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	<title>Medical Inspection - Health Blog &#187; Health</title>
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		<title>Inflammatory bowel diseases in Indo-Canadians: Treatment and complications</title>
		<link>http://www.medicalinspection.net/inflammatory-bowel-diseases-in-indo-canadians-treatment-and-complications.html</link>
		<comments>http://www.medicalinspection.net/inflammatory-bowel-diseases-in-indo-canadians-treatment-and-complications.html#comments</comments>
		<pubDate>Sun, 01 Jan 2012 01:10:32 +0000</pubDate>
		<dc:creator>Kristina Albers</dc:creator>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[Antineutrophil cytoplasmic autoantibodies]]></category>
		<category><![CDATA[Crohn's disease]]></category>
		<category><![CDATA[Granulocytes]]></category>
		<category><![CDATA[Inflammatory bowel disease]]></category>
		<category><![CDATA[Ulcerative colitis]]></category>

		<guid isPermaLink="false">http://www.medicalinspection.net/?p=2143</guid>
		<description><![CDATA[Treatment and complications: Medications included 5- aminosalicylates, steroids and immunosuppressants as well as antimicrobial agents. In most patients, more than one medi­cation was administered during the course of their treatment, particularly for Crohn&#8217;s disease. For both groups, most were treated with corticosteroids and/or immunosuppressants dur­ing a mean follow-up period of five to six years. Some [...]]]></description>
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		<title>Hypoxic Pulmonary Vasoconstriction: Alteration of the Response in Other Clinical States &#8211; part 2</title>
		<link>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-alteration-of-the-response-in-other-clinical-states-part-2.html</link>
		<comments>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-alteration-of-the-response-in-other-clinical-states-part-2.html#comments</comments>
		<pubDate>Mon, 16 May 2011 21:40:43 +0000</pubDate>
		<dc:creator>Kristina Albers</dc:creator>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[clinical relevance]]></category>
		<category><![CDATA[Hypoxic Pulmonary]]></category>
		<category><![CDATA[Vasoconstriction]]></category>

		<guid isPermaLink="false">http://www.medicalinspection.net/?p=2017</guid>
		<description><![CDATA[Nitroprusside is frequently employed to lower blood pressure in a variety of situations where precise control over systemic hemodynamics is imperative. In the normal lung, this vasodilator does not produce any significant change in gas exchange. In contrast, a significant deterioration in gas exchange is produced when the drug is infused during pulmonary edema in [...]]]></description>
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		<title>Hypoxic Pulmonary Vasoconstriction: Alteration of the Response in Other Clinical States</title>
		<link>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-alteration-of-the-response-in-other-clinical-states.html</link>
		<comments>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-alteration-of-the-response-in-other-clinical-states.html#comments</comments>
		<pubDate>Sun, 15 May 2011 14:39:40 +0000</pubDate>
		<dc:creator>Kristina Albers</dc:creator>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[clinical relevance]]></category>
		<category><![CDATA[Hypoxic Pulmonary]]></category>
		<category><![CDATA[Vasoconstriction]]></category>

		<guid isPermaLink="false">http://www.medicalinspection.net/?p=2016</guid>
		<description><![CDATA[There are a group of diverse, unrelated clinical states where alteration of the normal AHPR is ob­served, but the mechanisms remain unclear. The influence of lung inflation on the response is contro­versial. An increase in lung inflation is associated with a decrease in the magnitude of the response. Pul­monary hypertension and elevations of left atrial [...]]]></description>
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		<title>Hypoxic Pulmonary Vasoconstriction: Loss or Attentuation of the Response after Chronic Hypoxia</title>
		<link>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-loss-or-attentuation-of-the-response-after-chronic-hypoxia.html</link>
		<comments>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-loss-or-attentuation-of-the-response-after-chronic-hypoxia.html#comments</comments>
		<pubDate>Sun, 15 May 2011 02:38:43 +0000</pubDate>
		<dc:creator>Kristina Albers</dc:creator>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[clinical relevance]]></category>
		<category><![CDATA[Hypoxic Pulmonary]]></category>
		<category><![CDATA[Vasoconstriction]]></category>

		<guid isPermaLink="false">http://www.medicalinspection.net/?p=2015</guid>
		<description><![CDATA[The pathophysiologic role of the AHPR in patients with acute cor pulmonale presenting with right ven­tricular failure, increased right ventricular afterload, and an elevated pulmonary vascular resistance is well known. A more controversial subject is whether hypoxic vasoconstriction is a stimulus for the vascular changes that occur during chronic hypoxic exposure. Chronic hypoxia is associated [...]]]></description>
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		<title>Hypoxic Pulmonary Vasoconstriction: PATHOPHYSIOLOGIC RELEVANCE OF ALTERATION OF AHPR</title>
		<link>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-pathophysiologic-relevance-of-alteration-of-ahpr.html</link>
		<comments>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-pathophysiologic-relevance-of-alteration-of-ahpr.html#comments</comments>
		<pubDate>Sat, 14 May 2011 01:37:58 +0000</pubDate>
		<dc:creator>Kristina Albers</dc:creator>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[clinical relevance]]></category>
		<category><![CDATA[Hypoxic Pulmonary]]></category>
		<category><![CDATA[Vasoconstriction]]></category>

		<guid isPermaLink="false">http://www.medicalinspection.net/?p=2014</guid>
		<description><![CDATA[The clinical implications of alterations of the AHPR are not widely appreciated. Our discussion of modifi­cation of the normal response will be arbitrarily divided into three areas: loss of the response in lung injury states; alteration of the response after chronic hypoxic exposure; and the alteration of the response in a diverse set of clinical [...]]]></description>
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		<title>Hypoxic Pulmonary Vasoconstriction: Direct Effects on the Vasculature</title>
		<link>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-direct-effects-on-the-vasculature.html</link>
		<comments>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-direct-effects-on-the-vasculature.html#comments</comments>
		<pubDate>Thu, 12 May 2011 22:37:06 +0000</pubDate>
		<dc:creator>Kristina Albers</dc:creator>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[clinical relevance]]></category>
		<category><![CDATA[Hypoxic Pulmonary]]></category>
		<category><![CDATA[Vasoconstriction]]></category>

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		<description><![CDATA[Direct effects of hypoxia on the vasculature are often discussed using a three-part model: sensor, transducer, and effector. The key questions for the oxygen sensor are its location and what specific cell or cell organelle plays this role. The likely site for the sensor is the precapillary arteriole, but the specific identity of the sensor [...]]]></description>
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		<title>Hypoxic Pulmonary Vasoconstriction: Mechanism</title>
		<link>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-mechanism.html</link>
		<comments>http://www.medicalinspection.net/hypoxic-pulmonary-vasoconstriction-mechanism.html#comments</comments>
		<pubDate>Thu, 12 May 2011 06:32:02 +0000</pubDate>
		<dc:creator>Kristina Albers</dc:creator>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[clinical relevance]]></category>
		<category><![CDATA[Hypoxic Pulmonary]]></category>
		<category><![CDATA[Vasoconstriction]]></category>

		<guid isPermaLink="false">http://www.medicalinspection.net/?p=2012</guid>
		<description><![CDATA[Mechanism Two main hypotheses underlie most investigations of the mechanism of the AHPR. The first is that the response is dependent on the release of a vasoactive mediator from some site within the lung. The opposing view states that acute hypoxia elicits vasoconstriction via a direct effect on pulmonary vascular smooth muscle without the involvement [...]]]></description>
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