## 4 Discussion  
The key finding of this study is that rats drinking white wine for 4 weeks prior to a surgically induced MI had significantly better survival than control animals drinking only water. In contrast to the wine group, consumption of a corresponding amount of ethanol did not result in significantly better survival relative to the water group. In addition, a more detailed analysis linking drinking volumes to survival outcomes revealed that lower ethanol consumption was more prevalent in rats that survived. These results indicate an upper limit for the protective effect of ethanol. Contrary to the ethanol drinking group, there seems to be no such limit for wine, as no deaths occurred in rats with an average daily white wine consumption of approximately 10 mL or more. This implies that the \begin{table}
\begin{tabular}{c c c c c c c} \hline \hline  & \multicolumn{3}{c}{**White Wine**} & \multicolumn{3}{c}{**Ethanol**} \\ \cline{2-7}  & **Wine (mL)** & **Water (mL)** & **Mass (g)** & **Ethanol (mL)** & **Water (mL)** & **Mass (g)** \\ \hline Survived & \(10.5\pm 3.7\) & \(20.1\pm 1.2\) & \(329\pm 13\) & \(11.0\pm 2.0\) & \(12.1\pm 2.1\) & \(330\pm 37\) \\ Died & \(8.21\pm 0.93\) & \(19.4\pm 8.2\) & \(351\pm 11\) & \(14.3\pm 1.6\) & \(11.9\pm 2.3\) & \(345\pm 1\) \\ Significance & ns & ns & ns & ** & ns & ns \\ \hline \hline \end{tabular}
\end{table} 
Table 2: Intake of white wine, ethanol and water based on the outcome after MI. The last row contains \(p\)-values for tests of differences between the corresponding measurements within the same treatment group. The results are presented as mean \(\pm\) SD. A \(p\)-value smaller than 0.05 was considered statistically significant. ns = not significant. ** denotes a \(p\)-value between 0.001 and 0.01. Figure 4: Comparison of daily intake of ethanol and white wine depending on the outcome (died or survived) four days after induction of MI. ns = not significant. ** denotes a \(p\)-value between 0.001 and 0.01.  
cardioprotective effect of white wine cannot be attributed solely to ethanol, but to other wine constituents as well. The fact that we were able to separate outcomes based on different levels of ethanol intake indicates the suitability of the experimental model used in terms of the intensity of the pathophysiological challenge and its sensitivity in detecting the effects of different drinking protocols. It should be pointed out that the intake of both ethanol and white wine by the animals in our study falls into the low to moderate drinking regime [20; 23]. Nonetheless, an upper limit for protective effects was observed in the ethanol group, indicating a hormetic physiological behavior of ethanol in which the effects of small quantities are opposite to that of large quantities. In other words, low-intensity stress in a living system provoked by low doses of ethanol triggers a series of countering mechanisms to ensure subsequent protection and homeostasis [24; 25]. Indeed, depending on the amount consumed, ethanol may increase or decrease the risk of CVDs, reflecting a J-shaped relationship between CVDs and alcohol intake [26]. It has been well established that the beneficial cardiovascular effects of moderate alcohol consumption can partly be attributed to alcohol-associated increases in both HDL cholesterol and fibrinolytic activity, as well as decreased platelet aggregation [27]. In the case of wine, cardioprotective effects may be attributed to both alcoholic and non-alcoholic bioactive compounds, primarily wine polyphenols and, possibly, other bioactive phytochemicals such as melatonin and phytosterols [28; 29]. Because of the positive effects of low amounts of alcohol on HDL-cholesterol and hemostatic factors, ethanol and polyphenols may exert additive and/or synergistic protective effects on the cardiovascular system [30]. Due to the differences in wine-making techniques, the total phenolic content in standard white wines is much lower than in red wines.