Physiological mechanisms of temperature biofeedback.

Research on the physiological mechanisms of finger temperature biofeedback with normal subjects and Raynaud's disease patients is reviewed. Studies conducted in the author's laboratory have shown that feedback-induced vasodilation is mediated through a non-neural, beta-adrenergic mechanism rather than through reductions in sympathetic nervous system activation. In contrast, feedback-induced vasoconstriction is mediated through the traditional, sympathetic nervous pathway. When used with primary Raynaud's disease patients, feedback-induced vasodilation has achieved reductions in reported symptom frequency ranging from 66% to 92% in controlled investigations. Future research directions are discussed.     

Physiological mechanism of digital vasoconstriction training

Recent work in our laboratory has shown that vasodilation produced during temperature biofeedback training is mediated through a nonneural, beta-adrenergic mechanism. Here we sought to determine if the effects of feedback training for vasoconstriction are produced through a neural or nonneural pathway and whether other measures of physiological activity are correlated with these changes. Nine normal subjects received temperature feedback vasoconstriction training in which feedback was delivered only during periods of successful performance. In a subsequent session, the nerves to one finger were blocked with a local anesthetic while finger blood flow was recorded from this and other fingers. Vasoconstriction occurred during feedback in the intact fingers but not in the nerve-blocked finger and was accompanied by increased skin conductance and heart rate. These data demonstrate that temperature feedback vasoconstriction training is mediated through an efferent, sympathetic nervous pathway. In contrast, temperature feedback vasodilation training is mediated through a nonneural, beta-adrenergic mechanism.This work was supported by research grant HL-30604 from the National Heart, Lung, and Blood Institute.     

Plasma catecholamine levels during temperature biofeedback training in normal subjects

Thirty-nine normal volunteers of both sexes were randomly assigned to receive 8 sessions of temperature biofeedback or autogenic training to increase finger temperature. Temperature biofeedback subjects produced significant elevations in finger temperature during training, whereas those who received autogenic training did not. Temperature feedback subjects had significantly higher heart rates and diastolic blood pressures during training compared to autogenic subjects. There were no significant changes or group differences in plasma catecholamine levels. These data do not support the hypothesis that feedback-induced vasodilation is accompanied by decreased sympathetic activation in normal populations, when only temperature biofeedback is employed.Supported by research grant No. HL-30604 from NHLBI. Dr. Angela McGuady served as Action Editor for this paper.     

Training to vasodilate in a cooling environment: A valid treatment for Raynaud's phenomenon?

While many reports indicate that voluntary modification of skin temperature is possible and may be useful in the treatment of Raynaud's phenomenon, little attention has been paid to the ecological validity of training skin temperature increases when a considerable amount of vasodilation of digital vessels may already exist (room temperature, 22–24° C). Patients with Raynaud's vasospastic attacks may benefit from learning to avoid attacks when they are impending by voluntarily vasodilating the vessels of their digits under conditions when vasoconstriction has begun. The results in 14 patients with primary and secondary Raynaud's phenomenon indicated that (a) patients learned to voluntarily increase digital skin temperatures in a cooling environment during documented vasoconstriction, and (b) there was a 31% decrease in the occurrence of vasospastic attacks following such learning. These data suggest that a new methodology may be useful in the biofeedback treatment of Raynaud's phenomenon, but further research is needed to determine the specific mechanism(s) involved, and the limits to its usefulness.This research was supported by grants from the Manitoba Heart and St. Boniface General Hospital Research Foundations. We gratefully acknowledge John Arnett, Garry Hawryluk, and Charles Weinstein for their critical reading of a draft of this paper. Portions of this paper were presented at the Canadian Psychological Association meeting, Winnipeg, 1983.     

