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Biomedical subjects

S Ehrenpreis

Publications and source records attributed to S Ehrenpreis.

At least 19 recordsLinked to original sources
PubMed1993

Risk factors not addressed in antihypertensive therapy based solely on blood pressure control.

There has been a considerable revolution in the field of hypertension therapy. We have gone through an era in which patients with severe hypertension and those with accelerated hypertension had a very short life expectancy. Currently blood pressure can be readily controlled with a marked improvement in longevity. We have gone from an era in which stroke was common due to hypertensive cardiovascular disease to an era in which patients are effectively treated and there has been a marked reduction in the incidence of stroke. The challenge is whether we can reduce the very high mortality due to coronary artery disease in patients with hypertension as we have done with stroke. New groups of drugs that may have a more favorable effect on metabolic and hemodynamic risk considerations have been developed over the last decade. These agents may reduce the risk for coronary heart disease to a greater extent than previously employed therapy. While there are no randomized placebo-controlled studies demonstration this, a theoretical basis does exist to give the physician reason to think about prioritizing therapies and tailoring them to the needs of the individual patient.

Animals↗
PubMed1993

The clinical implications of first-pass metabolism: treatment strategies for the 1990s.

The first-pass effect is real. It may pose obstacles to the treatment of disease, and strategies need to be developed to address the problem that first pass can cause. First we have to look at identifying the problem, and this symposium has helped to further emphasize that the problem exists and awareness is increasing. The first-pass effect has been a basic tenant of pharmacology but an area not receiving active research interest and one that is often overlooked in the clinical arena. Avoiding drug interactions is a consideration, and that is a major challenge to the field of clinical pharmacology. Clinicians need to be aware of the problem, aware of the danger areas with drugs, and first pass. Another alternative is to turn to chemical modification of a drug that avoids needing to take first pass into consideration.

Drug Therapy↗
PubMed1988

Histologic changes in the guinea pig gastrointestinal tract following 1 weeks' administration of chlorpromazine, haloperidol or atropine.

A comparison was made between the toxic effects of chronic chlorpromazine, haloperidol or atropine on the guinea pig intestinal tract. Chlorpromazine, administered at a dose of 30 mg/kg/day, IP for 7 days, produced marked pathologic changes in the guinea pig cecum, consisting of inflammation, edema and hemorrhage. None of these effects were noted when haloperidol, 2 or 10 mg/kg/day or atropine 30 mg/kg/day were similarly administered. Similar toxic effects may occur in humans on long-term chlorpromazine or other phenothiazine therapy, thereby accounting for the paralytic ileus observed with these drugs.

Animals↗
PubMed1988

Use of oral sodium polyacrylate in rat gastrointestinal alkali burns.

Alkali-induced injuries of the esophagus and stomach are currently medically managed with steroids and antibiotics. We investigated whether treatment with sodium polyacrylate (PANa), a proposed mucosal protectant, could decrease the deleterious effect of alkali injuries or prevent alkali injuries. Rats were randomized in 4 groups. Group I (control; n = 7) received 0.1 ml normal saline via gastric gavage. Groups II-IV received 0.1 ml 25% NaOH. Group II (n = 22) received no further treatment. Group III (n = 9) received 0.25% PANa ad lib in drinking water for 3 days prior to NaOH. Group IV received 0.25% PANa for 6 days after NaOH. Animals were weighed daily. At 6 days post NaOH, stomachs were removed from animals in Groups II-IV and burn lesions were outlined on tracing paper. 1 x 1 cm sections of burned areas were fixed, stained with H&E and histologically evaluated. In another study, 0.1 ml of 10% NaOH was given to 2 groups of animals. Group I (n = 22) received no other treatment, while Group II (n = 13) received PANa ad lib in drinking water for 3 days prior to NaOH. Of the animals treated with 25% NaOH, only those in Group II showed a decrease mean weight which was statistically significant on Day 4, p = 0.016. Mean burn areas were statistically greater in Group II than in Group IV (p = 0.025), while histologically, lesions were similar. Pretreatment with PANa prior to 10% NaOH prevented the weight loss which occurred daily in the control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylic Resins↗
PubMed1987

Histamine release as the basis for morphine action on bile duct and sphincter of Oddi.

We have investigated the mechanism by which morphine contracts hog bile duct and sphincter of Oddi. Morphine contraction is antagonized by naloxone, competitively on the sphincter, noncompetitively on the bile duct. Diphenhydramine at low concentration (3.4 X 10(-6)M) also antagonizes both actions of morphine. Histamine has a very potent contracting action on the sphincter and bile duct and this is antagonized by diphenhydramine. Burimamide only weakly antagonizes the actions of morphine or histamine. Compound 48/80 causes a pronounced contraction of sphincter and bile duct following which morphine effects are greatly attenuated. These results suggest that morphine-induced contraction of the sphincter of Oddi and bile duct is mediated by a two step reaction involving interaction with a specific opiate receptor leading to the release of histamine which combines with an H1 receptor to produce the effect.

Animals↗
PubMed1986

Inhibition by indomethacin of naloxone-precipitated opiate withdrawal contraction in isolated guinea pig myenteric plexus-longitudinal muscle preparation.

The isolated myenteric plexus-longitudinal muscle preparation from guinea pigs which had previously been administered morphine chronically 100 mg/kg/day, 7 days) shows a pronounced contraction when exposed to naloxone. Exposure of the preparation to indomethacin (6.7 micrograms/ml) for 10 minutes prior to naloxone inhibits this withdrawal response. A single dose of indomethacin, 1 mg/kg, given on the 6th day on morphine, also inhibits the naloxone contraction. These results suggest the involvement of a prostaglandin in the opiate withdrawal response in the ileum.

