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Biomedical subjects

W Oliver

Publications and source records attributed to W Oliver.

At least 37 records · Page 2Linked to original sources
PubMed1983

Histamine receptor blocking effects of cimetidine in the airways.

We investigated the modification of histamine-induced bronchoconstriction by the H2-antagonist cimetidine in conscious sheep. One hundred breaths of 5% histamine aerosol increased mean (SD) pulmonary resistance (RL) by 5.6 (1.4) cmH2O/l/sec. This increase in RL was completely blocked by intravenous clemastine (0.5 mg), a specific H1-antagonist, indicating that the histamine-induced bronchoconstriction was mediated by H1-receptors. Intravenous cimetidine caused a dose-dependent enhancement of the histamine response between 1 and 1000 mg with a mean peak delta RL of 15.3 (5) cmH2O/l/sec (p less than 0.05) at the 1000 mg dose, while it blocked the histamine response at a dose of 2400 mg [delta RL = 1.9 (2) cmH2O/l/sec, p = NS]. This paradoxic effect was not related to an anticholinergic mechanism as intravenous cimetidine (2400 mg) failed to block carbachol-induced (25 breaths of 1% solution) bronchoconstriction. We conclude that in the ovine airway, cimetidine is a selective H2-histamine receptor blocker at lower tissue concentrations, and a combined H2- and H1-histamine receptor blocker at high tissue concentrations.

Airway Resistance↗
PubMed1983

Variability of hypoxic pulmonary vasoconstriction in sheep. Role of prostaglandins.

In a minority of conscious sheep, the hypoxic pulmonary vasoconstrictor response is blunted ("nonresponders"). The purpose of this investigation was to determine if this blunted response is related to an increased activity of H2-histamine receptors, beta-adrenergic receptors, or the generation of inhibitory prostaglandins. We measured pulmonary arterial pressure, pulmonary arterial wedge pressure, and pulmonary blood flow for the calculation of pulmonary vascular resistance (PVR) in 5 "nonresponders" and 5 sheep with a typical hypoxic pulmonary vasoconstrictor response ("responders") while breathing room air and 13% O2 (balance, N2). Arterial oxygen tension (PaO2) was also determined as a measure of the severity of hypoxia. During hypoxia, mean PVR increased by 6% (p = NS) in the "nonresponders" (PaO2, 49 +/- 4 mmHg), and by 70% (p less than 0.01) in the "responders" (mean PaO2, 46 +/- 4 mmHg). Metiamide (H2-blocker) and propranolol (beta-adrenergic blocker) pretreatments did not restore the hypoxic pulmonary vascular response in the "nonresponders," whereas pretreatment with indomethacin (prostaglandin synthetase inhibitor) caused mean PVR to increase by 48% (p less than 0.01) during hypoxia, indicating a partial restoration of hypoxic pulmonary vasoconstriction. In the "responders," the hypoxic pulmonary vascular response was not potentiated by indomethacin pretreatment (68% increase in mean PVR). We conclude that some sheep exhibit a blunted hypoxic pulmonary vasoconstrictor response caused by enhanced production of inhibitory prostaglandins.

Animals↗
PubMed1983

Does slow-reacting substance of anaphylaxis mediate hypoxic pulmonary vasoconstriction?

We have previously established a relationship between mast cell degranulation and hypoxic pulmonary vasoconstriction (HPV). In the present study, we investigated the possible role of slow-reacting substance of anaphylaxis (SRS-A) in the mediation of HPV. In 18 conscious sheep, pulmonary artery pressure, pulmonary arterial wedge pressure, and cardiac output were measured for the calculation of pulmonary vascular resistance (PVR) along with arterial oxygen tension (PaO2) while breathing room air and while breathing 13% O2 (balance, N2). Before and during 13% O2 breathing (pretreatment), Group 1 received an intravenous infusion of cromolyn sodium (3 mg/kg-1/min-1) and Group 2 was infused with FPL-57231, a SRS-A antagonist (2 mg/kg-1/min-1); Groups 3 and 4 received infusions of cromolyn sodium or FPL-57231 after induction of HPV. During 13% O2 breathing (mean PaO2, 47 mmHg), mean PVR increased to 190% of baseline. Pretreatment with cromolyn sodium prevented HPV, whereas infusion of cromolyn sodium after induction of HPV failed to reverse it; FPL-57231 both prevented HPV (pretreatment) and reversed it when infused after induction of HPV. Pretreatment with the prostaglandin synthetase inhibitor indomethacin (2 mg/kg) 1 h before the experiment failed to modify the FPL-57231-induced reversal of hypoxic vasoconstriction, thus excluding the release of inhibitory prostaglandins by this compound. We conclude that cromolyn sodium prevented HPV, presumably by inhibiting the release of SRS-A, which mediates pulmonary vasoconstriction directly or indirectly through other mechanisms.

