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Biomedical subjects

W Maixner

Publications and source records attributed to W Maixner.

At least 91 records · Page 5Linked to original sources

Pharmacological effects of 2-aminotetralins, octahydrobenzo[f]quinolines and clonidine on the isolated guinea pig ileum.

The ability of derivatives of 2-aminotetralins (2AT), cis- or trans-isomers of octahydrobenzo[f]quinolines (BfQ) and clonidine to modulate acetylcholine release was studied using field-stimulated guinea pig ilea (GPI). Antihistaminic and antiacetylcholine activities were also determined using isolated superfused segments of GPI. Hydroxylated 2AT, BfQ and clonidine inhibited field stimulation-induced contractions through alpha-adrenoceptor mechanisms which were antagonized by phentolamine. In contrast, the inhibition produced by nonhydroxylated 2AT was not attenuated by alpha-adrenoceptor antagonism. 2AT, trans-7,8-dihydro-BfQ and cis-8,9-dihydroxy-BfQ inhibited contractions induced by nicotine bitartrate using superfused GPI. Clonidine was inactive as an antinicotinic agent and there was no correlation between a compound's ability to inhibit contractions induced by field stimulation and its antinicotinic activity. Various 2AT derivatives demonstrated weak antimuscarinic and/or antihistaminic activities on superfused ileal segments. These data demonstrate that these agents possess a spectrum of pharmacological activity.

2-Naphthylamine↗

Reactive hyperemia vs treadmill exercise testing in arterial disease.

We compared the ankle pressure response during reactive hyperemia to the response to treadmill exercise in 28 limbs of 14 normal individuals and 26 legs of 15 patients with arterial occlusive disease. The mean percent maximum drop in ankle blood pressure during reactive hyperemia in normal limbs, 17% +/- 11% (+/- 1 SD) was significantly less than that of legs with arterial disease, 54% +/- 15% (P less than .001). Abnormal values were recorded in all but three diseased limbs. There was good correlation between the ankle pressure responses to reactive hyperemia and treadmill exercise (r = 0.71, P less than .001). This study suggests that measurement of ankle pressure during reactive hyperemia may be a useful substitute for treadmill testing to determine the functional capacity of the circulation during stress in patients with arterial occlusive disease. Reactive hyperemia testing requires less time and equipment and may be performed in patients who might be at risk or unable to carry out treadmill exercise.

Adult↗

Early detection of hypovolemia from directional arterial flow velocity.

The effect of hypovolemia on femoral artery vascular resistance and directional arterial flow velocity was determined in six mongrel dogs. Progressive withdrawal of blood was associated with an increase in femoral arterial resistance and reverse flow velocity and a decrease in forward flow velocity. The percentage increase in the ratio of peak reverse to peak forward flow velocity (Vr/Vf) varied in a positive linear fashion with the percent increase in femoral artery vascular resistance, (r = 0.69, P less than 0.001). The femoral arterial peripheral vascular resistance and peak Vr/Vf increased significantly before arterial pressure declined. These alterations in peak Vr/Vf occur early in the course of hypovolemia and are a sensitive index of extremity hemodynamics associated with hemorrhagic induced hypovolemia.

Animals↗

Value of concomitant sympathectomy in aortoiliac reconstruction. Results of a prospective, randomized study.

The efficacy of concomitant lumbar sympathectomy in improving results of aortoiliac reconstruction was assessed by a prospective, randomized study of 51 patients undergoing operation for occlusive or aneurysmal disease. Sympathectomy was performed on 50 limbs, while 52 extremities served as controls. Sympathectomy resulted in a significant reduction in foot vascular resistance determined by plethysmography. However, the procedure had no effect on leg circulation, assessed by ankle/arm pressure indices determined by Doppler ultrasound. In the sympathectomy group, there were three early postoperative amputations for ischemia, despite patent grafts. In the control group, there was one late graft occlusion, caused by progressive atherosclerotic disease. Although sympathectomy may improve pedal circulation, the procedure does not appear to improve the results of aortoiliac reconstruction.

Adult↗

The role of prostaglandin E in the hemodynamic response to aortic clamping and declamping.

