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<title>Biomedical Sciences (Pharmacology)</title>
<link>http://hdl.handle.net/10125/1935</link>
<description/>
<pubDate>Sun, 19 May 2013 06:12:43 GMT</pubDate>
<dc:date>2013-05-19T06:12:43Z</dc:date>
<item>
<title>Effects of adrenergic agonists and antagonists in potassium intoxication</title>
<link>http://hdl.handle.net/10125/11789</link>
<description>Typescript.; Bibliography: leaves 132-142.; xii, 142 l illus
</description>
<pubDate>Mon, 01 Jan 1973 00:00:00 GMT</pubDate>
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<dc:date>1973-01-01T00:00:00Z</dc:date>
<dc:creator>Lockwood, Raymond H</dc:creator>
</item>
<item>
<title>The chemistry and pharmacology of a central nervous system stimulant from the sea anemone, Stoichactis kenti</title>
<link>http://hdl.handle.net/10125/11788</link>
<description>Typescript.; Bibliography: leaves 87-94.; ix, 94 l illus
</description>
<pubDate>Fri, 01 Jan 1971 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/11788</guid>
<dc:date>1971-01-01T00:00:00Z</dc:date>
<dc:creator>Turlapaty, Prasad D. M. V</dc:creator>
</item>
<item>
<title>The nature and action of a hypotensive agent from Eucalyptus robusta</title>
<link>http://hdl.handle.net/10125/11787</link>
<description>Typescript.; Bibliography: leaves 80-90.; viii, 90 l illus
</description>
<pubDate>Wed, 01 Jan 1969 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/11787</guid>
<dc:date>1969-01-01T00:00:00Z</dc:date>
<dc:creator>Read, George Wesley</dc:creator>
</item>
<item>
<title>Chemistry and pharmacology of adrenergic blocking agents</title>
<link>http://hdl.handle.net/10125/11786</link>
<description>Typescript.; Bibliography: leaves [173]-194.; ix, 194 l illus
</description>
<pubDate>Wed, 01 Jan 1969 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/11786</guid>
<dc:date>1969-01-01T00:00:00Z</dc:date>
<dc:creator>Ghouri, Mohammad Sarfraz Khan</dc:creator>
</item>
<item>
<title>The contractile mechanisms of sodium metavanadate in isolated vascular smooth muscle</title>
<link>http://hdl.handle.net/10125/9413</link>
<description>Thesis (Ph. D.)--University of Hawaii at Manoa, 1995.; Includes bibliographical references (leaves 60-67).; Microfiche.; xii, 67 leaves, bound ill. 29 cm
</description>
<pubDate>Sun, 01 Jan 1995 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/9413</guid>
<dc:date>1995-01-01T00:00:00Z</dc:date>
<dc:creator>Zhou, Qin</dc:creator>
</item>
<item>
<title>Effects of drugs which alter blood cell deformability in circulatory shock produced by endotoxin</title>
<link>http://hdl.handle.net/10125/9412</link>
<description>Thesis (Ph. D.)--University of Hawaii at Manoa, 1991.; Includes bibliographical references (leaves 77-89); Microfiche.; xiv, 89 leaves, bound ill. (some col.) 29 cm
</description>
<pubDate>Tue, 01 Jan 1991 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/9412</guid>
<dc:date>1991-01-01T00:00:00Z</dc:date>
<dc:creator>Yao, Zhenhai</dc:creator>
</item>
<item>
<title>Studies on homocarnosinosis and on human tissue carnosinase and its inhibition by bestatin and by endogenous inhibitors</title>
<link>http://hdl.handle.net/10125/9411</link>
<description>Typescript.; Thesis (Ph. D.)--University of Hawaii at Manoa, 1984.; Bibliography: leaves 139-157.; Photocopy.; Microfilm.; xii, 157 leaves, bound ill. 29 cm
</description>
<pubDate>Sun, 01 Jan 1984 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/9411</guid>
<dc:date>1984-01-01T00:00:00Z</dc:date>
<dc:creator>Peppers, Steven Carl</dc:creator>
</item>
<item>
<title>Effect of gender on the antidiuretic activity of vasopressin in the spontaneously hypertensive rat</title>
<link>http://hdl.handle.net/10125/6880</link>
<description>Recently, studies have found that circulating vasopressin levels, as well as the cardiovascular and antidiuretic actions of vasopressin are greater in males than in females, but the consequences of these gender differences are unclear. Further, animal and human studies have revealed that hypertension develops more rapidly and is more prevalent in males than in females. Because vasopressin is involved with blood pressure regulation, whether vasopressin gender differences are involved in the gender difference of hypertension development should be examined. Thus, this dissertation tested the hypothesis that a gender effect on vasopressin renal action contributes to gender differences in hypertension. Renal function of male and female adult spontaneously hypertensive rats (SHR) were compared to that of normotensive (WKY) rats. Vasopressin V2 receptors were pharmacologically stimulated with a selective V2 receptor agonist, which revealed that maximal urine concentrating abilities of SHR were higher than that of WKY. While there were significant differences in concentrating abilities with hypertension, there were no significant gender differences in responses to maximal V2 stimulation in normotensive or hypertensive rats. The contribution of endogenous vasopressin on renal fluid handling to a gender difference in hypertension was also examined. Vasopressin inhibition with a selective V2 antagonist resulted in higher free water clearance in females than in males of both strains. Also, the renal response to endogenous vasopressin blockade was lower in SHR than WKY in both sexes. Expression of V2 receptors in renal inner medulla of male SHR and WKY showed that levels of V2 receptor mRNA in SHR were significantly lower than those in WKY. Thus, differences in renal fluid handling abilities between strains and gender, may be due to the differences in endogenous vasopressin levels, renal concentrating abilities, or expression of renal vasopressin receptors. In conclusion, vasopressin influence on renal fluid handling is altered in established hypertension. While there are differences in vasopressin renal action between males and females in both strains, there were no significant differences in the gender effect between normotensive and hypertensive adult rats. Thus, whether gender differences in fluid handling contribute to gender differences in hypertension development remains to be determined.