Skin temperature biofeedback for Raynaud's disease: A double-blind study

The lack of control procedures inherent in most of the experiments conducted to assess the effectiveness of skin temperature biofeedback in the treatment of Raynaud's disease renders the results inconclusive. In this study, control groups and a double-blind approach are adopted. Thirty-six patients, carefully screened for a diagnosis of primary Raynaud's disease, were assigned to a skin temperature increase group (N=12), to an EMG relaxation control group (N=12), or to a notreatment control group (N=12). All patients kept records of their symptoms for the duration of the study. Each subject in the two training groups received 20 sessions, the last 2 conducted under cold stress. Data analysis according to original group assignment, as well as following regrouping of subjects according to several learning criteria, showed that while all patients reported a marked decrease in the number of vasospastic attacks, no significant differences were found among the three groups on the clinical measures used to assess symptomatic relief. The general improvement reported must therefore be attributed to nonspecific factors.This study was supported in part by Rehabilitation Services Administration Grant No. 16-P-56810/5–17 to the University of Minnesota Medical Rehabilitation Research and Training Center. We are grateful to Gail Gaebe, Carla Grossman, Steve Janousek, Linda Rubbelke, and Scott Williamson, who served as blind assistants, and to Steve Sheffield for his technical support.     

Physiological mechanism of digital vasoconstriction training

Recent work in our laboratory has shown that vasodilation produced during temperature biofeedback training is mediated through a nonneural, beta-adrenergic mechanism. Here we sought to determine if the effects of feedback training for vasoconstriction are produced through a neural or nonneural pathway and whether other measures of physiological activity are correlated with these changes. Nine normal subjects received temperature feedback vasoconstriction training in which feedback was delivered only during periods of successful performance. In a subsequent session, the nerves to one finger were blocked with a local anesthetic while finger blood flow was recorded from this and other fingers. Vasoconstriction occurred during feedback in the intact fingers but not in the nerve-blocked finger and was accompanied by increased skin conductance and heart rate. These data demonstrate that temperature feedback vasoconstriction training is mediated through an efferent, sympathetic nervous pathway. In contrast, temperature feedback vasodilation training is mediated through a nonneural, beta-adrenergic mechanism.     

Training to vasodilate in a cooling environment: a valid treatment for Raynaud's phenomenon?

While many reports indicate that voluntary modification of skin temperature is possible and may be useful in the treatment of Raynaud's phenomenon, little attention has been paid to the ecological validity of training skin temperature increases when a considerable amount of vasodilation of digital vessels may already exist (room temperature, 22-24 degrees C). Patients with Raynaud's vasospastic attacks may benefit from learning to avoid attacks when they are impending by voluntarily vasodilating the vessels of their digits under conditions when vasoconstriction has begun. The results in 14 patients with primary and secondary Raynaud's phenomenon indicated that (a) patients learned to voluntarily increase digital skin temperatures in a "cooling" environment during documented vasoconstriction, and (b) there was a 31% decrease in the occurrence of vasospastic attacks following such learning. These data suggest that a new methodology may be useful in the biofeedback treatment of Raynaud's phenomenon, but further research is needed to determine the specific mechanism(s) involved, and the limits to its usefulness.     

Brain Areas Controlling Heart Rate Variability in Tinnitus and Tinnitus-Related Distress

Background

Tinnitus is defined as an intrinsic sound perception that cannot be attributed to an external sound source. Distress in tinnitus patients is related to increased beta activity in the dorsal part of the anterior cingulate and the amount of distress correlates with network activity consisting of the amygdala-anterior cingulate cortex-insula-parahippocampus. Previous research also revealed that distress is associated to a higher sympathetic (OS) tone in tinnitus patients and tinnitus suppression to increased parasympathetic (PS) tone.

Methodology

The aim of the present study is to investigate the relationship between tinnitus distress and the autonomic nervous system and find out which cortical areas are involved in the autonomic nervous system influences in tinnitus distress by the use of source localized resting state electroencephalogram (EEG) recordings and electrocardiogram (ECG). Twenty-one tinnitus patients were included in this study.

