Heat shock proteins and myocardial protection : comparative physiology and the role of cardiac energetics /
We hypothesized that cardiac tissue from highly hypoxia tolerant animals might superexpress specific HSPs either by induction or constructively. We measured myocardial HSP6O and HSP72/73 in painted and softshelled turtles during nontoxic, anoxia (12 hr), after recovery (12 or 24 hr) and in nontoxic...
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| Format: | Thesis Book |
| Language: | English |
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[Place of publication not identified] :
[publisher not identified] ;
1999.
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| Online Access: | http://proxy.library.tamu.edu/login?url=http://proquest.umi.com/pqdweb?did=733670141&sid=1&Fmt=2&clientId=2945&RQT=309&VName=PQD |
| Summary: | We hypothesized that cardiac tissue from highly hypoxia tolerant animals might superexpress specific HSPs either by induction or constructively. We measured myocardial HSP6O and HSP72/73 in painted and softshelled turtles during nontoxic, anoxia (12 hr), after recovery (12 or 24 hr) and in nontoxic rats and rabbits. During nontoxic, painted turtles, which are the most hypoxia tolerant, expressed the highest levels of HSP6O followed by softshells, which are the relatively hypoxia sensitive and rabbits and rats, which are the most hypoxia sensitive. HSP6O levels from both painted and softshelled turtles did not deviate significantly from control values after either 12 hr of anoxia or after either 12 or 24 hr of recovery. For HSP72/73, anoxia induced a significant increase in myocardial HSP72/73 in painted turtles. By 12 hr of recovery, HSP72/73 had returned to control levels and remained there through 24 hr. In softshelled turtles, HSP72/73 decreased significantly after 12 hr of anoxia and then rose to significantly above control after 24 hr of recovery. Our data support our hypothesis for HSP6O but not for HSP72/73. Previously Knowlton et al. have observed that the isolated rabbit heart in the absence of injury has increased levels of heat shock protein 72. We hypothesized that this increase was mediated by stretch-activated ion channels (SACs). We Langendorff perfused isolated rat hearts and demonstrated that HSF1 was activated, but not in non-perfused hearts or in hearts perfumed with an empty left ventricle. In a separate set of hearts, gadolinium, an inhibitor of SACs, was added to the perforate and it inhibited the activation of HSF1. Because gadolinium can inhibit both SACs and L-type calcium channels, we perfumed another group of hearts with diltiazem, an L-type calcium channel blocker. Diltiazem failed to inhibit the activation of HSF1. Thus, Langendorff perfusion of rat hearts results in activation of HSF1 through SACs. Heat Shock Factor (HSF) can be activated by cardiac ischemia and/or reperfusion. We hypothesized that a decreased intercellular ATP and/or intercellular pH (pH[]) might be sufficient to activate HSF in the isolated perused rat heart. Hearts were subjected to either ischemia or repercussion. Intercellular ATP, Per and pH levels were monitored by ³¹P-NMR spectrometer and free energy of ATP hydrolysis ([]G[]) was calculated. Using gel mobility shift assays, we measured the activation of HSF. Our conclusions are 1) a moderate decrease in intercellular ATP correlates with the activation of HSF1 in the isolated perused rat heart; 2) a severe depletion in ATP correlates with an attenuation in HSF1 activation, suggesting that a critical ATP level is required for HSF1 activation; 3) a high AGATP might be required for HSF1 activation; 4) changes in pH may be synergistic for the activation of the heat shock response. |
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| Item Description: | Vita. "Major Subject: Veterinary Physiology". |
| Physical Description: | x, 79 leaves : illustrations ; 28 cm. Issued also on microfiche from University Microfilm Inc. |
| Bibliography: | Includes bibliographical references (leaves 65-78). |