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Journal of Pain Research 2024We aimed to assess uterine and arcuate artery Doppler indices in patients with mild primary dysmenorrhea.
PURPOSE
We aimed to assess uterine and arcuate artery Doppler indices in patients with mild primary dysmenorrhea.
PATIENTS AND METHODS
A total of 55 patients were included, consisting of women without dysmenorrhea (n=26, group A) and women with mild primary dysmenorrhea (n=29, group B). Doppler measurements of the uterine and arcuate arteries were performed in both groups on the 1st-2nd days and 21st-24th days (midluteal phase) of the menstrual cycle using transvaginal ultrasound and compared between the groups. The severity of dysmenorrhea was assessed using visual analog scale scores.
RESULTS
Doppler measurements of the uterine and arcuate arteries performed on the 1st-2nd days of the menstrual cycle and the midluteal phase were similar between the groups (p>0.05). There was a significant decrease in the intragroup measurements of uterine and arcuate arteries performed on the first day of menstruation and the luteal phase in both groups (p<0.01).
CONCLUSION
Doppler findings of the uterine and arcuate arteries did not differ between patients with and without mild primary dysmenorrhea. The etiology of primary dysmenorrhea mainly involves ischemia and vasoconstriction, but mild primary dysmenorrhea appears to be associated with a different etiology other than decreased tissue perfusion.
PubMed: 38887385
DOI: 10.2147/JPR.S456239 -
Thyroid Research Jun 2024Primary hypothyroidism (PHT) is associated with an increased risk for the development of atherosclerosis (AS) and other cardiovascular disorders. PHT induces... (Review)
Review
Primary hypothyroidism (PHT) is associated with an increased risk for the development of atherosclerosis (AS) and other cardiovascular disorders. PHT induces atherosclerosis (AS) through the induction of endothelial dysfunction, and insulin resistance (IR). PHT promotes vasoconstriction and the development of hypertension. However, patients with subclinical PHT with normal thyroid hormones (THs) are also at risk for cardiovascular complications. In subclinical PHT, increasing thyroid stimulating hormone (TSH) levels could be one of the causative factors intricate in the progression of cardiovascular complications including AS. Nevertheless, the mechanistic role of PHT in AS has not been fully clarified in relation to increased TSH. Therefore, in this review, we discuss the association between increased TSH and AS, and how increased TSH may be involved in the pathogenesis of AS. In addition, we also discuss how L-thyroxine treatment affects the development of AS.
PubMed: 38880884
DOI: 10.1186/s13044-024-00199-3 -
Fetal Diagnosis and Therapy Jun 2024Reduced middle cerebral artery resistance indices (MCA-RI) in fetuses with spina bifida (fSB) are commonly observed. Compression of neuronal pathways in the brainstem...
INTRODUCTION
Reduced middle cerebral artery resistance indices (MCA-RI) in fetuses with spina bifida (fSB) are commonly observed. Compression of neuronal pathways in the brainstem due to hindbrain herniation (HH) and disturbed cerebrospinal fluid circulation likely cause an imbalance of the autonomic nervous system. This may increase systemic vasoconstriction and compensatory increase cerebral vasodilation (like brain sparing). Aim of this study was to systematically analyze all fetal MCA-RI before and after fSB repair and to compare their correlation with the presence and post-surgical resolution of HH.
METHODS
173 patients were included. Standardized ultrasound examinations including MCA and umbilical artery (UA) Doppler as well as assessment of HH presence and regression were performed. Fetuses with MCA-RI<5th percentile (P.) before fetal surgery were compared to the group with normal MCA-RI and correlated to the presence of HH before and its regression after fSB repair.
RESULTS
30% (49/161) fetuses showed RI's <5thP before fSB repair. All fetuses had normal UA-RI. 99.4% of fetuses (160/161) showed normal of MCA-RI before delivery. Normalization occurred within a mean of 1.3±1.2 weeks. HH regression was observed in 97% in the group with normal MCA-RI and in 96% in the group with MCA-RI <5thP. before surgery (p = 0.59). Time lapse to HH regression after fSB repair was 1.8±1.7 and 1.9±1.6 weeks respectively.
CONCLUSION
In fetuses with MCA-RIs <5.P before fSB repair, a parallel timely course of MCA-RI normalization and HH regression was noted. To suggest common pathogenic factor(s), more studies are needed. However, normalization of the fetal cerebral circulation could be a further benefit of fSB repair.
PubMed: 38880089
DOI: 10.1159/000539773 -
Clinical Autonomic Research : Official... Jun 2024Central and peripheral chemoreceptors are hypersensitized in patients with heart failure with reduced ejection fraction. Whether this autonomic alteration occurs in...