The infrarenal aorta was occluded for one hour in 11 control dogs and in eight dogs in which biosynthesis of prostaglandin E (PGE) was inhibited by administration of indomethacin (2.5 mg. per kilogram). The mean arterial pressure (MAP) in the indomethacin group was significantly (p less than 0.001) higher than in the control group at the end of 60 minutes of aortic occlusion (187 +/- 3 vs. 137 +/- 4 mm. Hg, mean +/- S.E.M.) and remained higher (p less than 0.001) after declamping. However, the decline in MAP at the time of aortic declamping was essentially the same for both groups. Total peripheral resistance (TPR) was higher in the indomethacin group than in the control group at the end of one hour of occlusion (159 +/- 13 vs. 124 +/- 12%, p less than 0.001) and remainded higher throughout the period following occlusion. The plasma concentration of PGE in the control group increased significantly (p less than 0.05) above control (630 +/- 110 to 1,299 +/- 261 pg. per milliliter) during the 60 minute period of occlusion with further increases to 1,447 +/- 389 and 1,523 +/- 256 pg. per milliliter (p less than 0.001) at 10 and 60 seconds after declamping, respectively. In the indomethacin group, PGE remained essentially unchanged throughout the clamping and declamping period and therefore was significantly (p less than 0.05) lower than in the control group. A similar pattern was observed in the tissue levels of PGE. This study suggests that PGE is released during and after infrarenal aortic occlusion and may be responsible for maintaining reduced TPR and MAP. However, hypotension after declamping is not affected by inhibition of PGE biosynthesis.

Animals↗

Estrous cycle modulation of nociceptive behaviors elicited by electrical stimulation and formalin.

The impact of circulating ovarian hormones on nociceptive behaviors elicited by phasic and tonic stimuli was evaluated in rats using two behavioral tests: an operant escape task and the formalin test. The operant escape task was structured to separately evaluate hindlimb flexion reflexes, the latency of escape, and the amplitude of peak vocalization to a series of phasic electrocutaneous stimuli (0.05-0.8 mA), whereas the formalin test evaluated nociceptive behaviors elicited by tonic stimulation following a subcutaneous injection of dilute formalin (1%). Hindlimb reflex amplitude, escape latency, and peak vocalization varied across the estrous cycle, such that rats were most sensitive to electrical stimuli during proestrus (reflex and escape latency) and diestrus (vocalization). Furthermore, morphine-induced (3 mg/kg sc) attenuation of hindlimb reflex amplitude was sensitive to estrous cycling. During proestrus, morphine produced less attenuation of hindlimb reflex amplitude than during nonproestrus phases. However, estrous cycling did not alter nociceptive behaviors elicited by 1% formalin. These data support the notion that circulating ovarian hormones may differentially modulate behaviors associated with phasic and tonic pain.

Analgesics, Opioid↗

Peripheral vascular effects of a new dopamine analog: 5-6-dihydroxy-2-methylaminotetralin (M-8).

It has been reported that the cyclic dopamine analog 5,6-dihydroxy-2-methylaminotetralin (M-8) in an adrenergic agonist in the dog. In this study, the effects of M-8 on hindlimb vascular responses was determined in the dog. In group I (n = 10), hindlimb vascular responses to ipsilateral femoral artery injections of M-8 before and after adrenergic blockade were determined. Mean femoral artery and peripheral venous pressures and heart rate responses to intra-arterial injections of M-8 were recorded. Mean femoral artery flows were measured by an electromagnetic flowmeter. Low doses of M-8 (0.0001-01 micrograms/kg) elicited transient dilatory responses, while higher doses (1-10 micrograms/kg) produced a biphasic response consisting of a dilation followed by constriction. The dilatory responses were attenuated following pretreatment with propranolol and were augmented by pretreatment with phenoxybenzamine. The constrictor responses were attenuated by pretreatment with phenoxybenzamine. The constrictor responses were attenuated by pretreatment with pehnoxybenzamine and augmented by pretreatment with propranolol. These responses were not reflex-mediated, since the hemodynamic parameters in the contralateral limb were not altered during the depressor or pressor phases. In group II (n = 5), the effects of intra-arterially infused M-8 (0.01 micrograms/kg/min) on plethysmographically determined hindlimb venous capacitance were determined. Intra-arterial infusion increased venous capacitance through beta-adrenergic mechanisms without altering mean arterial pressure and heart rate or contralateral limb mean femoral artery flows. M-8 is a potent peripherally acting adrenergic agent.

Animals↗

The influence of resting blood pressure and gender on pain responses.