Conclusions

The results indicate that the dorsal and subgenual anterior cingulate, as well as the left and right insula are important in the central control of heart rate variability in tinnitus patients. Whereas the sympathovagal balance is controlled by the subgenual and pregenual anterior cingulate cortex, the right insula controls sympathetic activity and the left insula the parasympathetic activity. The perceived distress in tinnitus patients seems to be sympathetically mediated.     

Hemodynamic effects of calcitonin gene-related peptide in conscious rats

The cardiovascular effects of calcitonin gene-related peptide (CGRP) were examined in conscious, unrestrained rats. Changes in mean arterial pressure, heart rate and cardiac output were continuously monitored before and after i.v. bolus injection of CGRP (0.1-5 micrograms/kg). Injection of the peptide caused dose-dependent reductions in mean arterial pressure (-24 +/- 4 mmHg), which were accompanied by marked tachycardia. Cardiac output was significantly increased after CGRP but little change was observed in stroke volume. CGRP also reduced total peripheral resistance (-46 +/- 6%). These data indicate that the hypotensive actions of CGRP are mediated through peripheral vasodilation rather than through reductions in cardiac output. Pretreatment with propranolol significantly reduced the tachycardia responses to CGRP from 81 +/- 11 beats/min to 36 +/- 4 beats/min, but did not abolish the increase in heart rate. These data suggest that CGRP produces a tachycardia through reflex increases in cardiac sympathetic tone and through possible direct positive chronotropic effects on the heart.     

Inhibition of Neuronal Apoptosis and Axonal Regression Ameliorates Sympathetic Atrophy and Hemodynamic Alterations in Portal Hypertensive Rats

Background and Aim

A neuronal pathway participates in the development of portal hypertension: blockade of afferent sensory nerves in portal vein ligated (PVL) rats simultaneously prevents brain cardiovascular regularory nuclei activation, neuromodulator overexpression in superior mesenteric ganglia, sympathetic atrophy of mesenteric innervation and hemodynamic alterations. Here we investigated in PVL rats alterations in neuromodulators and signaling pathways leading to axonal regression or apoptosis in the superior mesenteric ganglia and tested the effects of the stimulation of neuronal proliferation/survival by using a tyrosine kinase receptor A agonist, gambogic amide.

Results

The neuronal pathway was confirmed by an increased neuronal afferent activity at the vagal nodose ganglia and the presence of semaphorin3A in sympathetic pre-ganglionic neurons at the intermediolateral nucleus of the spinal cord of PVL rats. Expression of the active form of tyrosine kinase receptor A (phosphorylated), leading to proliferation and survival signaling, showed a significant reduction in PVL comparing to sham rats. In contrast, the apoptotic and axonal retraction pathways were stimulated in PVL, demonstrated by a significant overexpression of semaphorin 3A and its receptor neuropilin1, together with increases of cleaved caspase7, inactive poly(ADP-ribose) polymerase and Rho kinase expression. Finally, the administration of gambogic amide in PVL rats showed an amelioration of hemodynamic alterations and sympathetic atrophy, through the activation of survival pathways together with the inhibition of apoptotic cascades and Rho kinase mediated axonal regression.

Conclusion

The adrenergic alteration and sympathetic atrophy in mesenteric vessels during portal hypertension is caused by alterations on neuromodulation leading to post-ganglionic sympathetic regression and apoptosis and contributing to splanchnic vasodilation.     