PURPOSE
Central and peripheral chemoreceptors are hypersensitized in patients with heart failure with reduced ejection fraction. Whether this autonomic alteration occurs in patients with heart failure with preserved ejection fraction (HFpEF) remains little known. We test the hypothesis that the central and peripheral chemoreflex control of muscle sympathetic nerve activity (MSNA) is altered in HFpEF.
METHODS
Patients aged 55-80 years with symptoms of heart failure, body mass index ≤ 35 kg/m, left ventricular ejection fraction > 50%, left atrial volume index > 34 mL/m, left ventricular early diastolic filling velocity and early diastolic tissue velocity of mitral annulus ratio (E/e' index) ≥ 13, and BNP levels > 35 pg/mL were included in the study (HFpEF, n = 9). Patients without heart failure with preserved ejection fraction (non-HFpEF, n = 9), aged-paired, were also included in the study. Peripheral chemoreceptors stimulation (10% O and 90% N, with CO titrated) and central chemoreceptors stimulation (7% CO and 93% O) were conducted for 3 min. MSNA was evaluated by microneurography technique, and forearm blood flow (FBF) by venous occlusion plethysmography.
RESULTS
During hypoxia, MSNA responses were greater (p < 0.001) and FBF responses were lower in patients with HFpEF (p = 0.006). Likewise, MSNA responses during hypercapnia were higher (p < 0.001) and forearm vascular conductance (FVC) levels were lower (p = 0.030) in patients with HFpEF.
CONCLUSIONS
Peripheral and central chemoreflex controls of MSNA are hypersensitized in patients with HFpEF, which seems to contribute to the increase in MSNA in these patients. In addition, peripheral and central chemoreceptors stimulation in patients with HFpEF causes muscle vasoconstriction.
PubMed: 38878143
DOI: 10.1007/s10286-024-01041-4 -
Neurointervention Jul 2024Delayed ischemic stroke associated with intractable vasospasm after clipping of unruptured intracranial aneurysms (UIAs) has been rarely reported. We report a patient...
Delayed ischemic stroke associated with intractable vasospasm after clipping of unruptured intracranial aneurysms (UIAs) has been rarely reported. We report a patient with delayed ischemic stroke associated with intractable vasospasm following UIA clipping. A middle-aged female underwent surgery for unruptured middle cerebral artery bifurcation aneurysms. The patient tolerated the neurosurgical procedure well. Seven days postoperatively, the headache was unbearable; a postcraniotomy headache persisted and abruptly presented with global aphasia and right-sided hemiplegia after a nap. Emergency digital subtraction angiography showed severe luminal narrowing with segmental vasoconstriction, consistent with severe vasospasm. The patient's neurological deficit improved after chemical angioplasty. Neurosurgeons should pay close attention to this treatable/preventive entity after neurological deterioration following UIA clipping, even in patients without subarachnoid hemorrhage.
PubMed: 38871004
DOI: 10.5469/neuroint.2024.00150 -
Revue Medicale de Liege Jun 2024Contrast-induced nephropathy (CIN) is a renal complication occurring after the administration of iodinated contrast agents routinely used in medical imaging. CIN causes... (Review)
Review
Contrast-induced nephropathy (CIN) is a renal complication occurring after the administration of iodinated contrast agents routinely used in medical imaging. CIN causes acute renal failure of varying severity. The pathophysiology of CIN is probably multifactorial: it involves (i) renal vasoconstriction inducing tissue hypoxia, and (ii) a possible direct toxicity of iodine derivatives leading to tubular inflammation and necrosis. Several risk factors are associated with CIN, some related to the procedure itself, others to the patient's co-morbid profile. In particular, the pre-existence of chronic renal failure, dehydration, congestive heart failure, diabetes or hypotension has been associated with an increased risk of CIN, as summarized in the Mehran score. Prevention of CIN relies essentially on adequate i.v. hydration before and after the procedure, and on the administration of the lowest possible volumes of contrast. In patients at high risk of CIN, the use of metformin and non-steroidal anti-inflammatory drugs is contraindicated at the time of contrast medium i.v. injection. In these patients, renal function assessment after 3-7 days post imaging is required.
Topics: Humans; Contrast Media; Kidney Diseases; Risk Factors; Acute Kidney Injury
PubMed: 38869133
DOI: No ID Found -
Journal of Neurophysiology Jun 2024Fentanyl is the leading contributor to drug overdose deaths in the US. Its potency, rapid onset of action, and lack of effective reversal treatment make the drug more...
