Human experimentation: No accurate, quantitative data?

Abstract

This Viewpoint addresses two issues in comparing data from humans and animals in studies of cardiovascular physiology: 1) accuracy of methods and 2) limits in extrapolating data from one species to another. You are invited to submit a brief commentary on this Viewpoint, which will be reviewed by Journal of Applied Physiology editors for possible publication in the Journal. Please limit your comment to 250 words and 5 peer-reviewed published references.IN A RECENT POINT:COUNTERPOINT debate in the Journal of Applied Physiology, Hainsworth and Drinkhill (5) state: "Unfortunately, as it is not possible to obtain accurate quantitative data from humans, we have to rely on results extrapolated from animal studies, mainly on dogs and cats." The purpose of this viewpoint, which takes Hainsworth's unqualified comment at face value, is to rebut this notion. Understanding of human physiology indeed rests in part on what we have learned from other species, but a great body of knowledge comes from studies performed on human subjects that entailed measurements as accurate and quantitative as those possible in work with animals.

Neuroprotection and stroke: time for a compromise

“…Nevertheless, more and more publications (De Keyser et al. 1999; Green and Shuaib 2006; Rowell 2007; Sacco et al. 2007) suggest that clinical testing of such compounds may also be flawed.…”

“…Indeed, what factors determine the right of access of an experimental drug to a clinical trial? Nevertheless, more and more publications (De Keyser et al 1999;Green and Shuaib 2006;Rowell 2007;Sacco et al 2007) suggest that clinical testing of such compounds may also be flawed. It may be argued that failed stroke trials were the result of not applying the information supplied by animal models to the clinical trial (Green and Shuaib 2006).…”

Peripheral vasodilatation determines cardiac output in exercising humans: insight from atrial pacing

“…Moreover, ventricular pacing over a wide range of heart rates (HRs) results in little or no change in in exercising dogs (White et al 1971; Wyss et al 1982; Sheriff et al 1993), indicating that a change in HR is not a regulatory mechanism of the exercise‐induced increase in . Whether these findings in dogs apply to humans remain uncertain, because of anatomical and physiological species differences (Rowell, 2007). Firstly, and in contrast to humans, dogs have most of the blood volume above the level of the heart (Rowell, 2003).…”

Response to: Control of muscle exercise hyperaemia: are the mechanisms found in transition?

“…Our human studies have often been inspired by results obtained in advanced animal studies, and we have turned to animal models when limited in our human models. That said, there are clear anatomical and physiological differences between animals and humans that are important to cardiovascular regulation, and one should be very careful before extrapolating findings in animals to humans (see Rowell, 2007). It is my opinion that observations from animal studies should never be seen as definitive before they have been confirmed in humans.…”