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The purpose of this study was to determine the contribution of prostaglandins to the reflex cardiovascular responses induced by static contraction of the hind limb in cats, i.e., the exercise reflex. To accomplish this, the cardiovascular responses to hind limb contraction induced by electrical stimulation of spinal cord ventral roots L^ and S, were compared before and after inhibition of prostaglandin synthesis (indomethacin, 2-6 mg/kg i.v., n = 5, or sodium meclofenamate, 2-6 mg/kg i.v., n = 5) or after injection of prostaglandin E 2 into the hind limb arterial blood supply. Treatment with indomethacin attenuated the contraction-induced increase in mean arterial pressure and left ventricular dP/dt by 76% and 86%, respectively. Heart rate and average developed triceps surae muscle tension were unchanged. After administering sodium meclofenamate, the reflex response was attenuated to a similar degree. In the indomethacin-treated animals, injection of exogenous prostaglandin E 2 (PGE 2 ) partially restored the pressor and myocardial contractile responses. In 6 animals, treatment with exogenous PGE 2 without prior inhibition of prostaglandin synthesis did not significantly augment the contraction-induced cardiovascular response. Using the radioactive microsphere technique, we measured skeletal muscle blood flow during contraction before and after treatment with indomethacin (n = 6) to determine if an indomethacin-induced alteration in blood flow could account for the attenuated contraction-induced cardiovascular response. Blood flow during static muscle contraction was not significantly altered by indomethacin. We conclude that prostaglandins contribute to the exercise reflex through an action on afferent nerve endings rather than through a regional vascular effect. (Circulation Research 1986;59:645-654)

To investigate blood pressure and pulse rate responses to dental surgery, 21 patients 18 to 73 years of age (mean age, 42 ± 4 years) who visited our hospital for tooth extraction were studied. Before dental treatment, the patients underwent a mental arithmetic stress test, electrocardiography, and an anxiety evaluation with the State-Trait Anxiety Inventory. Baseline blood pressure and pulse rate were 118±4/ 70±3 mmHg and 69±2 beats/min, respectively. Blood pressure rose by 24±3117±2 mmHg during the mental stress test, and the magnitude of the rise in systolic blood pressure was significantly correlated with age (r=0.81, p<0.001) and baseline blood pressure (r=0.56, p<0.01). After the topical injection of local anesthetic containing 1: 80,000 epinephrine, a transient increase in systolic blood pressure was observed. The maximum blood pressure and pulse rate increases during dental surgery were 24±4/13 ±2 mmHg and 17±3 beats/min, respectively. Similarly, the rate pressure product increased from 8,196 ± 486 to 11,802 ± 682. The magnitude of the blood pressure increase during dental surgery was not correlated with age, sex, family history of hypertension, baseline blood pressure, anxiety score, or response to mental stress. On the other hand, when the subjects were divided into two subgroups according to the blood pressure response during dental surgery, the larger response group (increase in mean blood pressure greater than 15 mmHg, n=9) required a significantly larger dose of local anesthetic than did the smaller response group. The number of cases of pericoronitis of the third molar tended to be greater in the larger response group. These results indicate that an increase in blood pressure during dental surgery cannot be predicted on the basis of baseline blood pressure or the response to mental stress, but is related to the cause of tooth extraction and the volume of local anesthetics required to control the pain. (Hypertens Res 1996; 19: 189-194)

Harada H, Mitsuyasu T, Seta Y. Maruoka Y, Toyoshima K, Yasumoto S: Overexpression of bcl‐2 protein inhibits terminal differentiation of oral keratinocytes in vitro. J Oral Pathol Med 1998; 27: 11–7. © Munksgaard, 1998. The bcl‐2 proto‐oncogene is a known inhibitor of apoptosis; in normal human stratified squamous epithelium, its expression is restricted to the basal cell layer. To investigate the functional role of bcl‐2 protein in the process of differentiation of oral keratinocytes, bcl‐2 expression vector was transfected into SCC‐25 cells, which normally undergo squamous cell differentiation in vitro while expressing specific differentiation markers, e.g., keratin 10/11 and involucrin. In bcl‐2 transfected SCC‐25 cells, the expression of these differentiation markers was markedly suppressed. The bcl‐2 proto‐oncogene may play a critical role in opposing the commitment to terminal differentiation and apoptosis of oral keratinocytes.

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