Animals↗
PubMed1982

Role of ciliary motility in acute allergic mucociliary dysfunction.

The purpose of this investigation was to determine if abnormal ciliary function contributes to allergic mucociliary dysfunction. In conscious sheep with Ascaris suum hypersensitivity, ciliated cells were obtained with a cytology brush and tracheal mucous velocity (TMV) was determined before and serially for 2 h following antigen inhalation. The recovered cells (also containing mast cells) were suspended in a chamber, and ciliary activity was viewed microscopically and recorded on videotape for subsequent slow-motion analysis of ciliary beat frequency (CBF). One hour after A. suum challenge mean CBF (+/- SE) showed a slight increase from a base-line value of 630 +/- 16 to 716 +/- 30 beats/min (P less than 0.05) when mean TMV was decreased to 57% of base line (P less than 0.05). After 2 h, both mean CBF and TMV returned toward base line. Since possible in vivo actions of chemical mediators liberated by antigen challenge may have been lost after suspension of the brushed cells, we also assessed the effects of antigen on CBF in vitro. A. suum caused a dose-dependent increase in CBF that was blocked by cromolyn sodium. We conclude that 1) allergic mucociliary dysfunction is not caused by a decrease in CBF and 2) antigen-induced release of chemical mediators increases CBF.

Acute Disease↗
PubMed1982

Characterization of H1- and H2-receptor function in pulmonary and systemic circulations of sheep.

We investigated the histamine H1- and H2-receptor function in the pulmonary and systemic circulations of sheep by in vivo and in vitro techniques. Combined H1 and H2 stimulation (by intravenous histamine) in vivo increased pulmonary vascular resistance (PVR) to 435% of base line and decreased systemic vascular resistance (SVR) to 49% of base line. Selective H2 stimulation (histamine after chlorpheniramine pretreatment) decreased PVR and SVR to 86 and 82% at base line, respectively, while selective H1 stimulation (histamine after metiamide pretreatment) increased PVR to 424% of base line and decreased SVR to 64% of base line. Combined H1- and H2-antagonist pretreatment completely blocked the effects of histamine on SVR, while PVR still decreased to 85% of base line, suggesting a mild "atypical" H2-receptor response in the pulmonary circulation under conditions of resting vascular tone. With increased pulmonary vascular tone (hypoxia), histamine decreased PVR to 55% (H1-antagonist pretreatment) and to 58% (combined H1- and H2-antagonist pretreatment) of posthypoxia values, respectively, demonstrating a marked atypical H2-receptor response. In vitro, both pulmonary arterial and venous strips showed a contractile dose-response to histamine, which was blocked by the H1-antagonist pyrilamine (mepyramine). In precontracted strips, both histamine and the H2-agonists (dimaprit and impromidine) elicited a relaxant response, which was neither blocked by H1-antagonist alone nor by combined H1- and H2-antagonists. We conclude that in sheep the histamine-induced pulmonary vasoconstrictor response is mediated by H1-receptors, while the pulmonary vasodepressor response is mediated by atypical H2-receptors. The systemic vasodepressor response is mediated by both H1- and typical H2-receptors.

Animals↗
PubMed1982

Hypoxic pulmonary vasoconstriction in conscious sheep: role of mast cell degranulation.

We used pharmacologic and histologic techniques to investigate the role of mast cells in the mediation of hypoxic pulmonary vasoconstriction in conscious sheep. Breathing a hypoxic gas mixture (13%, 02, 87% nitrogen) caused hypoxic pulmonary vasoconstriction (HPV) with increases in mean pulmonary artery pressure and pulmonary vascular resistance by 97 and 90%, respectively. Intravenous pretreatment with the mast cell membrane stabilizing agent cromolyn sodium (3 mg/kg/min) completely blocked HPV, whereas the H1-histamine receptor antagonist chlorpheniramine, alone or in combination with the H2-receptor antagonist metiamide and the prostaglandin synthetase inhibitor indomethacin, failed to prevent HPV. Cromolyn sodium failed to modify the pulmonary pressor response to infusions of norepinephrine (alpha-agonist), tyramine (catecholamine-releasing agent), and histamine, indicating the specificity of cromolyn sodium action on the mast cells. Electromicroscopic studies of pulmonary perivascular mast cells showed that a 90-min exposure to the hypoxic gas mixture reduced the total number of granules per mast cell to 75% of control. This was blocked by cromolyn sodium pretreatment. We conclude that in conscious sheep], HP[V is initiated by the liberation of a mast cell product (other than histamine) that either directly or indirectly causes pulmonary vasoconstriction.

Animals↗
PubMed1981

Impaired tracheal mucus transport in allergic bronchoconstriction: effect of terbutaline pretreatment.