Acetylcholine↗
PubMed1985

Methionine-enkephalin and beta-endorphin levels in brain, pancreas, and adrenals of db/db mice.

Levels of methionine-enkephalin immunoreactivity (MEI) and beta-endorphin immunoreactivity (BEI) were measured by means of a specific RIA in pituitary, hypothalamus, pancreas, and adrenal glands of db/db and control mice. We found significantly higher levels of MEI in the pituitaries of db/db mice than in either littermate or background strain controls. There was no significant difference in MEI levels in pancreas, adrenal glands, and hypothalamus. There was a significant difference in the BEI levels in the pituitaries of db/db mice compared with those in controls. No significant difference in BEI levels was observed between db/db and control mice in any of the other regions examined. We conclude from the above data that the opiate peptide system in the hypophyseal-hypothalamic axis of the db/db mouse is abnormal and warrants further investigation. The significance of this finding with respect to the possible etiology of diabetes mellitus is discussed.

Adrenal Glands↗
PubMed1985

Pharmacology of enkephalinase inhibitors: animal and human studies.

We have shown that a number of compounds which inhibit the degradation of met-enkephalin can produce naloxone-reversible analgesia in mice. These compounds also potentiate the analgesia produced by acupuncture, foot shock, and transcutaneous nerve stimulation in animals and humans. The potency of their effectiveness as analgesics or potentiators parallels their potency as inhibitors of mouse brain enkephalinase. D-Phenylalanine (DPA), one of these enkephalinase inhibitors, has been used successfully for the management of chronic intractable pain in humans and to potentiate the treatment of many painful conditions by acupuncture. Other aspects of pharmacology of DPA will be discussed, including its effects on the cardio-vascular system, behavior, and lack of development of tolerance and dependence when used chronically in animals and humans.

Acupuncture Therapy↗
PubMed1985

Analgesic properties of enkephalinase inhibitors: animal and human studies.

D-phenylalanine, bacitracin and puromycin produce long-lasting, naloxone-reversible analgesia in mice. Analgesic potency parallels potency of these compounds as inhibitors of met-enkephalin degradation by mouse brain enzymes. D-phenylalanine potentiates acupuncture analgesia in mice and humans and has been used to ameliorate a variety of human chronic pain conditions.

Acupuncture Therapy↗
PubMed1982

D-phenylalanine and other enkephalinase inhibitors as pharmacological agents: implications for some important therapeutic application.

A number of compounds have been shown to inhibit the degradation of enkephalins. As expected, these compounds produce naloxone reversible analgesia and potentiate the analgesia produced by enkephalins and by acupuncture. One of these, D-phenylalanine, is also anti-inflammatory. D-phenylalanine has proven to be beneficial in many human patients with chronic, intractable pain. It is proposed the enkephalinase inhibitors may be effective in a number of human "endorphin deficiency diseases" such as depression, schizophrenia, convulsive disorders and arthritis. Such compounds may alleviate other conditions associated with decreased endorphin levels such as opiate withdrawal symptoms.

Acupuncture Therapy↗
PubMed1979

Phenothiazine effect on gastrointestinal tract function.

Clinical evidence indicates that phenothiazines, specifically chlorpromazine (CPZ), used extensively in the treatment of patients with mental and/or neurologic disorders produce an ileus characterized by pseudoobstruction with an extended barium transit time of eight to ten days. Postoperatively, these patients have a protracted ileus, lasting from ten to fourteen days. In our present study we investigated the mechanism of action by which phenothiazines block gastrointestinal tract function as well as the possible reversal of this effect by pharmacologic agents. Guinea pigs were injected intraperitoneally with CPZ at a dose of 30 mg/kg/day for five to seventeen days. This caused deleterious effects in the gastrointestinal tract, such as cessation of peristalsis of small intestine and colon, and marked distension of the cecum. In vitro pharmacologic studies were performed on the electrically stimulated longitudinal muscle-myenteric plexus of the guinea pigs. We found that phenothiazines interfered with the neuromuscular mechanism of the intestine, as exemplified by a lack of response to electrical current stimulation. The effect was protracted, lasting at least 24 hours. These effects were reversed by the administration of the anticholinesterase, physostigmine (PGM), provided the block was less than 80 per cent. The paralytic ileus produced was similar to that found in man.

Animals↗
PubMed1978

Effect of lithium chloride on electrically stimulated guinea-pig longitudinal muscle-myenteric plexus.

Lithium chloride, in the concentration range of 10(-4)M to 10(-2)M, increases the height of electrically induced contractions of guinea-pig longitudinal muscle-myenteric plexus preparation. Higher concentrations of the salt cause a progressive block of contractions. Sodium chloride shows no augmentation of contraction height, but concentrations above 10(-2)M only cause block of contractions. Inhibition of contractions by LiCl exactly parallels inhibition of responses of the tissue to exogenous acetylcholine (ACh); thus, the site of action is considered to be directly on the muscle. Sodium chloride causes insignificant inhibition of responses to exogenous ACh. Guinea-pigs injected chronically with high doses of LiCl (2 months, 5 mEq/kg show no stimulatory effect on LiCl in vitro, only inhibition. This finding suggests that tolerance to at least some of the actions of LiCl may occur upon chronic administration, particularly if the dose used is very high.

Acetylcholine↗