Effect of nifedipine on ocular pulse amplitude in normal pressure glaucoma
Ocular pulse amplitude (OPA) is reduced in normal tension glaucoma (NTG) patients when compared to non-glaucomatous, healthy control subjects. This might be related to a vasospastic reaction. The objective of this study was to determine if low OPA in NTG is associated with a vasospastic reaction and...
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Veröffentlicht in: | Klinische Monatsblätter für Augenheilkunde 1997-06, Vol.210 (6), p.355 |
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description | Ocular pulse amplitude (OPA) is reduced in normal tension glaucoma (NTG) patients when compared to non-glaucomatous, healthy control subjects. This might be related to a vasospastic reaction. The objective of this study was to determine if low OPA in NTG is associated with a vasospastic reaction and its response to vasodilation.
Nifedipine, a calcium channel blocker, vasodilator and systemic antihypertensive agent improves visual fields in NTG patients following acute and chronic dosing. The effect of 60 mg of daily orally administered nifedipine on OPA, intraocular pressure (IOP, German abbreviation: IOD), blood pressure (BP, German abbreviation: RR) and pulse rate (PR, German abbreviation: HF) were measured prior to and for 3 months after initiating nifedipine therapy in 32 NTG patients with and without a vasospastic reaction as manifested by a local cold exposure test. Before treatment, all patients had reduced OPA evaluated with the Langham Ocular Blood Flow System.
During nifedipine treatment NTG patients with a vasospastic reaction showed a significant (p < 0.001) increase in OPA, whereas NTG patients without a vasospastic reaction showed no sig. (p > 0.05) change in OPA.
There may be two different subgroups of NTG patients, those who have a vasospastic reaction and react to nifedipine, while others lack the ability to react to nifedipine or might have a different, non-vasospastic pathology. Calcium channel blockers and other vasodilators may be useful in the treatment of vasospastic NTG patients. |
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Nifedipine, a calcium channel blocker, vasodilator and systemic antihypertensive agent improves visual fields in NTG patients following acute and chronic dosing. The effect of 60 mg of daily orally administered nifedipine on OPA, intraocular pressure (IOP, German abbreviation: IOD), blood pressure (BP, German abbreviation: RR) and pulse rate (PR, German abbreviation: HF) were measured prior to and for 3 months after initiating nifedipine therapy in 32 NTG patients with and without a vasospastic reaction as manifested by a local cold exposure test. Before treatment, all patients had reduced OPA evaluated with the Langham Ocular Blood Flow System.
During nifedipine treatment NTG patients with a vasospastic reaction showed a significant (p < 0.001) increase in OPA, whereas NTG patients without a vasospastic reaction showed no sig. (p > 0.05) change in OPA.
There may be two different subgroups of NTG patients, those who have a vasospastic reaction and react to nifedipine, while others lack the ability to react to nifedipine or might have a different, non-vasospastic pathology. Calcium channel blockers and other vasodilators may be useful in the treatment of vasospastic NTG patients.</description><identifier>ISSN: 0023-2165</identifier><identifier>PMID: 9333660</identifier><language>ger</language><publisher>Germany</publisher><subject>Administration, Oral ; Adult ; Blood Flow Velocity - drug effects ; Blood Flow Velocity - physiology ; Calcium Channel Blockers - administration & dosage ; Calcium Channel Blockers - adverse effects ; Choroid - blood supply ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Eye - blood supply ; Female ; Glaucoma, Open-Angle - drug therapy ; Glaucoma, Open-Angle - physiopathology ; Humans ; Intraocular Pressure - drug effects ; Intraocular Pressure - physiology ; Male ; Middle Aged ; Nifedipine - administration & dosage ; Nifedipine - adverse effects ; Pulse - drug effects ; Pulse - physiology ; Vascular Resistance - drug effects ; Vascular Resistance - physiology ; Vasodilator Agents - administration & dosage ; Vasodilator Agents - adverse effects</subject><ispartof>Klinische Monatsblätter für Augenheilkunde, 1997-06, Vol.210 (6), p.355</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9333660$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schmidt, K G</creatorcontrib><creatorcontrib>von Rückmann, A</creatorcontrib><creatorcontrib>Geyer, O</creatorcontrib><creatorcontrib>Mittag, T W</creatorcontrib><title>Effect of nifedipine on ocular pulse amplitude in normal pressure glaucoma</title><title>Klinische Monatsblätter für Augenheilkunde</title><addtitle>Klin Monbl Augenheilkd</addtitle><description>Ocular pulse amplitude (OPA) is reduced in normal tension glaucoma (NTG) patients when compared to non-glaucomatous, healthy control subjects. This might be related to a vasospastic reaction. The objective of this study was to determine if low OPA in NTG is associated with a vasospastic reaction and its response to vasodilation.