The transport velocity of mucus within the trachea, pulmonary resistance, and arterial blood gas composition were measured in intubated conscious sheep with Ascaris suum sensitivity before and during allergic bronchoconstriction. Inhalation of A. suum extract for 15 min increased mean pulmonary resistance significantly from 1.9 cm H2O . L-1 sec-1 to 5.1 cm H2O . L-1 sec-1 after 60 min and to 4.5 cm H2O . L-1 sec-1 after 120 min, while it decreased mean arterial PO2 from 85 to 59 and 53 mm Hg, respectively, without altering arterial PCO2 or pH. This was associated with a decrease in mean mucus velocity from 11.2 to 6.0 and 5.7 mm min-1, respectively. The decrease in mucus velocity was accompanied by endoscopically visible increases in the quantity of tracheal mucus. No alterations in mucus velocity or pulmonary resistance were observed in animals who inhaled a control antigen (ragweed) or breathed a mixture of 10% oxygen 90% nitrogen, which produced a mean arterial PO2 of 51 mm Hg. The administration of 0.25 mg terbutaline sulfate by subcutaneous injection prior to A. suum challenge prevented the changes in mucus velocity, pulmonary resistance, and arterial PO2. We conclude that the decreased mucus velocity in the trachea during antigen-induced bronchoconstriction in conscious sheep is related to the allergic response, and can be prevented by the subcutaneous administration of terbutaline sulfate, a beta adrenergic agonists. This suggests that the protective effect of terbutaline sulfate in antigen-induced bronchoconstriction includes the effect on the associated impairment of mucociliary function.

Animals↗
PubMed1981

Differences in airway reactivity in normal and allergic sheep after exposure to sulfur dioxide.

The effect of breathing 5 ppm sulfur dioxide (SO2) on airway reactivity was studied in both normal and allergic conscious sheep. Allergic sheep were defined as animals in which inhalation of Ascaris suum extract resulted in bronchospasm as evidenced by an increase in mean pulmonary flow resistance (RL), hyperinflation, and a fall in dynamic compliance. Airway reactivity was assessed by measuring the increase of RL after 18 breaths of 0.25% carbachol (c), from an initial RL value obtained after 18 breaths of buffered saline (s) [RL(c-s)]. RL and RL(c-s) were determined prior to, immediately after, and 24 h after exposure to 5 ppm SO4 for 4 h. In both groups RL remained unchanged after SO2 exposure. Prior to exposure, RL(c-s) was not significantly different in seven normal (0.3 +/- 0.1) and seven allergic sheep [0.4 +/- 0.2 (SD) cmH2O X l-1 X s], and there was no significant change in RL (c-s) immediately after SO2 exposure in either group. Twenty-four h later, RL(c-s) RL(c-s) increased to 0.7 +/- 0.8 (P less than 0.2) in normal and to 1.8 +/- 0.9 cmH2O X l-1 X s (P less than 0.01) in allergic sheep. Because the increase in RL(c-s) after 24 h was greater (P less than 0.01) in allergic than in normal sheep, we conclude that SO2 exposure increased airway reactivity more in the former than in the latter.

Animals↗
PubMed1981

Effect of pharmacologic agents on antigen-induced decreases in specific lung conductance in sheep.

The purpose of this investigation was to determine the primary mediators responsible for the decrease in specific lung conductance (SGL) after airway challenge with Ascaris suum antigen in allergic sheep. On different occasions, separated by 10 to 14 days, pulmonary resistance and thoracic gas volume were measured in 5 sheep with Ascaris suum hypersensitivity before and for 2 h after a standard inhalation challenge with this antigen. Initially and at the end of the study, inhalation challenge decreased mean SGL to 38 and 44% of baseline, respectively. Pretreatment by intravenous injection of the H1 receptor antagonist chlorpheniramine (2 mg/kg) completely prevented the antigen-induced decrease in SGL. Similar results were obtained with inhalation of the mediator release blocking agent, disodium cromoglycate (1 mg/kg), prior to antigen challenge. The decrease in SGL after inhalation challenge was not modified by pretreatment with the H2 receptor antagonist, metiamide (3 mg/kg), the anticholinergic agent, atropine (0.2 mg/kg), the prostaglandin synthetase inhibitor, indomethacin (2 mg/kg) by intravenous injection, or with inhalation of FPL-55712 (1% solution), an antagonist of slow-reacting substance of anaphylaxis (SRS-A). We concluded that during allergic bronchoconstriction in sheep (1) the decrease in SGL is mediated by histamine via H1 receptors, (2) other liberated or activated mediators including SRS-A do not decrease SGL, and (3) cholinergic reflex mechanisms are not involved in this response.

Airway Resistance↗
PubMed1980

Sulfur dioxide induced airway hyperreactivity in allergic sheep.