Inflammation,endothelial function and atherosclerosis in rheumatoid arthritis

Different techniques have proven to be useful in determining the presence of subclinical cardiovascular disease in patients with rheumatoid arthritis (RA). Doppler imaging with iontophoresis of acetylcholine and flow-mediated, endothelium-dependent vasodilation give information on endothelial dysfunction, an early step in the atherogenesis process. However, there is no good correlation between these two surrogate markers of cardiovascular disease in RA. A single determination of routine laboratory markers of inflammation does not seem to relate to endothelial function in RA. Further research is needed to determine whether microvascular endothelial function is a better predictor of cardiovascular outcome than macrovascular endothelial function in patients with RA.Endothelial dysfunction is an early step in the atherogenesis process of rheumatoid arthritis (RA). In the previous issue of Arthritis Research & Therapy, Sandoo and colleagues [1] reported a cross-sectional study performed on 99 unselected patients with RA to determine the presence of microvascular and macrovascular endothelial function in parallel with disease activity, individual cardiovascular (CV) disease risk factors, and global CV disease. The authors also longitudinally studied 23 patients who had RA and who started on anti-tumor necrosis factor-alpha (anti-TNFα) therapy [1]. In the cross-sectional study, markers of RA-related inflammation were not associated with microvascular or macrovascular endothelium-dependent function, and global CV disease risk inversely correlated with microvascular endothelium dependent function. In the longitudinal study, only microvascular endothelium-dependent function showed an improvement following 2 weeks of anti-TNFα treatment in comparison with baseline, but no association between change in endothelial function and change in inflammatory markers was evident. Considering these results, the authors concluded that classic CV disease risk may influence endothelial function more than disease-related markers of inflammation in RA. They stated that classic CV disease risk factors and anti-TNFα medication have different effects on microvascular and macrovascular endothelial function [1].This interesting study raises a series of points that deserve to be addressed. First, endothelial dysfunction in RA is the result of a complex effect mediated by classic CV risk factors, genetic predisposition, chronic inflammation, pro-oxidative stress, a prothrombotic status, and metabolic abnormalities (such as insulin resistance or dyslipidemia) that to a greater or lesser extent may influence the development of this systemic pathological state [2]. The results reported by Sandoo and colleagues suggest that systemic markers of inflammation - erythrocyte sedimentation rate, C-reactive protein (CRP), and disease activity score using 28 joint counts (DAS28) - and disease duration do not relate to endothelial function in microvascular and macrovascular vascular beds [1]. With respect to this, we feel that a single determination of routine laboratory markers of inflammation may not be useful to provide accurate information on the whole atherosclerotic burden associated with this chronic disease. In this regard, when we conducted a study to assess the association between inflammation measured by CRP values and carotid intima-media thickness (IMT)(another surrogate marker of CV disease) [3], we could not find a correlation between CRP at the time of disease diagnosis or at the time of the ultrasound study and the carotid IMT [4]. Nevertheless, the magnitude and chronicity of the inflammatory response measured by the average CRP values in patients with at least 5 years'' disease duration correlated directly with the presence of atherosclerosis determined by carotid IMT [4]. Therefore, considering the results observed using carotid IMT, we think that an overall assessment of the values of biomarkers of inflammation over a prolonged period of time (that is, the mean value of CRP over at least 5 years'' time), rather than a single determination of these biomarkers, might yield more useful information on the implication of these biomarkers of inflammation in the assessment of endothelial dysfunction of patients with RA.Another important result derived from the study [1] was the poor correlation between different surrogate markers of atherosclerosis. This result is expected given that, in a study we conducted to determine whether a correlation between flow-mediated, endothelium-dependent macrovascular vasodilation and carotid IMT values exists, a correlation between these two surrogate markers of atherosclerosis was observed only in RA patients with a long disease duration (more than 7 years) [5]. Therefore, different techniques may provide information on different stages of the atherosclerotic disease [3]. Unlike laser Doppler imaging with iontophoresis of acetylcholine or flow-mediated, endothelium-dependent vasodilation (which give functional information on endothelial function), carotid ultrasound allows the identification of structural morphological damage that was reported to predict CV events in RA [6,7].An unexpected result from the study by Sandoo and colleagues [1] was the absence of change of flow-mediated, macrovascular, endothelial-dependent function in response to 3 months of anti-TNFα treatment. This finding is in contrast to that of previous reports [8-10]. The authors'' explanation of a better baseline macrovascular endothelial-dependent function in their cohort compared with previous series of RA patients undergoing anti-TNFα therapy may be plausible, as treatment with anti-TNFα may have less impact in RA patients who have an endothelial function similar to that of healthy individuals.Finally, the authors highlight the importance of assessing endothelial function in more than one vascular bed. This conclusion is based on the observations that micro-vascular, but not macrovascular, endothelium-dependent function was associated with global CV disease risk algorithms and that only microvascular endothelium dependent function changed following treatment with anti-TNFα [1]. At this point, replication of these observations by other investigators would be of great help to shed light on this matter.Whether classic CV risk factors are more important than chronic inflammation to establish endothelial dysfunction in RA is, at this point, rather speculative. We feel that, as previously pointed out by Kitas and Gabriel [11], classic CV risk factors are important but not sufficient to explain all of the CV excess risk found in RA. We feel that additional research is needed to determine whether microvascular endothelial function is a better predictor of CV outcome than macrovascular endothelial function in patients with RA.     

