Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred eight consecutive patients with proved coronary artery disease and reproducible exercise-induced myocardial ischemia were studied. During repeated exercise testing, 52 patients (Group I) had myocardial ischemia in the absence of pain (silent ischemia) whereas 56 patients (Group II) experienced anginal symptoms in the presence of electrocardiographic signs of ischemia. A pulpal test was carried out in all patients using an electrical dental stimulator commonly used in dentistry. Electrical current was delivered in increasing intensity from 10 to 500 mA, and the dental pain threshold and the reaction of the patients to maximal stimulation were determined. During the pulpal test, 71.2% of the patients in Group I did not experience pain, even at maximal stimulation (threshold 0), 11.5% were sensitive at threshold I (10 to 200 mA) and 17.3% felt pain at threshold II (210 to 500 mA). In Group II, 69.7% of the patients complained of dental pain at the low intensity test current (threshold I), 10.7% at threshold II and 19.6% at threshold 0. In Group I, 71.2% of patients did not have discomfort (reaction -), even at maximal stimulation, 21.1% had a mild reaction (reaction +) and 7.7% had an intense painful reaction (reaction ++). In Group II, 80.4% of patients were sensitive to the pulpar test (67.9% reported intense painful sensation at maximal stimulation, 12.5% had a mild reaction); 19.6% of patients had no reaction. The two groups of patients were similar with respect to age, sex and angiographic features.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dental pain threshold and angina pectoris in patients with coronary artery disease. 339 25

Ischemic pain was produced by a blood pressure cuff placed to the arm of healthy human subjects for 15 min which produced a mean pain score of 59% (visual analogue scale). Ischemia induced a significant dental pain threshold elevation (mean 67%) and 2 mg of naloxone did not reduce it. Thermal sensitivity of the upper lip had a tendency to reduction during ischemia and 2 mg of naloxone reduced this effect. Tactile thresholds in the forehead or in the contralateral arm were not markedly elevated. Neither ACTH nor prolactin level in the plasma was related to the dental pain threshold elevation during ischemia. The findings of the present study suggest that ischemic pain nonsegmentally produces a predominant inhibition of responses to thin afferents. Endogenous opioids may markedly contribute to the reduction of thermal sensitivity induced by ischemia, but their contribution to dental pain threshold elevations seems to be less important. Stress or other adenohypophyseal mechanisms involving the release of ACTH or prolactin do not explain the effects of ischemia found in the present study.
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PMID:Ischemic pain nonsegmentally produces a predominant reduction of pain and thermal sensitivity in man: a selective role for endogenous opioids. 629 48

It is commonly accepted that application of a sustained noxious stimulus frequently suppresses the perception of pain. In this investigation, we have determined whether painful forearm ischemia suppresses tooth pain resulting from an acute irreversible pulpitis. We have also determined whether the physiological responses to toothache alter the perception of pain evoked by experimental procedures. Ten male subjects experiencing a painful toothache (group TA) and 7 age-matched pain-free male subjects (group PF) participated in these studies. During session 1, heat pain threshold and tolerance values were determined for both groups. The times to ischemic pain onset and ischemic pain tolerance were determined for both groups using the submaximal effort tourniquet procedure. The effect of the tourniquet procedure on the intensity, unpleasantness, and spatial distribution of toothache was also assessed. Session 2 was conducted on 7 TA and 7 PF subjects 1 week later and was conducted like session 1 with the exception that group TA was not experiencing tooth pain during this session. Measures of thermal pain perception and forearm ischemic pain perception were not altered by the occurrence of toothache. In contrast, sustained noxious forearm ischemia produced a marked reduction in the intensity, unpleasantness and spatial distribution of pulpal pain. These effects on pulpal pain remained for at least 5 min after removal of the tourniquet while the arm was pain free. These findings suggest that a noxious conditioning stimulus does not universally inhibit pain perception but instead depends on unidentified interactions between the noxious test and conditioning stimuli.
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PMID:Effects of experimental and clinical noxious counterirritants on pain perception. 793 6

An association between a decreased responsiveness to varying painful stimuli and arterial hypertension both in animals and in humans has been documented. The relationship between essential hypertension and silent myocardial ischemia in coronary artery disease (CAD) populations is not well understood. The aims of this study in CAD patients with and without essential hypertension were (1) to determine dental pain threshold and reaction to tooth pulp stimulation and (2) to ascertain whether hypertensive CAD patients differ from normotensive ones in reactivity to pain. This study involved 182 patients who were affected by mild and moderate hypertension (G1) and 174 normotensive patients (G2). The inclusion criteria were reproducible exercise-induced myocardial ischemia, CAD documented at angiography, and dental formula suitable for pulp test. All patients underwent an ergometric stress test, coronary angiography, and pulp test. Our CAD hypertensive patients showed a lower prevalence of angina during daily life (64.8% in G1 versus 81.6% in G2, P<.05) and a higher incidence of exercise-induced silent myocardial ischemia (60.4% in G1 versus 48.8% in G2, P<.05) than the normotensive group. The mean anginal pain intensity, which was suffered both during spontaneous transitory episodes of ischemia and/or during acute myocardial infarction, was significantly lower in G1 than in G2 patients (P<.05). During pulp test, 31.8% of G1 and 13.7% of G2 referred no symptoms, even at the highest current intensity of 500 mA. The hypertensive patients with symptoms during pulp test had a higher mean dental pain threshold and lower mean threshold reaction and maximal reaction than did the normotensive symptomatic ones. In patients of both groups, a positive correlation between the mean maximal reaction during pulp test and the prevalence of angina during daily life was also found. In conclusion, patients with CAD and essential hypertension differ from normotensive CAD patients in reactivity to pain. Significantly higher pain thresholds and lower reactions to tooth pulp stimulation characterized patients with increased blood pressure values.
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PMID:Susceptibility to pain in hypertensive and normotensive patients with coronary artery disease: response to dental pulp stimulation. 936 88

Preferential blocks of peripheral nerves have shown that myelinated nerves are more susceptible to local compression and less resistant to asphyxia than unmyelinated fibers. Since two groups of functionally different nociceptors exist in the dental pulp, it is of theoretical and clinical interest to determine the influence of ischemia on the sensitivity of human dental pulp, using standard means for testing tooth vitality and at the same time investigating the intensity coding in one pathway of the afferent trigeminal system. Adrenaline was used to study the differential effect of adrenaline-induced ischemia on intradental A-delta nerve activity (INA) and the concomitant sharp pain, as well as on the detection threshold for monopolar electrical stimulation. Cold (ethyl chloride) and heat (heated gutta-percha) stimulation was applied to the tooth surface. In accordance with the hydrodynamic theory of dentin sensitivity the rapid fluid flow induced in the dentinal tubuli by these thermal stimuli is an adequate stimulus for selectively activating the A-delta nerves in healthy pulps. Consistency plots of the magnitude of the perceptual experience of sharp pain against the neural population response in linear coordinates yielded a high product-moment correlation, implying linearity for the intensity coding relationship. In contrast to the significant reduction of INA and its perceptual correlate of sharp pain after adrenaline administration, the electrical detection threshold remained constant during the full test period, suggesting that electrical threshold measurements have their limitations as a diagnostic tool or criterion for assessing the sensitivity of the dental pulp. The absence of A-delta activity was parallelled by no sensation of sharp pain. These findings suggested that the integrated neural A-delta activity constituted the underlying peripheral neurophysiological mechanism of the sensory intensity of sharp dental pain.
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PMID:Pulpal ischemia in man: effects on detection threshold, A-delta neural response and sharp dental pain. 1021 48