Recent research suggests that resting blood pressure is inversely related to pain sensitivity, even among normotensives; however, most of these studies have included only male participants. To determine whether this hypoalgesic effect of blood pressure was also present in females, we investigated thermal and ischemic pain responses in a group of age-matched, normotensive females and males as a function of resting blood pressure. Thermal pain threshold and tolerance were determined, and a cross-modality thermal magnitude matching procedure was conducted, after which ischemic pain threshold and tolerance were determined using the submaximal effort tourniquet procedure. Systolic pressure, diastolic pressure, and heart rate were obtained using an automated blood pressure monitor with a pneumatic cuff positioned around the left ankle. Females provided higher normalized thermal magnitude estimates and a shorter time to ischemic pain tolerance, but no gender differences emerged on other pain measures. Systolic, diastolic, and mean arterial pressures were significantly correlated with thermal and ischemic pain responses among males but not females, with higher blood pressure being associated with lower pain sensitivity. After adjusting for resting blood pressure, the gender difference in normalized magnitude estimates was only marginally significant, and the gender difference in ischemic pain tolerance became nonsignificant. These findings are consistent with previous research indicating an inverse relationship between blood pressure and pain sensitivity. Additionally, the findings also suggest that blood pressure may partially moderate gender differences in pain sensitivity. Potential mechanisms and clinical implications of the current findings are discussed.

Adult↗

Relationship between pain sensitivity and resting arterial blood pressure in patients with painful temporomandibular disorders.

OBJECTIVE: Patients experiencing temporomandibular disorders (TMD) show greater sensitivity to painful stimuli than age- and gender-matched control subjects. This enhanced pain sensitivity may result, at least in part, from an alteration in pain regulatory systems that are influenced by resting arterial blood pressure. In this study, we examined the relationship between resting systolic blood pressure and pain perception in 64 female TMD and 23 age-matched pain-free female subjects. METHOD: Resting arterial blood pressure and measures of thermal and ischemic pain threshold and tolerance were determined for each participant. Subjective ratings of thermal pain evoked by suprathreshold noxious thermal stimuli (45-49 degrees C) using a magnitude matching procedure were also obtained for both groups. RESULTS: TMD patients had lower thermal and ischemic pain thresholds and tolerances than pain-free subjects (ps < .05). Both groups provided equivalent intensity ratings to suprathreshold noxious thermal stimuli. A median split of each group based on resting systolic blood pressure revealed an influence of blood pressure on both thermal and ischemic pain perception for the Pain-Free group. The Pain-Free high resting blood pressure subgroup had higher thermal pain tolerances, higher ischemic pain thresholds, and provided lower magnitude estimates of the intensity of graded heat pulses compared with the Pain-Free low blood pressure subgroup. A trend toward a significant effect of blood pressure level on ischemic pain tolerance was also observed for the Pain-Free group. In contrast to the Pain-Free group, blood pressure level did not influence ischemic or thermal pain perception for TMD patients. Similar to the lack of effect of resting blood pressure on experimental pain perception in TMD patients, resting blood pressure was not related to measures of clinical orofacial pain in TMD patients. CONCLUSIONS: These findings confirm our previous findings that TMD patients are more sensitive to noxious stimuli and suggest that painful TMD may result, at least in part, from an impairment in central pain regulatory systems that are influenced by resting arterial blood pressure.

Adult↗

Ischemic but not thermal pain sensitivity varies across the menstrual cycle.

OBJECTIVE AND METHOD: Findings from both animal and human research suggest that pain sensitivity changes across the menstrual cycle; however, among humans the nature of these menstrual cycle effects remains unclear. The present study used a repeated-measures design to evaluate changes in thermal and ischemic pain responses during three phases of the menstrual cycle, midfollicular (postmenstrual), ovulatory, and mid-to-late luteal (premenstrual), in 11 healthy women. The cycle phase during which subjects began their participation was determined randomly. Plasma levels of estrogen, progesterone, luteinizing hormone (LH), testosterone, and beta-endorphin were determined at each experimental session. Participants also completed a daily diary of physical and emotional symptoms for two complete menstrual cycles before the experimental sessions. RESULTS: The results indicated that women showed less ischemic pain sensitivity during the midfollicular compared with the ovulatory and mid-to-late luteal phases, but thermal pain responses did not vary significantly across menstrual cycle phases. Physical and emotional symptoms were minimal and did not change significantly across the menstrual cycle. CONCLUSIONS: These findings indicate greater ischemic but not thermal pain sensitivity among women after the midcycle LH surge. The practical relevance and potential mechanisms of these findings are discussed.