Examining the impact of health research facilitated by small peer-reviewed research operating grants in a women's and children's health centre

Background

There has been limited research on the impact of research funding for small, institutional grants. The IWK Health Centre, a children and women's hospital in Maritime Canada, provides small amounts (up to $15,000) of research funding for staff and trainees at all levels of experience through its Research Operating Grants. These grants are rigorously peer-reviewed. To evaluate the impact of these grants, an assessment was completed of several different areas of impact.

Findings

An online questionnaire was sent to 64 Principal Investigators and Co-Investigators from Research Operating Grants awarded from 2004 to 2006. The questionnaire was designed to assess five areas of potential impact: (1) research, (2) policy, (3) practice, (4) society and (5) personal. Research impact reported by participants included publications (72%), presentations (82%) and knowledge transfer beyond the traditional formats (51%). Practice impact was reported by 67% of participants, policy impact by 15% and societal impact by 18%. All participants reported personal impact.

Conclusions

Small research grants yield similar impacts to relatively large research grants. Regardless of the total amount of research funds awarded, rigorously peer-reviewed research projects have the potential for significant impact at the level of knowledge transfer and changes in clinical practice and policy. Additional findings in the present research indicate that small awards have the potential to have significant impact on the individual grant holder across a variety of capacity building variables. These personal impacts are particularly noteworthy in the context of developing the research programs of novice researchers.

     

An individual with “Miyada”-like hemoglobin indistinguishable from hemoglobin A2

The hemoglobin of a 24-year-old man of Italian descent who has the phenotypic characteristics of thalassemia intermedia contains about 12% hemoglobin F, 73% hemoglobin A, and 15% hemoglobin A₂. Chemical analysis definitely identifies the last as hemoglobin A₂. So elevated a percentage of hemoglobin A₂ has not been reported before. In addition, the amount of hemoglobin A is unusually large for an individual with presumed homozygosity for -thalassemia. Although the evidence is indirect, it is suggested that he is heterozygous for two conditions: -thalassemia and a Miyada type of gene that produces a hemoglobin indistinguishable from hemoglobin A₂.The work was supported in part by grants HL-02558 and HL-05168 and Training Grant HD-00048 from the National Institutes of Health, U.S. Public Health Service, as well as funds from the Southern California Chapter of the Cooley's Anemia Blood and Research Foundation.     

Neurotransmitter Release Mechanisms in Sympathetic Neurons: Past,Present, and Future Perspectives

In 1969, Paton and Vizi (1) described the inhibitory actions of noradrenaline on acetylcholine release from the innervation of the guinea-pig ileum longitudinal muscle. They concluded that acetylcholine output by the nervous networks of the longitudinal strip is under the normal control of the sympathetic by a species of presynaptic inhibition mediated by receptors. This work was carried out in the Pharmacology Department at Oxford University. Clearly, a period in the Dreaming Spires of Oxford sufficiently inspired Sylvester to take up a life long career in scientific research. He has published more than 300 papers on a wide range of topics but clearly has a strong interest in neurotransmitter release mechanisms and recently, non-synaptic interactions between neurons. It seems fitting therefore to write a brief review on the continuing studies on neurotransmitter release mechanisms in sympathetic neurons in a volume honoring the now distinguished Professor Vizi.     

