 2) control--no pharmacological treatment; and 3) NE-norepinephrine was added to the KHS. The effective CO2 buffer values (delta[HC03-]i/deltapHi) during respiratory acidosis were: beta blockade, 11; control, 35; and NE, 84. The production of metabolic acidosis resulted in the following [H+]i changes: beta blockade, 52 mM; control, 60 nM; and NE 7 nM. These results suggest that NE markedly attenuates the changes in [H+]i accompanying respiratory and metabolic acidosis and may account in part for previous observations that the effective C02 buffer value of cardiac muscle in vivo is greater than that in vitro.

Acid-Base Imbalance↗

Circulating T and B lymphocytes in progressive systemic sclerosis.

Thymus derived (T) and bone-marrow derived (B) lymphocytes were quantitated in 11 untreated patients with progressive systemic sclerosis (PSS) and in 11 age and sex matched controls. T and B lymphocytes were identified according to their receptor sites for sheep red blood cells and activated complement, respectively. All patients had a normal lymphocyte count. The mean per cent value of circulating T lymphocytes was less in PSS patients (38 per cent) as compared with controls (56 per cent) (P less than 0.005), while no significant difference existed for the circulating B lymphocytes (PSS 14 per cent; controls 11 per cent). The mitogenic response to phytohemagglutinin (PHA) was assessed by comparing dose response curves in PSS with those obtained from matched controls. No significant difference could be detected between these groups.

B-Lymphocytes↗

Repopulation with IgA-containing cells of bronchial and intestinal lamina propria after transfer of homologous Peyer's patch and bronchial lymphocytes.

Transfer of 50 million rabbit allogeneic lymphocytes from either bronchus-associated lymphoid tissue (BALT) or Peyer's patches into 1000 R x-irradiated recipients results, 6 days later, in predominant repopulation of gut and bronchial lamina propria, as well as spleen with IgA-containing cells. After repopulation with BALT or Peyer's patch cells, lymphoid follicles in both gut and lung showed peripheral cellular membrane type of fluorescence with fluorescein-conjugated anti-IgA antisera only. Six days after x-irradiation alone, little evidence of repopulation was seen and immunofluorescent qualitative observations of gut and lung, and quantitative data in the spleen, confirmed these findings. After transfer of 50 million lymph node cells, very few immunoglobulin-containing cells were seen in the gut or bronchial lamina propria. These results suggest that there may be a common mucosal immunologic system, and that repopulation of gut and lung lamina propria may be through the organized lymphoid tissue therein.

Animals↗

The distribution of a rabbit thymic antigen and membrane immunoglobulins in lymphoid tissue, with special reference to mucosal lymphocytes.

We have examined rabbit lymphocytes from several tissue sources for membrane immunoglobulins with anti-antiserum for alpha, mu and iota heavy chains, as well as with an antiserum specific for a rabbit thymus lymphocyte antigen (RTLA). Among lymphocytes from bronchus-associated lymphoid tissue (BALT), Peyer's patches, thoracic duct and gut mucosa exclusive of Peyer's patches, alpha and mu predominated with roughly equal percentages of each being found. The distribution of cells with iota receptors was approximately half that of either of the two other classes. In splenic lymphocytes mu predominated, followed, respectively, in numbers by iota and alpha. Detection of RTLA on almost all thymus lymphocytes (94%), most thoracic duct lymphocytes (72%), and lower numbers of peripheral blood lymphocytes (44%), Peyer's patch lymphocytes (17%), and splenic lymphocytes (20%) indicated a similar distribution of this antigen between the lymphoid organs as has been found for the mouse thymus lymphocyte-specific antigens. Low numbers of RTLA-bearing lymphocytes were detected in both the BALT (18%) and the gut mucosa (11%). An unexpected finding was the number of "null" cells among the gut mucosa population, bearing neither thymic nor heavy chain markers. These results in toto support the view that lymphoid aggregates in lung and gut may both contain precursor populations of B cells destined for IgA production.

Animals↗