Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
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Proc. Soc. Exp. Biol. Med. · Apr 1989
Phospholipid changes during adaptation to acidosis in urinary bladder of Bufo marinus.
The purpose of this study was to determine whether phospholipids (PL) play a role in the adaptation to metabolic acidosis by toad urinary bladder epithelium. Toads were placed in an NH4Cl acidosis for 48 hr. Quarter bladders were removed and incubated with [32P]orthophosphate or [3H]arachidonic acid for 1 hr at 25 degrees C. ⋯ Fractional PL (reported as percentage of fraction of total PL based on total lipid phosphorus) analysis in normal toads revealed phosphatidylinositol = 8.1 +/- 0.6% and PE = 27 +/- 1.2%, whereas for acidotic toads phosphatidylinositol = 11 +/- 0.6% and PE = 32 +/- 1.0% (P less than 0.01 for both). Aldosterone, a known stimulator of acidification, had no effect on 32P incorporation into PL fractions of the bladder. The increase in PL turnover following induction of acidosis is consistent with increased membrane synthesis or turnover during metabolic acidosis and this may reflect an increased transport of vesicular H+-ATPase into the apical membrane or the result of a proliferation of acid-secreting mitochondria-rich cells or both.
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Proc. Soc. Exp. Biol. Med. · Sep 1988
Comparative StudyComparison of effects of surgical and chemical sympathectomy on beta adrenergic and muscarinic receptors of parotid gland of young and adult rats.
Surgical (removal of a superior cervical ganglion) or chemical [(administration of a single dose of 6 hydroxydopamine (6 OHDA) (50 mg/kg dose body wt)] sympathectomy of rats at 2 or 8 days of age resulted in an increase in [3H]DHA binding of membranes of parotid gland of young rats (age range 21 days to 48 days). The increase progressed with postnatal age; at 21 days of age (surgical sympathectomy), it was 13%; at 32 days of age with 6 OHDA, it was as much as 34%, but only 26% at 42 days of age with surgical sympathectomy. No change in [3H]QNB binding was observed at any postnatal ages following neonatal sympathectomy. ⋯ In the adult, however, the duration of the denervation was of no importance since change in number of beta adrenoceptors did not occur at 1, 2, 3, or 4 weeks after surgical denervation but did occur after only 1 week after of reserpine-induced denervation. QNB binding was decreased with surgical sympathectomy as well as reserpine-induced sympathectomy of adult parotid gland; norepinephrine concentration was decreased to levels of a few percent of innervated glands. The relation between development of glandular supersensitivity and increase in beta adrenoceptors is discussed.
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Proc. Soc. Exp. Biol. Med. · Jan 1988
Interleukin 1 bioactivity in the lungs of rats with monocrotaline-induced pulmonary hypertension.
A single subcutaneous injection of monocrotaline in rats provokes lung injury, inflammation, and progressive pulmonary hypertension. The specific mediators of the lung injury and inflammation and the relation of these events to the ensuing hypertensive pulmonary vascular disease are not understood. Since the monokine interleukin 1 (IL-1) has been implicated in acute inflammatory reactions, the present study tested the hypotheses that monocrotaline promotes the appearance of IL-1 in the bronchoalveolar spaces of treated rats and that accumulation of the monokine coincides temporally with development of lung injury, inflammation, and/or pulmonary hypertension. ⋯ Lung inflammation also was present at Days 14 and 21 after monocrotaline as indicated by the accumulation of leukocytes in the bronchoalveolar lavage fluid and by an increase in the lung tissue activity of the granulocyte-specific enzyme myeloperoxidase. Interleukin 1, bioassayed in bronchoalveolar lavage fluid using the standard D10 T-cell assay system, was increased slightly at Day 4 postmonocrotaline, returned to baseline at Day 7, and was markedly elevated at Days 14 and 21 after monocrotaline treatment. These observations indicate that increases in the bronchoalveolar lavage fluid content of IL-1 bioactivity are temporally related to the evolution of monocrotaline-induced lung injury, inflammation, and pulmonary hypertension and suggest that the monokine may play a pathogenetic role in these events.
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Proc. Soc. Exp. Biol. Med. · Sep 1986
Monocrotaline-induced cardiopulmonary damage in rats: amelioration by the angiotensin-converting enzyme inhibitor CL242817.
Pulmonary injury induced by the plant alkaloid monocrotaline is partially prevented by the angiotensin-converting enzyme (ACE) inhibitor captopril. CL242817 [(S-[R*,S*])-1-([3-acetylthio]-3-benzoyl-2-methyl-propionyl)- L-proline] is a new orally active ACE inhibitor under evaluation as an antihypertensive agent. To determine whether CL242817 also can modify monocrotaline-induced pulmonary injury, male rats were divided into four groups: control; CL242817 (60 mg/kg/day, po); monocrotaline (2.4 mg/kg/day, po); or monocrotaline plus CL242817, and were sacrificed after 6 weeks of continuous treatment. ⋯ In contrast, concomitant CL242817 did not significantly influence the suppressed lung ACE and PLA activities in monocrotaline-treated rats. CL242817 alone produced retarded weight gain, decreased heart weight relative to body weight, decreased lung hydroxyproline content and ACE activity, and increased serum ACE activity and plasma AII concentration. Thus CL242817 resembles captopril, both in its ability to ameliorate monocrotaline-induced pulmonary injury in rats, and in many of its side effects.
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Proc. Soc. Exp. Biol. Med. · Oct 1984
Effects of neuromuscular blocking agents and acetylcholinesterase inhibitors on the response of pectoral fin muscle of the sculpin (Enophrys bison) to indirect stimulation.
The neuromuscular junction of the buffalo sculpin (Enophrys bison) was characterized in situ by examining the effects of various neuromuscular blocking agents and acetylcholinesterase inhibitors (ACHE-I) on pectoral muscle response to indirect stimulation. The injection of either d-tubocurarine (350 micrograms/kg) or alpha-bungarotoxin (alpha-Butx) (1 mg/kg) resulted in a flaccid paralysis. ⋯ The administration of the ACHE-I, diisopropyl fluorophosphate (DFP), and eserine resulted in responses which were contrary to those expected based on similar experiments using mammalian skeletal muscle. Twitch potentiation did not occur and the ability to maintain a tetanic response was not abolished even after the administration of clearly lethal concentrations of ACHE-I.