The behavioral treatment of Raynaud's disease: A review

Raynaud's disease is a peripheral vascular system disorder characterized by episodes of vasoconstriction in the hands and feet resulting in a lowering of skin temperature and pain. Recent studies are reviewed that focus on the behavioral treatment of Raynaud's disease—in particular, biofeedback and autogenic training. Methodological problems and other difficulties include the measurement of skin temperature, schedules of reinforcement/feedback, and characteristics of the experimenter and subject. Studies in this area indicate some promise for certain behavioral interventions, especially finger temperature biofeedback under cold stress conditions. On the other hand, further research is needed to clarify the mechanisms, especially that of vasodilation, and the applications of temperature biofeedback, as well as the role of attitudinal, interpersonal, and cognitive factors.     

Biobehavioral treatment of essential hypertension: A group outcome study

In a group outcome and follow-up study of 77 patients with essential hypertension, significant reductions were seen in systolic and diastolic blood pressure (BP) and in hypotensive medication requirement. A multimodality biobehavioral treatment was used which included biofeedback-assisted training techniques aimed at teaching self-regulation of vasodilation in the hands and feet. Of the 54 medicated patients, 58% were able to eliminate hypotensive medication while at the same time reducing BP an average of 15/10 mm Hg. An additional 19 (35%) of the medicated patients were able to cut their medications approximately in half while reducing BP by 18/10 mm Hg. The remaining 4 (7%) medicated patients showed no improvement in either BP or medication requirement. Similar reductions in BP were seen in initially unmedicated patients. Seventy percent of the 23 unmedicated patients achieved average pressures below 140/90 mm Hg, with an additional 22% of these patients making clinically significant reductions in pressure without becoming normotensive, and with 8% unsuccessful at lowering pressures to a clinically significant extent. Follow-up data available on 61 patients over an average of 33 months indicated little regression in these results with 51% of the total patient sample remaining well-controlled off medication, an additional 41% partially controlled, and 8% unsuccessful in lowering either medications and/or blood pressures to a clinically significant extent.This research was partially supported by grant HL-32136. The Authors wish to thank Sarah Bremer for her assistance in preparing this article.     

Distribution of ichthyoplankton in the eastern Peter the Great Bay,Sea of Japan,in June and July of 2007

Comparison of the results of ichthyoplankton surveys conducted at 97 stations in the eastern part of the Peter the Great Bay of the Sea of Japan, in June–July 2007 with the similar research data of the 1950s shows that at present, as was the case 50 years ago, flatfish eggs belonging mainly to the yellowfin sole Limanda aspera and brown sole Pleuronectes herzensteini prevail in the local ichthyoplankton (up to 86%). The highest concentrations of these species’ eggs were recorded in the Vostok Bay and Strelok Bay. The spawning activity of flatfish in 2007 is found to be lower than in the mid 1900s, but the significance of the eastern part of the Peter the Great Bay for flatfish reproduction remains large. The importance of long-term monitoring in this area, which is being subjected to steadily growing anthropogenic impacts, is also proven.     

The impact of a 6-year comprehensive community trial on the awareness, treatment and control rates of hypertension in Iran: experiences from the Isfahan healthy heart program

Background

Acute mental stress may contribute to the cardiovascular disease progression via autonomic nervous system controlled negative effects on the endothelium. The joint effects of stress-induced sympathetic or parasympathetic activity and endothelial function on atherosclerosis development have not been investigated. The present study aims to examine the interactive effect of acute mental stress-induced cardiac reactivity/recovery and endothelial function on the prevalence of carotid atherosclerosis.

