Continuous light exposure and sympathectomy suppress circadian rhythm of blood pressure in rats.

BACKGROUND: Although the 24-hour rhythm in blood pressure is well known, it is not clear how environmental light controls circadian cardiovascular and behavioral rhythms. METHODS AND RESULTS: The prolonged exposure of Wistar rats to continuous light for 17 weeks, beginning at 5 weeks old, induced a complete suppression of their blood pressure, heart rate, spontaneous locomotor activity, and body temperature circadian rhythms. Daily subcutaneous melatonin injections at the theoretical onset of darkness for 21 days could not restore light-suppressed blood pressure circadian rhythm, whereas it partially synchronized heart rate and body temperature rhythms and it fully restored spontaneous locomotor activity rhythms, as measured by radiotelemetry. The transfer of these rats from constant light to a standard 12:12-hour light/dark photoperiod fully restored circadian rhythmicity within 2 to 5 days, although their 24-hour diastolic blood pressure remained elevated. Synchronized rats were then subjected to superior cervical ganglionectomy (SCGx) and 6-hydroxydopamine sympathectomy (SYMPx). SCGx plus SYMPx completely abolished the circadian rhythm in blood pressure and significantly reduced those in heart rate, spontaneous locomotor activity, and body temperature. CONCLUSIONS: We conclude that in Wistar rats exposed to continuous light, the light-induced increase in sympathetic outflow can suppress blood pressure circadian rhythm, and sustained cardiac wall stress can alter diastolic function at rest. Preserved inotropy in these conditions must result from an adaptative hypertrophic response of myocytes.

Leukocyte trafficking and myocardial reperfusion injury in ICAM-1/P-selectin-knockout mice.

P-selectin and intercellular adhesion molecule-1 (ICAM-1) mediate early interaction and adhesion of neutrophils to coronary endothelial cells and myocytes after myocardial ischemia and reperfusion. In the present study, we examined the physiological consequences of genetic deletions of ICAM-1 and P-selectin in mice. In wild-type mice, after 1 h of ischemia followed by reperfusion, neutrophil influx into the area of ischemia was increased by 3 h with a peak at 24 h and a decline by 72 h. ICAM-1/P-selectin-deficient mice showed a significant reduction in neutrophils by immunohistochemistry or by myeloperoxidase activity at 24 h but no significant difference at 3 h. Infarct size (area of necrosis/area at risk) assessed 24 h after reperfusion was not different between wild-type and deficient mice after 30 min and 1 h of occlusion. Mice with a deficiency in both ICAM-1 and P-selectin have impaired neutrophil trafficking without a difference in infarct size due to myocardial ischemia-reperfusion.