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Biomedical subjects

R C Reynolds

Publications and source records attributed to R C Reynolds.

At least 91 records · Page 5Linked to original sources
PubMed1977

Vasoactive intestinal polypeptide in brain: localization in and release from isolated nerve terminals.

The vasoactive intestinal polypeptide was present in synaptosomal (nerve ending) preparations from cerebral cortex, hypothalamus, and striatum of rat brain in higher concentrations than in these tissues as a whole. The total content and relative specific activity of the peptide increased with progressive purification of the synaptosomal fractions and generally followed the distribution of known synaptosomal constituents--dopamine, norepinephrine, and lactate dehydrogenase (L-lactate:NAD+ oxidoreductase, EC 1.1.1.27). The peptide was also released from synaptosomal pellets with increased K+ concentration, and this release was Ca2+-dependent. The findings suggest a role for vasoactive intestinal polypeptide as a transmitter or modulator of synaptic function.

Animals↗
PubMed1977

Primary pulmonary sporotrichosis.

A 34-year-old alcoholic and drug addict developed cavitary pulmonary sporotrichosis that progressed slowly during 6 years. Pulmonary resection and pre- and postoperative therapy with amphotericin B were associated with prompt clinical improvement with no evidence of relapse during a 2-year follow-up. Histologic examination of lung revealed granulomatous inflammation with organisms consistent with Sporothrix schenckii, and interstitial talc (magnesium silicate) granulomas. The latter finding was consistent with the history of intravenous drug abuse. Although the presence of silicates in lung enhances the pathogenicity of some microorganisms, the relation of these findings to the pathogenesis of sporotrichosis in our patient is unclear.

Adult↗
PubMed1977

Leukocytic response to inhaled bacteria.

Using histologic techniques, we have quantified the amount of infiltration of bronchi and alveoli by polymorphonuclear leukocytes during the 4 hours after an aerosol inoculation of mice with bacteria. Although the lungs of animals challenged with Staphylococcus aureus differed little from those of animals exposed only to a water aerosol, the lungs of animals exposed to Klebsiella pneumoniae or to Escherichia coli demonstrated significantly greater polymorphonuclear leukocyte infiltrations in bronchi and alveoli 2 and 4 hours afer exposure. These results suggest that the polymorphonuclear leukocyte may contribute to the early defense of the lung against some bacteria.

Aerosols↗
PubMed1977

Release of luteinizing hormone releasing hormone and thyrotropin releasing hormone from a synaptosome-enriched fraction of hypothalamic homogenates.

A mitochondrial fraction prepared from homogenates of rat hypothalamic tissue was found by means of electron microscopy to be enriched with synaptosomes. The release of luteinizing hormone releasing hormone (LHRH) and thyrotropin releasing hormone (TRH) from this preparation was investigated. After incubation, the synaptosomes were re-isolated by ultrafiltration; and the concentration of LHRH and TRH in the ultrafiltrate was determined by radioimmunoassay. When the synaptosome-enriched preparation was incubated in 0.32M sucrose at 1 or 30 C, less than 10% of the total LHRH and TRH was recovered in the ultrafiltrate. The two hormones were released by depolarizing concentrations (60 mM) of K+ in a Ca++-dependent manner, and the stimulatory effect of K+ was essentially complete within 2 min. In the presence of 2 mM Ca++, the release of LHRH and TRH increased with increasing K+ concentrations in the range 30-120 mM. Prostaglandin E2 (PGE2), PGF2 alpha, and PGF2 beta had little if any effect on LHRH or TRH release. When the synaptosome-enriched fraction was incubated in Hanks' balanced salt solution, the release of LHRH and TRH was about 10 times greater than that seen in 0.32M sucrose. It is concluded that a synaptosome-enriched fraction from the hypothalamus contains readily releasable pools of LHRH and TRH which are mobilized rapidly by depolarizing concentrations of K+ in a Ca++-dependent manner.

Animals↗
PubMed1977

Metabolism of kinins and angiotensins in the isolated glomerulus and brush border of rat kidney.