Methods

Participants were 81 healthy young adults aged 24-39 years. Preclinical atherosclerosis was assessed by carotid intima-media thickness (IMT) and endothelial function was measured as flow-mediated dilatation (FMD) using ultrasound techniques. We also measured heart rate, respiratory sinus arrhythmia (RSA), and pre-ejection period (PEP) in response to the mental arithmetic and speech tasks.

Results

We found a significant interaction of FMD and cardiac RSA recovery for IMT (p = 0.037), and a significant interaction of FMD and PEP recovery for IMT (p = 0.006). Among participants with low FMD, slower PEP recovery was related to higher IMT. Among individuals with high FMD, slow RSA recovery predicted higher IMT. No significant interactions of FMD and cardiac reactivity for IMT were found.

Conclusions

Cardiac recovery plays a role in atherosclerosis development in persons with high and low FMD. The role of sympathetically mediated cardiac activity seems to be more important in those with impaired FMD, and parasympathetically mediated in those with relatively high FMD. The development of endothelial dysfunction may be one possible mechanism linking slow cardiac recovery and atherosclerosis via autonomic nervous system mediated effect.     

Sympathetic nervous dysregulation in the absence of systolic left ventricular dysfunction in a rat model of insulin resistance with hyperglycemia

Background

Diabetes mellitus is strongly associated with cardiovascular dysfunction, derived in part from impairment of sympathetic nervous system signaling. Glucose, insulin, and non-esterified fatty acids are potent stimulants of sympathetic activity and norepinephrine (NE) release. We hypothesized that sustained hyperglycemia in the high fat diet-fed streptozotocin (STZ) rat model of sustained hyperglycemia with insulin resistance would exhibit progressive sympathetic nervous dysfunction in parallel with deteriorating myocardial systolic and/or diastolic function.

Methods

Cardiac sympathetic nervous integrity was investigated in vivo via biodistribution of the positron emission tomography radiotracer and NE analogue [¹¹C]meta-hydroxyephedrine ([¹¹C]HED). Cardiac systolic and diastolic function was evaluated by echocardiography. Plasma and cardiac NE levels and NE reuptake transporter (NET) expression were evaluated as correlative measurements.

Results

The animal model displays insulin resistance, sustained hyperglycemia, and progressive hypoinsulinemia. After 8 weeks of persistent hyperglycemia, there was a significant 13-25% reduction in [¹¹C]HED retention in myocardium of STZ-treated hyperglycemic but not euglycemic rats as compared to controls. There was a parallel 17% reduction in immunoblot density for NE reuptake transporter, a 1.2 fold and 2.5 fold elevation of cardiac and plasma NE respectively, and no change in sympathetic nerve density. No change in ejection fraction or fractional area change was detected by echocardiography. Reduced heart rate, prolonged mitral valve deceleration time, and elevated transmitral early to atrial flow velocity ratio measured by pulse-wave Doppler in hyperglycemic rats suggest diastolic impairment of the left ventricle.

Conclusions

Taken together, these data suggest that sustained hyperglycemia is associated with elevated myocardial NE content and dysregulation of sympathetic nervous system signaling in the absence of systolic impairment.     

Biofeedback treatment of Raynaud's disease and phenomenon

Six Raynaud's disease and four Raynaud's phenomenon patients were treated with 12 sessions of finger temperature biofeedback. The mean frequency of vasospastic attacks was reduced to 7.5% of that reported during the pretreatment baseline and was maintained for a 1 year follow-up period. Significant control of digital temperature was demonstrated during laboratory training sessions. Raynaud's phenomenon patients showed significantly greater temperature increases during feedback periods than Raynaud's disease patients. Correlations between finger temperature and other physiological measures suggested that results could not be attributed to general physical relaxation. The role of imagery in self-control of digital temperature is considered.Portions of this paper were presented at the annual meeting of the Biofeedback Society of America, Albuquerque, March 1978.