Fentanyl is the leading contributor to drug overdose deaths in the US. Its potency, rapid onset of action, and lack of effective reversal treatment make the drug more lethal than other opioids. Although it is understood that fentanyl is dangerous at higher doses, literature surrounding fentanyl's physiological effects remains contradictory at lower doses. To explore this discrepancy, we designed a study incorporating electrochemical assessment of oxygen in the brain (nucleus accumbens; NAc) and subcutaneous (SC) space, multi-site thermorecording (brain, skin, muscle), and locomotor activity at varying doses of fentanyl (1.0, 3.0, 10, 30, 90 µg/kg) in rats. In the NAc, lower doses of fentanyl (3.0, 10 µg/kg) led to an increase in oxygen levels while higher doses (30, 90 µg/kg) led to a biphasic pattern, with initial dose-dependent decrease followed by increase. In the SC space, oxygen decreases started to appear at relatively lower doses (>3 µg/kg), had shorter onset latencies, and were stronger and prolonged. In the temperature experiment, lower doses of fentanyl (1.0, 3.0, 10 µg/kg) led to an increase in brain, skin, and muscle temperatures, while higher doses (30 and 90 µg/kg) resulted in a dose-dependent biphasic temperature change, with an increase followed by a prolonged decrease. We also compared oxygen and temperature responses induced by fentanyl over six consecutive days and found no evidence of tolerance in both parameters. In conclusion, we report that fentanyl's effects are highly dose-dependent, drawing attention to the importance of better characterization to adequately respond in emergent cases of fentanyl misuse.
PubMed: 38863429
DOI: 10.1152/jn.00177.2024 -
Bioscience Reports Jun 2024High blood pressure in the portal vein, portal hypertension (PH), is the final common pathway in liver cirrhosis regardless of aetiology. Complications from PH are the...
High blood pressure in the portal vein, portal hypertension (PH), is the final common pathway in liver cirrhosis regardless of aetiology. Complications from PH are the major cause of morbidity and mortality in these patients. Current drug therapy to reduce portal pressure is mainly limited to β-adrenergic receptor blockade but about forty percent of patients do not respond. Our aim was to use microarray to measure the expression of ~20,800 genes in portal vein from patients with PH undergoing transplantation for liver cirrhosis (PH, n = 12) versus healthy vessels (control, n = 9) to identify potential drug targets to improve therapy. Expression of 9,964 genes above background was detected in portal vein samples. Comparing PH veins versus control (adjusted p value < 0.05, fold change > 1.5) identified 548 upregulated genes and 1,996 downregulated genes. The 2,544 differentially expressed genes were subjected to pathway analysis. We identified 49 significantly enriched pathways. The endothelin pathway was ranked the tenth most significant, the only vasoconstrictive pathway to be identified. ET-1 gene (EDN1) was significantly upregulated, consistent with elevated levels of ET-1 peptide previously measured in PH and cirrhosis. ETA receptor gene (EDNRA) was significantly downregulated, consistent with an adaptive response to increased peptide levels in the portal vein but there was no change in the ETB gene (EDNRB). The results provide further support for evaluating the efficacy of ETA receptor antagonists as a potential therapy in addition to β-blockers in patients with PH and cirrhosis.
PubMed: 38860875
DOI: 10.1042/BSR20240528 -
American Journal of Physiology. Lung... Jun 2024Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vasoconstriction and remodeling of small pulmonary arteries (PAs). Central to the...
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vasoconstriction and remodeling of small pulmonary arteries (PAs). Central to the remodeling process is a switch of pulmonary vascular cells to a proliferative, apoptosis-resistant phenotype. Plasminogen activator inhibitor-1 (PAI-1) is the primary physiological inhibitor of urokinase-type and tissue-type plasminogen activators (uPA and tPA), but its role in PAH is unsettled. Here, we report that: (1) PAI-1 is deficient in remodeled small PAs and in early-passage PA smooth muscle and endothelial cells (PASMCs and PAECs) from subjects with PAH compared to controls; (2) PAI-1 mice spontaneously develop pulmonary vascular remodeling associated with up-regulation of mTORC1 signaling, pulmonary hypertension (PH), and right ventricle (RV) hypertrophy; and (3) pharmacological inhibition of uPA in human PAH PASMCs suppresses pro-proliferative mTORC1 and SMAD3 signaling, restores PAI-1 levels, reduces proliferation and induces apoptosis , and prevents the development of SU5416/hypoxia-induced PH and RV hypertrophy in mice. These data strongly suggest that down-regulation of PAI-1 in small PAs promotes vascular remodeling and PH due to unopposed activation of uPA and consequent up-regulation of mTOR and TGF-b signaling in PASMCs, and call for further studies to determine the potential benefits of targeting the PAI-1/uPA imbalance to attenuate and/or reverse pulmonary vascular remodeling and PH.
PubMed: 38860847
DOI: 10.1152/ajplung.00110.2024