In order to localize the activities of kallikrein, kininase, angiotensin I converting enzyme, and angiotensinase in the kidney, rat kidneys were homogenized and glomeruli and brush border were isolated. The yield and purity of glomeruli preparations were high. The similarity of the structure of the isolated glomeruli in situ was established by scanning and transmission electron microscopy and freeze-fracture. The morphology of isolated brush border of proximal tubules was compared to brush border in situ. Isolated brush border, devoid of core material, retained its converting enzyme, kininase, and angiotensinase activity confirming our previous findings that these enzymes are bound to plasma membrane. Isolated glomeruli contained little or no kallikrein. In addition, compared to renal brush border, renal glomeruli contained a relatively low concentration of kininase, angiotensin I converting enzyme, and angiotensinase. The results of these experiments support the idea that the brush border of the proximal tubule is the major site of inactivation of kinins and angiotensins and that renal kallikrein enters the tubular filtrate distal to the glomeruli and proximal tubule.

Angiotensin II↗
PubMed1976

Isolation of membrane-bound renal enzymes that metabolize kinins and angiotensins.

Cortex of rat kidney was homogenized and fractions enriched in plasma membrane, endoplasmic reticulum or brush border were prepared by several techniques of differential centrifugation. The identity and homogeneity of the membrane fragments were investigated by assaying marker enzymes and by transmission and scanning electron microscopy. Kallikrein was present in both plasma-membrane- and endoplasmic-reticulum-enriched fractions isolated by two fractionation procedures. Kallikrein was highly concentrated in a plasma-membrane fraction but was absent from the brush-border membrane of proximal tubular cells. Cells of transplanted renal tumours of the rat, originating from the proximal tubule, had no kallikrein activity. Kininase activity, angiotensin I-converting enzyme (kininase II) and angiotensinase were found in a plasma-membrane-enriched fraction and especially in the fraction containing isolated brush border. It is suggested that after renal kallikrein is synthesized on endoplasmic reticulum, it is subsequently reoriented to a surface membrane for activation and release. Renal kallikrein may enter the tubular filtrate distal to the proximal tubules. The brush-border membrane of proximal tubule is the major site of inactivation of kinins and angiotensin II..

Adenosine Triphosphatases↗
PubMed1976

Pulmonary hypertension and foreign body granulomas in intravenous drug abusers. Documentation by cardiac catheterization and lung biopsy.

In this report we confirm the presence of pulmonary hypertension by cardiac catheterization in four intravenous drug abusers with biopsy-documented foreign body granulomas in the pulmonary vessels and interstitium. Each patient had a history of intravenous injections of alpha-sympathomimetic agents obtained from nasal inhalers. There agents may have contributed to the disease by constricting small vessels when simultaneously injected foreign bodies were passing through the vasculature of the lung. The severity of the pulmonary hypertension correlated well with the decrease in single breath diffusing capacity in each case. Pulmonary hypertension may contribute significantly to the increased morbidity and mortality observed in intravenous drug users.

Adult↗
PubMed1976

Malignant hyperpyrexia during anesthesia in childhood.

Malignant hyperpyrexia is a highly lethal complication of general anesthesia. It occurs with sufficient frequency, particularly in children and young adults, to justify use of continuous temperature monitoring during adminnstration of general anesthesia. Fever may be a late manifestation of the malignant hyperpyrexia syndrome, and it is important to be aware of the early signs. Prompt recognition and aggressive management should lower the high mortality known to occur with this complication. Family members should be screened for CPK elevations to determine possible susceptibility to malignant hyperpyrexia. Two case reports illustrate these points of diagnosis and management.

Anesthesia, General↗
PubMed1976

Isolation of renal membranes that contain kallikrein, angiotensin I-converting enzyme (kininase II) and angiotensinase in the rat.

1. Fractions highly enriched in plasma membrane, endoplasmic reticulum or brush border were prepared from rat kidney cortex. Kallikrein was concentrated in the plasma membrane fraction, but not in the brush border fraction. Angiotensin I-converting enzyme (kininase II) and angiotensinase were localized in the brush border membrane. 2. It is suggested that kallikrein in the urine may originate from plasma membrane distal to the brush border of proximal tubules and the conversion of angiotensin I and the inactivation of bradykinin and angiotensin II may occur on the lumen membrane of the proximal tubular cells.

Animals↗