scholarly journals Vagosympathetic imbalance induced thyroiditis following subarachnoid hemorrhage: a preliminary study

2020 ◽  
Vol 8 (1) ◽  
pp. 17-17
Author(s):  
Ozgur Caglar ◽  
Erdem Karadeniz ◽  
Irem Ates ◽  
Sevilay Ozmen ◽  
Mehmet Dumlu Aydin

Introduction: This preliminary study evaluates the possible responsibility of ischemia-induced vagosympathetic imbalances following subarachnoid hemorrhage (SAH), for the onset of autoimmune thyroiditis. Methods: Twenty-two rabbits were chosen from our former experimental animals, five of which were picked from healthy rabbits as control (nG-I=5). Sham group (nG-II=5) and animals with thyroid pathologies (nG-III=12) were also included after a one-month-long experimental SAH follow-up. Thyroid hormone levels were measured weekly, and animals were decapitated. Thyroid glands, superior cervical ganglia, and intracranial parts of vagal nerve sections obtained from our tissue archives were reexamined with routine/immunohistochemical methods. Thyroid hormone levels, hormone-filled total follicle volumes (TFVs) per cubic millimeter, degenerated neuron density (DND) of vagal nuclei and neuron density of superior cervical ganglia were measured and statistically compared. Results: The mean neuron density of both superior cervical ganglia was estimated as 8230±983/ mm3 in study group animals with severe thyroiditis, 7496±787/mm3 in the sham group and 6416±510/mm3 in animals with normal thyroid glands. In control group (group I), T3 was 107±11 μg/dL, T4: 1,43±0.32 μg/dL and TSH <0.5, while mean TFV was 43%/mm3 and DND of vagal nuclei was 3±1/mm3. In sham group (group II), T3 was 96±11 μg/dL, T4: 1.21±0.9 μg/ dL and TSH>0.5 while TFV was 38%/mm3 and DND of vagal nuclei was 13±4. In study group, T3 was 54±8 μg/dL, T4: 1,07±0.3 μg/dL and TSH >0.5, while TFV was 27%/mm3 and DND of vagal nuclei was 42±9/mm3. Conclusion: Sympathovagal imbalance characterized by relative sympathetic hyperactivity based on vagal insufficiency should be considered as a new causative agent for hypothyroidism.

2019 ◽  
Vol 80 (06) ◽  
pp. 430-440 ◽  
Author(s):  
Huseyin Findik ◽  
Ayhan Kanat ◽  
Mehmet Dumlu Aydin ◽  
Murteza Cakir ◽  
Sevilay Akalp Ozmen ◽  
...  

Abstract Background The pterygopalatine ganglion (PPG) and ophthalmic arteries (OpAs) have important roles in ocular autoregulation and retinal and visual functions. The relationship between PPG neuron density, OpA vasospasm, and retinal detachment in subarachnoid hemorrhage (SAH) has never been studied. Methods This study was conducted on 25 rabbits. Five animals were in the control group (GI; n = 5), five in the sham group (GII; n = 5), and 15 in the study group (GIII; n = 15). After injection of 1 cc serum saline into the cisterna magna in the sham group, and autologous blood in the SAH group, the animals were followed for 3 weeks. All animals underwent a retinal examination five times a week for 3 weeks before and after the experiment. After the experiment, the neuron density of PPGs of the facial nerves, vasospasm index (VSI) of OpAs, and total basal surface values of the detached retinal parts (DRPs) were calculated. Results In the funduscopic examination, intravitreous hemorrhage ( Terson's syndrome) was detected in four animals in the SAH group. In the control groups, neuron density was 12,000 ± 1,240/mm3, VSI = 0.345 ± 0.076, and DRP = 0 to 1.5 mm2. Mean neuron density was 9,450 ± 940/mm3, VSI = 1.645 ± 0.940, and DRP = 6.23 ± 1.61 mm2 in the sham group (p < 0.05). Neuron density was 6,890 ± 932/mm3, VSI = 2.92 ± 0.97, and DRP = 9.43 ± 2.54 mm2 in SAH group. Conclusion Mean neuron density, VSI of OpAs, and DRP values differed statistically significant between the SAH group and other groups (p < 0.005). There is an inverse relationship between PPG neurons and DRP. However, a direct relationship was observed between the mean VSI and DRP values.


2017 ◽  
Vol 79 (04) ◽  
pp. 302-308 ◽  
Author(s):  
Cengiz Ozturk ◽  
Nuriye Ozdemir ◽  
Mehmet Aydin ◽  
Huseyin Findik ◽  
Nazan Aydin ◽  
...  