xvii, 157 leaves
</description>
<pubDate>Fri, 01 Aug 2003 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/6880</guid>
<dc:date>2003-08-01T00:00:00Z</dc:date>
<dc:creator>Ye, Dailin</dc:creator>
</item>
<item>
<title>Studies on the effects of pharmacological agents on endotoxin induced pulmonary injury</title>
<link>http://hdl.handle.net/10125/6879</link>
<description>Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury, characterized by inflammation and increased capillary permeability, associated with a constellation of clinical, radiological and physiological abnormalities. The incidence of ARDS is uncertain but has been estimated to be as high as 75 cases per 100,000
hospitalized patients per year. The overall mortality of patients with ARDS remains at 40 to 60 percent. Many factors predispose to ARDS, with sepsis caused by gram negative bacteria being one of the most important. Experimentally, ARDS can be mimicked by the injection of bacterial endotoxin. Previous studies in our laboratory showed that pretreatment with pentoxifylline (a methylated xanthine), bepafant (a platelet activating factor antagonist) and nicardipine (a calcium channel blocker), 15 minutes before the administration of endotoxin, reduced the mortality and manifestations of disseminated intravascular coagulation caused by endotoxin in rats. The objective of the present study was to determine whether these drugs would also protect the rat lung against the deleterious effects of endotoxin. Anesthetized rats were given endotoxin (10 mg/kg) intravenously. One hour later, the lungs were removed and perfused with a buffered salt solution containing 4% Ficoll and aerated with air and 5% CO2 Pulmonary arterial pressure, capillary pressure, capillary permeability, and arterial and venous segmental resistances were significantly higher in lungs obtained from endotoxin-treated animals than in lungs from saline control rats. Endotoxin also caused an increase in lung weight, lung water content and the outflow of lung filtrate as compared to saline-treated controls. Pretreatment in vivo with nicardipine and bepafant, 15 minutes before the administration of endotoxin, significantly reduced the endotoxin-induced increases in capillary permeability and filtrate outflow but did not significantly affect the other parameters of measurement. Pretreatment with pentoxifylline differed from other two drugs in that the methylated xanthine significantly reduced the endotoxin-induced increases in all of the hemodynamic parameters as well as the increase in capillary permeability and filtrate outflow. Studies were also made on the effect of endotoxin on the pulmonary leukocyte count in rats. In these experiments, lungs were removed for histological examination one hour after the intravenous administration of endotoxin (10 mg/kg). Leukocyte numbers were significantly increased in the endotoxin group as compared to the saline group. Pretreatment with nicardipine and bepafant but not pentoxifylline significantly reduced the endotoxin-induced increase in pulmonary leukocyte count. The present results thus showed that the three drugs can protect against endotoxin-induced lung injury, in addition to preventing disseminated intravascular coagulation and death caused by the lipopolysaccharide. Pulmonary migration/sequestration of leucocytes and production/release of autacoids and cytokines from leucocytes are thought to play important roles in the lung injury caused by endotoxin. The results with nicardipine and bepafant suggest that these agents may act at least in part by inhibiting the pulmonary migration/sequestration of leucocytes.
xiii, 113 leaves
</description>
<pubDate>Fri, 01 Aug 2003 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/6879</guid>
<dc:date>2003-08-01T00:00:00Z</dc:date>
<dc:creator>Yang, Li</dc:creator>
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