Nifedipine, a calcium channel blocker, vasodilator and systemic antihypertensive agent improves visual fields in NTG patients following acute and chronic dosing. The effect of 60 mg of daily orally administered nifedipine on OPA, intraocular pressure (IOP, German abbreviation: IOD), blood pressure (BP, German abbreviation: RR) and pulse rate (PR, German abbreviation: HF) were measured prior to and for 3 months after initiating nifedipine therapy in 32 NTG patients with and without a vasospastic reaction as manifested by a local cold exposure test. Before treatment, all patients had reduced OPA evaluated with the Langham Ocular Blood Flow System.
During nifedipine treatment NTG patients with a vasospastic reaction showed a significant (p < 0.001) increase in OPA, whereas NTG patients without a vasospastic reaction showed no sig. (p > 0.05) change in OPA.
There may be two different subgroups of NTG patients, those who have a vasospastic reaction and react to nifedipine, while others lack the ability to react to nifedipine or might have a different, non-vasospastic pathology. Calcium channel blockers and other vasodilators may be useful in the treatment of vasospastic NTG patients.</description><subject>Administration, Oral</subject><subject>Adult</subject><subject>Blood Flow Velocity - drug effects</subject><subject>Blood Flow Velocity - physiology</subject><subject>Calcium Channel Blockers - administration & dosage</subject><subject>Calcium Channel Blockers - adverse effects</subject><subject>Choroid - blood supply</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Administration Schedule</subject><subject>Eye - blood supply</subject><subject>Female</subject><subject>Glaucoma, Open-Angle - drug therapy</subject><subject>Glaucoma, Open-Angle - physiopathology</subject><subject>Humans</subject><subject>Intraocular Pressure - drug effects</subject><subject>Intraocular Pressure - physiology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Nifedipine - administration & dosage</subject><subject>Nifedipine - adverse effects</subject><subject>Pulse - drug effects</subject><subject>Pulse - physiology</subject><subject>Vascular Resistance - drug effects</subject><subject>Vascular Resistance - physiology</subject><subject>Vasodilator Agents - administration & dosage</subject><subject>Vasodilator Agents - adverse effects</subject><issn>0023-2165</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNotj7tqAzEQAFUkOI7jTwjoBw5Wt9Y9ymCcF4Y07s1KWhkF6U7orCJ_n0BcTTMMzJ1YA7TYtKrTD-JxWb4B1G5UaiVWIyJ2HazF58F7tlc5ezkFzy7kMLGcJznbGqnIXOPCklKO4VodyzDJaS6JosyFl6UWlpdI1c6JnsS9pz97e-NGnF4Pp_17c_x6-9i_HJusERpEY5y2aiDuQY3t4KhVFjrdeXC0w5G0sczEnoy1zvTe-8EhABnVO6NxI57_s7maxO6cS0hUfs63JfwFP55I8g</recordid><startdate>199706</startdate><enddate>199706</enddate><creator>Schmidt, K G</creator><creator>von Rückmann, A</creator><creator>Geyer, O</creator><creator>Mittag, T W</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>199706</creationdate><title>Effect of nifedipine on ocular pulse amplitude in normal pressure glaucoma</title><author>Schmidt, K G ; von Rückmann, A ; Geyer, O ; Mittag, T W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p530-33bbd5c18ae701928da21c0656f0da439a5bceeaefabccdb7fff8d300ab17db53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>ger</language><creationdate>1997</creationdate><topic>Administration, Oral</topic><topic>Adult</topic><topic>Blood Flow Velocity - drug effects</topic><topic>Blood Flow Velocity - physiology</topic><topic>Calcium Channel Blockers - administration & dosage</topic><topic>Calcium Channel Blockers - adverse effects</topic><topic>Choroid - blood supply</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Administration Schedule</topic><topic>Eye - blood supply</topic><topic>Female</topic><topic>Glaucoma, Open-Angle - drug therapy</topic><topic>Glaucoma, Open-Angle - physiopathology</topic><topic>Humans</topic><topic>Intraocular Pressure - drug effects</topic><topic>Intraocular Pressure - physiology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Nifedipine - administration & dosage</topic><topic>Nifedipine - adverse effects</topic><topic>Pulse - drug effects</topic><topic>Pulse - physiology</topic><topic>Vascular Resistance - drug effects</topic><topic>Vascular Resistance - physiology</topic><topic>Vasodilator Agents - administration & dosage</topic><topic>Vasodilator Agents - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schmidt, K G</creatorcontrib><creatorcontrib>von Rückmann, A</creatorcontrib><creatorcontrib>Geyer, O</creatorcontrib><creatorcontrib>Mittag, T W</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Klinische Monatsblätter für Augenheilkunde</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schmidt, K G</au><au>von Rückmann, A</au><au>Geyer, O</au><au>Mittag, T W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of nifedipine on ocular pulse amplitude in normal pressure glaucoma</atitle><jtitle>Klinische Monatsblätter für Augenheilkunde</jtitle><addtitle>Klin Monbl Augenheilkd</addtitle><date>1997-06</date><risdate>1997</risdate><volume>210</volume><issue>6</issue><spage>355</spage><pages>355-</pages><issn>0023-2165</issn><abstract>Ocular pulse amplitude (OPA) is reduced in normal tension glaucoma (NTG) patients when compared to non-glaucomatous, healthy control subjects. This might be related to a vasospastic reaction. The objective of this study was to determine if low OPA in NTG is associated with a vasospastic reaction and its response to vasodilation.
Nifedipine, a calcium channel blocker, vasodilator and systemic antihypertensive agent improves visual fields in NTG patients following acute and chronic dosing. The effect of 60 mg of daily orally administered nifedipine on OPA, intraocular pressure (IOP, German abbreviation: IOD), blood pressure (BP, German abbreviation: RR) and pulse rate (PR, German abbreviation: HF) were measured prior to and for 3 months after initiating nifedipine therapy in 32 NTG patients with and without a vasospastic reaction as manifested by a local cold exposure test. Before treatment, all patients had reduced OPA evaluated with the Langham Ocular Blood Flow System.
During nifedipine treatment NTG patients with a vasospastic reaction showed a significant (p < 0.001) increase in OPA, whereas NTG patients without a vasospastic reaction showed no sig. (p > 0.05) change in OPA.
There may be two different subgroups of NTG patients, those who have a vasospastic reaction and react to nifedipine, while others lack the ability to react to nifedipine or might have a different, non-vasospastic pathology. Calcium channel blockers and other vasodilators may be useful in the treatment of vasospastic NTG patients.</abstract><cop>Germany</cop><pmid>9333660</pmid></addata></record> |
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source | MEDLINE; Thieme Connect Journals |
subjects | Administration, Oral Adult Blood Flow Velocity - drug effects Blood Flow Velocity - physiology Calcium Channel Blockers - administration & dosage Calcium Channel Blockers - adverse effects Choroid - blood supply Dose-Response Relationship, Drug Drug Administration Schedule Eye - blood supply Female Glaucoma, Open-Angle - drug therapy Glaucoma, Open-Angle - physiopathology Humans Intraocular Pressure - drug effects Intraocular Pressure - physiology Male Middle Aged Nifedipine - administration & dosage Nifedipine - adverse effects Pulse - drug effects Pulse - physiology Vascular Resistance - drug effects Vascular Resistance - physiology Vasodilator Agents - administration & dosage Vasodilator Agents - adverse effects |
title | Effect of nifedipine on ocular pulse amplitude in normal pressure glaucoma |
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