Adult↗

Blood pressure-related hypoalgesia in bulimia nervosa.

OBJECTIVE: This study examined pain sensitivity and its relationship to arterial blood pressure in bulimia nervosa (BN). METHODS: Fourteen women who met Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, criteria for BN, purging subtype, and 14 controls were tested for ischemic pain sensitivity after an extended baseline period. Blood pressure, cardiac output, stroke volume, and total peripheral resistance were assessed during baseline, during ischemic pain testing, and at the point of voluntary tolerance. RESULTS: Women with BN had significantly greater ischemic pain tolerance than controls. Additionally, only for BN women was blood pressure related to pain sensitivity. Systolic blood pressure during the pain procedure and at the point of tolerance was positively related to pain threshold and tolerance times and negatively related to rated unpleasantness of pain in BN, whereas no relationships involving blood pressure and pain sensitivity were observed in controls. CONCLUSIONS: These results may have implications for maladaptive changes in central pain-cardiovascular regulatory systems for women with BN.

Adult↗

Race and sex differences in cutaneous pain perception.

OBJECTIVE: The purpose of this study was to determine race and sex differences in cutaneous pain perception. METHODS: Pain perception was measured using a suprathreshold evaluation of pain intensity and pain unpleasantness to a series of thermal stimuli in 27 whites (14 men and 13 women) and 24 African Americans (12 men and 12 women). Blood pressure, depressive symptoms, anxiety state levels, and negative mood were assessed before pain testing to examine whether they might account for any sex or race differences in pain perception that emerged. RESULTS: African Americans rated the stimuli as more unpleasant and showed a tendency to rate it as more intense than whites. Women showed a tendency to rate the stimuli as more unpleasant and more intense than men. In addition, systolic blood pressure was inversely related to pain intensity. After statistically adjusting for systolic blood pressure, sex differences in pain unpleasantness were reduced and sex differences in pain intensity were abolished; race differences were unaltered. CONCLUSIONS: These differences in pain perception may be associated with different pain mechanisms: in the ease of sex, differences in opioid activity and baroreceptor-regulated pain systems; in the case of race, unmeasured psychological characteristics are suggested by the larger differences in ratings of pain unpleasantness than pain intensity.

Adult↗

Pharmacological comparison of isolated monkey and dog cerebral arteries.

Pharmacological differences between canine and monkey basilar arteries were studied in vitro. The constrictor response of canine basilar artery to either norepinephrine or an alpha 1-adrenoceptor agonist phenylephrine was partly inhibited by an alpha 2-adrenoceptor antagonist yohimbine but not by an alpha 1-adrenoceptor antagonist prazosin. The contraction elicited by an alpha 2-adrenoceptor agonist clonidine was inhibited by neither prazosin nor yohimbine. These results suggest that the receptors in canine basilar artery which mediate norepinephrine-induced contraction are different from classical alpha 1 or alpha 2-adrenoceptors, although they more closely resemble the alpha 2- rather than the alpha 1-subtype. Using monkey basilar artery, phenylephrine produced the same amplitude of maximum contractile response as norepinephrine, though a much higher concentration of phenylephrine than norepinephrine was needed in order to elicit that maximum response. Clonidine did not elicit contractions. The contraction induced by norepinephrine was markedly suppressed by both prazosin and yohimbine in a noncompetitive fashion. The constrictor response of monkey basilar artery to norepinephrine, therefore, appears to be mediated by alpha 1-like adrenoceptors. Comparison of ED50 values for thromboxane A2 revealed that the monkey basilar artery was more sensitive to thromboxane A2 than that of the canine. Prostaglandin F2 alpha produced a larger maximum contraction in monkey basilar arteries than in canine basilar arteries, although the ED50 values for monkey basilar arteries were larger than those for canine basilar arteries. The ED50 values for serotonin in canine basilar arteries were a little less than those for monkey basilar arteries, although both arteries produced nearly identical maximum contractions.

Adrenergic alpha-Agonists↗

Enlarged parietal foramina: MR imaging features in the fetus and neonate.

Enlarged parietal foramina are believed to be benign and familial and due to a variable degree of defective intramembranous ossification of the parietal bones. We report 2 patients with this condition in whom fetal and neonatal MR imaging studies illustrate the antenatal and perinatal evolution of this condition and the associated persistence of a falcine sinus. We discuss its relationship to the spectrum of cephalocoeles.

Female↗