Evaluating the reactivity hypothesis.

T1 - Cardiovascular reactivity to work stress predicts subsequent onset of hypertension

Therefore, it will be used as a prototype for the class.

BP and HR measurements were obtained before the test and every min for 4 min during the test and the recovery period. Because the pressor and chronotropic responses in each of the three tests were maximal at different times points, we selected the time of the greatest magnitude of the response; the 3rd min for the handgrip test, the 4th min for the Stroop test and the 2nd min for the cold pressor test. The BP and HR responses during the tests were compared to the baseline measurements.

T1 - Autonomic, neuroendocrine, and immune responses to psychological stress

Cardiovascular Reactivity - MacArthur SES & Health …

Cardiovascular reactivity may then influence either the development or clinical course of diagnosed cardiovascular disease as these processes are separable (e.g., initial vascular injury in comparison to ischemia / arrhythmia; ; ). However, as shown in , we hypothesize that received support should be associated only with the course of clinically diagnosed cardiovascular disease which can be either beneficial or detrimental depending on the contextual processes noted above. We do not predict that received support influences the development of cardiovascular disease because (a) of the variability associated with the effectiveness of received support in coping with stress, (b) of the potential for stress to erode support even from close relationships (), and (c) it is just one of many coping options available to individuals. These theoretical issues have important implications for the inconsistent epidemiological links observed between received support and mortality and its subsequent modeling in laboratory contexts.

T1 - Cardiovascular reactivity to the cold pressor test as a predictor of hypertension

DBP formation and requisite chlorine dosage for disinfection strongly correspond to the concentration of TOC at the point of chlorine addition, suggesting that optimized or enhanced removal of organic carbon prior to chlorination will decrease the formation of DBPs.

This has significant implications, for example, for precipitative softening facilities.

Cardiovascular Responses to Stress and Disease …

In comparison with other chemicals known to produce mutations via direct DNA reactivity such as aflatoxin B1 and ethylene dibromide, BDCM is a relatively weak mutagen.


In rats, P450-mediated metabolism of BDCM (Figure 1) is believed to proceed by the same two pathways established for chloroform: oxidation with phosgene the proposed active metabolite, and reduction with the dichloromethyl free radical proposed as the reactive product (Tomasi et al., 1985; IPCS, 1994; Gao et al., 1996).

Psychology Definition of CARDIOVASCULAR REACTIVITY: n

This may be due to the fact that the reactive intermediates suspected to be involved in THM mutagenicity must be generated within the target cells (Thier et al., 1993; Pegram et al., 1997).

Cardiovascular Reactivity to Psychological Stress ..

A number of recent studies support the hypothesis that chloroform acts to produce cancer in rodents through a non-genotoxic/cytotoxic mode of action, with carcinogenesis resulting from events secondary to chloroform-induced cytolethality and regenerative cell proliferation (Larson et al., 1994a,b, 1996; Pereira, 1994; Templin et al., 1996a,b,c, 1998).

and Health: The Cardiovascular Reactivity Hypothesis ..

The authors also observed a treatment-related increase in transforming growth factor-alpha (TGF-alpha) immunoreactivity in hepatocytes, bile duct epithelium, bile canaliculi and oval cells and an increase in transforming growth factor-beta (TGF-ß) immunoreactivity in hepatocytes, bile duct epithelium and intestinal crypt-like ducts.

Relationship of cardiovascular reactivity, stressful ..

Human GST T1-1 is expressed polymorphically and could therefore be a critical determinant of susceptibility to the genotoxicity of the brominated THMs.