Background and Study Aim  Basic neurophysiologic principles of the light reflex are well known. However, the effects of degenerated axon densities of oculomotor nerves (OMNs) secondary to posterior communicating artery (PComA) vasospasm following subarachnoid hemorrhage (SAH) have not been investigated. Our aim was to study this subject. Methods This study was conducted on 19 rabbits. There was a control group of five animals, a sham group of five animals in which saline was injected into the cisterna magna and a study group of nine animals in which homologous blood was injected into the cisterna magna. Pupillary diameters were measured for 1 week, then the animals were decapitated. The normal and degenerated axon densities of the OMNs were examined by stereological methods. Vasospasm indexes (VSIs) of posterior communicating arteries (PComAs) supplying OMNs were estimated and analyzed statistically. Results The pupillary diameter was 5.439 ± 368 µm, and the mean axon density of the OMNs was 0.924 ± 324/mm3 in the control group. The pupillary diameter and degenerated axon density of the OMNs in animals of the sham group were 6.980 ± 0.370 µm and 36 ± 8/mm3, respectively. The pupillary diameter was 9.942 ± 653 µm, and degenerated axon density of the OMNs was 265 ± 57/mm3 in animals with SAH. The mean VSI values of PComAs were 0.927 ± 0.224 in the control group, 1.542 ± 0.257 in the sham group, and 2.321 ± 0.324 in the SAH group. Conclusion We found a linear relationship between the axon density of the OMNs and pupillary diameters. High degenerated neuron density in the OMNs may be responsible for an unresponsive pupillary that has not been mentioned in the literature.


2015 ◽  
Vol 16 (2) ◽  
pp. 78
Author(s):  
Umit Kervan ◽  
Anil Ozen ◽  
Utku Unal ◽  
Irfan Tasoglu ◽  
Mahmut Mustafa Ulas ◽  
...  

<p><b>Objective:</b> The aim of this study was to examine the effects of positive inotropic drugs, including adrenaline, dopamine, and dobutamine on thyroid hormone levels following open heart surgery.</p><p><b>Methods:</b> We analyzed free thyroid hormones (FT3 and FT4) and thyroid-stimulating hormones (TSH) in 200 consecutive patients undergoing open heart surgery. Patients were divided into 5 groups according to the inotropic drug administration as follows: Group A (n = 46) received dopamine alone; Group B (n = 40), dopamine and dobutamine; Group C (n = 36), dopamine, dobutamine, and adrenaline; Group D (n = 32), adrenaline alone; and Group E (n = 46), placebo. Procedural factors affecting thyroid hormones were recorded and included cardiopulmonary bypass (CPB) time, cross-clamping time, degree of hypothermia, and the duration and doses of positive inotropic drugs. Blood samples for hormone assays were collected before initiation of inotropic drug therapy (baseline) and postoperatively at 24, 72, and 120 hours after drug therapy.</p><p><b>Results:</b> FT3, FT4, and TSH levels at baseline were similar in all groups. Although there was a trend showing very slight increases in thyroid hormone levels from baseline to the 24th, 72nd, and 120th postoperative hours after drug therapy, these changes were not significant, and there were also no significant differences between the groups. There was also no significant statistical difference in CPB time, cross-clamping time, degree of hypothermia, and duration and doses of positive inotropic drugs between groups.</p><p><b>Conclusion:</b> Although thyroid hormone levels were affected by positive inotropic drug usage after open heart surgery, this effect was not significant and thyroid hormone levels remained within normal ranges.</p>


1980 ◽  
Vol 95 (4) ◽  
pp. 472-478 ◽  
Author(s):  
A. Eugene Pekary ◽  
Jerome M. Hershman ◽  
Clark T. Sawin

Abstract. Basal serum TSH and the peak TSH response to a 500 μg TRH bolus were measured in 57 euthyroid and in 29 hypothyroid subjects either receiving graded thyroid hormone replacement or acutely removed from full replacement therapy. Serum TSH, total T4 and T3 were determined by sensitive radioimmunoassay methods. The peak versus basal TSH data for hypothyroid patients were linear within individuals. The regression slope of the peak versus basal TSH data for all hypothyroid subjects did not differ significantly from the corresponding slope for all euthyroid subjects. Basal and peak TSH versus T3 and T4 data for hypothyroid patients were also linear within each individual. Moreover, the regression of the basal TSH values averaged over the non-replacement to full replacement state against the TSH versus T3 slope had a significant negative correlation. This trend leads to an array of regression lines which average to the familiar hyperbolic relationship between thyrotrophin and thyroid hormone levels in man.


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