1. Heat shock improves recovery and provides protection against global ischemia after hypothermic storage 
Ashok Gowda, MS, Chunjie Yang, MD, Gregory K Asimakis, PhD, Sohi Rastegar, PhD, Massoud Motamedi, PhD 
The Annals of Thoracic Surgery 
Volume 66, Issue 6, Pages (December 1998)
DOI: /S (98)

2. Fig 1
Experimental protocol. Myocardial function (heart rate, developed pressure, rate of ventricular pressure increase, rate of ventricular pressure decrease, and coronary flow were measured at 20 minutes after the initial reperfusion and after an additional 15-minute period of warm global ischemia (n = 10/group). Additional animals were used to evaluate HSP72 expression at 6 hours of recovery (control, n = 2; sham-treated, n = 3; heat-shocked, n = 3), and after 6 hours of recovery and 12 hours at 4°C (control, n = 3; sham-treated, n = 3; heat-shocked, n = 3). (Hr = hours; LDH = lactate dehydrogenase; Min = minutes.)
The Annals of Thoracic Surgery  , DOI: ( /S (98) )

3. Fig 2
Typical core temperature and heating pad temperature recorded from an animal subjected to whole-body heating (heat-shock group). Heat-shocked animals were anesthetized and wrapped in a heating blanket. Temperatures were recorded by a thermocouple placed rectally. Core temperature was increased to between 42° and 43°C for 15 minutes.
The Annals of Thoracic Surgery  , DOI: ( /S (98) )

4. Fig 3
End-diastolic pressure (EDP) versus balloon volume for all three groups at baseline reperfusion after cold ischemia (12 hours at 4°C). Heat-shocked animals demonstrated significant differences in EDP at all three balloon volumes between both sham-treated and control groups. (a = p < 0.05 versus sham and control; b = p < versus sham and control.)
The Annals of Thoracic Surgery  , DOI: ( /S (98) )

5. Fig 4
End-diastolic pressure (EDP) versus balloon volume for all three groups after 15 minutes of additional warm global ischemia. Heat-shocked animals demonstrated significant differences in EDP at all three balloon volumes between both sham-treated and control groups. (a = p < versus sham and control; b = p < versus sham and control.)
The Annals of Thoracic Surgery  , DOI: ( /S (98) )

6. Fig 5
Lactate dehydrogenase (LDH) enzyme leakage measured at baseline reperfusion and at 1-minute intervals after the additional warm ischemic period. Enzyme leakage was significantly different at all time points greater than 1 minute measured between heat-shocked and control animals. Although enzyme leakage of heat-shocked animals was lower than that of sham-treated animals at all time points, these differences were not statistically significant. (a = p < 0.05 versus control.)
The Annals of Thoracic Surgery  , DOI: ( /S (98) )

7. Fig 6
(a) Total cell lysates from rat hearts were dissolved on sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotted with an antibody specific for HSP72. Study groups above included heat-shocked (1), sham-treated (2), and control (3) animals, with 6 hours of recovery and 12 hours of storage at 4°C, and heat-shocked (4), sham-treated (5), and control (6) animals with only 6 hours of recovery. (b) Bar graphs showing densitometric analysis of autoradiographs from all groups studied. Heat shock followed by 6 hours of recovery (before storage) and 6 hours of recovery and 12 hours of storage at 4°C resulted in a significant difference (a = p < 0.005) when compared with both sham-treated and control groups.
The Annals of Thoracic Surgery  , DOI: ( /S (98) )