The effects of a four-hour exposure (via a Plexiglas hood) to sulfur dioxide (SO2) on airway reactivity was studied in both normal and allergic conscious sheep. Allergic sheep were defined as animals in whom inhalation of Ascaris suum extract resulted in an increase in mean pulmonary flow resistance (RL). Airway reactivity (delta RL) was assessed by measuring the increase in RL after 18 breaths of 0.25% carbachol, from an initial value obtained after 18 breaths of buffered saline. RL and delta RL were determined prior to, immediately after and 24 hours following SO2 exposure in three groups of sheep: six normal sheep exposed to 5 ppm SO2 (group A); six normal sheep exposed to 10 ppm SO2 (group B) and seven allergic sheep exposed to 5 ppm SO2 (group C). RL was not affected by SO2 exposure in any group but both groups B and C showed increases in delta RL 24 hours after exposure. Since the increase in delta RL was greater in group C than in either groups A or B, we conclude that allergic sheep have enhanced susceptibility to the injurious airway effects of SO2.

Airway Resistance↗
PubMedDate not supplied

[Endoscopic resection in early gastric cancer].

Development of therapeutic endoscopy has permitted the treatment of early gastric cancer (EGC) in its different macroscopic forms. In this paper we present 9 cases of EGC treated endoscopically in our Institution. We describe the criteria we follow to perform this procedure. The patients selected were of advanced age and high surgical risk. Seven cases were macroscopically Type I and two were Type IIa. According to localization six were proximal tumors (body and fundus) and three were located in the antrum. Six of the nine patients are alive after resection, one more than 6 years and 3 more than 3 years. Three patients died of ailments no related to cancer.

Aged↗
PubMedDate not supplied

[Gastric cancer in hyperplasia polyps].

We present 3 cases of Early Gastric Cancer in 82 Hyperplastic Polyps (HP) resected endoscopically (3.6%) during the years 1985 to 1989, at the GI Cancer Center "Dr. Luis E. Anderson", San Cristobal, Venezuela. The diagnosis criteria followed were those of Nakamura, T and Nagayo T. This paper shows the possibility of malignant changes of these lesions, advising endoscopic resection of HP as a mean of treatment and in order to make a complete study of the polyps. We compare our data with existing bibliography, finding similitude in results.

Aged↗
PubMedDate not supplied

[Metastasis to lymph nodes in early gastric cancer].

The presence of metastasis in lymph nodes is one of the most important aspects to be evaluated in Early Gastric Cancer (EGC). In this paper we analyze the presence of that kind of metastasis in 70 EGC, in 66 patients studied in our Institute and surgically treated at the Central Hospital of San Cristobal. We found 3 cases with metastasis to perigastric (regional) lymph nodes (N1) and one case with extra perigastric lymph nodes metastasis (N3), that signify 5.7% of the total of all cases. We established the relationship of these metastasis and the following variables: macroscopic type, localization, size, depth of invasion within the gastric wall and the histological variety of the lesions. We found that the type IIa + IIc, the lesions located in the fundus, bigger that 3 cm, with invasion reaching the submucosa and histological differentiated (intestinal type), were the most important characteristics related with the presence of metastasis to the lymph nodes in our EGC.

Humans↗
PubMedDate not supplied

[Endoscopic polypectomy of the upper digestive tract].

From 1985 to 1987 we performed 82 endoscopic polipectomies in 80 patients. In this paper we refer the technics, epidemiological data and macro and microscopical findings of the resected specimens. Two patients with gastric cancer were treated in this way, these patients had formal surgical contraindication. In two patients in whom the endoscopic biopsies could not render a definitive diagnosis (cancer or atypical epithelium), the study of the resected tumor permitted the diagnosis of atypical epithelium, so two gastrectomies were avoided. Among our resected lesions we found 55 of inflammatory type, 6 adenomas and 7 atypical epithelium. We consider that this is a useful method for the diagnosis and treatment of some elevated lesions. Although this is not the treatment of choice for the elevated early cancer, it could be used to treat cancerous tumors in patients with high surgical risk.

Adult↗
PubMedDate not supplied

[Asymptomatic stomach ulcer].

The purpose of this paper is to evaluate the frequency and some of the clinical and epidemiological characteristics of asymptomatic gastric ulcer, found in persons who attend the Center for Control of Gastrointestinal Cancer of San Cristóbal, Venezuela, as part of a gastric cancer mass screening program. 350 patients with active peptic ulcer were found, 176 duodenal and 174 gastric, diagnosed by means of endoscopy. Of the patients with gastric ulcers, 67 (38.5%) had no symptoms. This group of asymptomatic patients were analyzed regarding age, sex, place of residence, type of work and also the location of the ulcer and the histology. We conclude that this entity is frequent in our region that it is associated with agricultural workers and house wives. It is necessary to continue a prospective periodical evaluation of these patients in order to understand the natural history of the entity.

Adult↗