Blunted peripheral but not cerebral vasodilator function in young otherwise healthy adults with persistent symptoms following COVID-19

Recent findings suggest that COVID-19 causes vascular dysfunction during the acute phase of the illness in otherwise healthy young adults. To date, no studies have investigated the longer-term effects of COVID-19 on vascular function. Herein, we hypothesized that young, otherwise healthy adults who are past the acute phase of COVID-19 would exhibit blunted peripheral (brachial artery flow-mediated dilation (FMD) and reactive hyperemia) and cerebral vasodilator function (cerebral vasomotor reactivity to hypercapnia; CVMR) and increased central arterial stiffness. Sixteen young adults who were at least 4 weeks past a COVID-19 diagnosis and 12 controls who never had COVID-19 were studied. Eight COVID subjects were symptomatic (SYM) and 8 were asymptomatic (ASYM) at the time of testing. FMD and reactive hyperemia were not different between COVID and Control groups. However, FMD was lower in SYM (3.8 ± 0.6%) compared to ASYM (6.8 ± 0.9%; P = 0.007) and Control (6.8 ± 0.6%; P = 0.003) with no difference between ASYM and Control. Similarly, peak blood velocity following cuff release was lower in SYM (47 ± 8 cm/s) compared to ASYM (64 ± 19 cm/s; P = 0.025) and Control (61 ± 14 cm/s; P = 0.036). CVMR and arterial stiffness were not different between any groups. In summary, peripheral macro- and microvascular function, but not cerebral vascular function or central arterial stiffness were blunted in young adults symptomatic beyond the acute phase of COVID-19. In contrast, those who were asymptomatic had similar vascular function compared to controls who never had COVID.

Consequences of Canine Ehrlichiosis: Clinical Case Successfully Resolved

This work aims to report the case of a canine that survived erlichiosis with severe consequences of the disease, such as meningitis, hind limb paresis, circle walking, cerebrovascular accident. The onset of paresis was sudden, soon after a hygienic grooming. X-ray examinations ruled out suspected trauma. A cerebrovascular accident is suspected due to vasculitis found by electrocardiogram examination. Traditional treatment for doxycycline-based erlichiosis (200 mg) 1 comp. 2 x day for 24 days was recommended; anti-inflammatory drug Prednisone - IDB for 15 days, antianemic Erythros - 1 comp./day, Leucogen (H) 5 mL (2 x day) immunomodulator for platelet elevation and a peripheral and cerebral vasodilator Revimax - 1 comp./ day were the drugs of choice. The case seems to suggest that the bacterium, through the hematogenous route, reaches the intervetbral discs, paralyzing the pelvic limbs, bladder, anal sphincter and tail, and may even cause neurological disorders and even lead to death of the animal. Since paresis and stroke, as well as hydrocephalus and meningitis, clinical signs were much more atypical and are currently becoming more frequent.

Profiling cerebrovascular function in migraine: A systematic review and meta-analysis

Previous studies have investigated whether migraine is a circulatory disorder, as migraineurs are at heightened risk of cerebrovascular disease. However, in most cases, systemic vascular function was evaluated, which may not reflect abnormalities in the cerebral circulation. Therefore, we aimed to determine whether cerebrovascular function differs between migraineurs and controls. A systematic literature search was conducted across three electronic databases to search for studies that compared cerebrovascular function in migraineurs to controls. Where applicable, meta-analyses were used to determine standardised mean differences (SMD) between migraineurs and controls. Seventy articles were identified, 40 of which contained quantitative data. Meta-analyses showed pulsatility index (PI) was higher (SMD = 0.23; 95%CI = 0.05 to 0.42, P = 0.01) and cerebrovascular responsiveness (CVR) to hypercapnia was lower (SMD=−0.34; 95%CI=−0.67 to −0.01, P = 0.04) in the posterior circulation of migraineurs, particularly those without aura. The meta-analyses also indicated that migraineurs have higher resting mean blood flow velocity in both anterior (SMD = 0.14; 95%CI = 0.05 to 0.23, P = 0.003) and posterior circulations (SMD = 0.20; 95%CI = 0.05 to 0.34, P = 0.007). Compared to healthy controls, migraineurs have altered cerebrovascular function, evidenced by elevated PI (representing arterial stiffness) and impaired CVR to hypercapnia (representing cerebral vasodilator function). Future studies should investigate whether improvement of cerebrovascular function is able to alleviate migraine.

THE ACTIVITY OF ANTIOXIDANT ENZYMES AND THE EXPRESSION OF THEIR GENES IN THE RAT BRAIN AFTER INJECTING OF VINDEBURNOL IN THE MULTIPLE SCLEROSIS MODEL

The article presents the results of a study on the effectiveness of vindeburnol, a structural analogue of the cerebral vasodilator vincamine, in the model of multiple sclerosis. The drug was injected subcutaneously in rats after modeling experimental allergic encephalomyelitis at a dose of 20 μg/kg, from the first manifestation of a neurological deficit over the next 10 days. In the somatosensory cortex of animals, the activity of superoxide dismutase, glutathione peroxidase and glutathione reductase, as well as the expression level of the SOD1, GPX4, GPX6 and GSR genes using real-time polymerase chain reaction were studied. It was found that vindeburnol does not affect the expression of the SOD1 gene, as well as the activity of superoxide dismutase, while increasing the expression of the GPS4, GPS6 and GRS genes, which determines the increased activity of glutathione peroxidase and glutathione reductase in rats in the model of multiple sclerosis.

Selective head cooling during neonatal seizures prevents postictal cerebral vascular dysfunction without reducing epileptiform activity

Epileptic seizures in neonates cause cerebrovascular injury and impairment of cerebral blood flow (CBF) regulation. In the bicuculline model of seizures in newborn pigs, we tested the hypothesis that selective head cooling prevents deleterious effects of seizures on cerebral vascular functions. Preventive or therapeutic ictal head cooling was achieved by placing two head ice packs during the preictal and/or ictal states, respectively, for the ∼2-h period of seizures. Head cooling lowered the brain and core temperatures to 25.6 ± 0.3 and 33.5 ± 0.1°C, respectively. Head cooling had no anticonvulsant effects, as it did not affect the bicuculline-evoked electroencephalogram parameters, including amplitude, duration, spectral power, and spike frequency distribution. Acute and long-term cerebral vascular effects of seizures in the normothermic and head-cooled groups were tested during the immediate (2–4 h) and delayed (48 h) postictal periods. Seizure-induced cerebral vascular injury during the immediate postictal period was detected as terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive staining of cerebral arterioles and a surge of brain-derived circulating endothelial cells in peripheral blood in the normothermic group, but not in the head-cooled groups. During the delayed postictal period, endothelium-dependent cerebral vasodilator responses were greatly reduced in the normothermic group, indicating impaired CBF regulation. Preventive or therapeutic ictal head cooling mitigated the endothelial injury and greatly reduced loss of postictal cerebral vasodilator functions. Overall, head cooling during seizures is a clinically relevant approach to protecting the neonatal brain by preventing cerebrovascular injury and the loss of the endothelium-dependent control of CBF without reducing epileptiform activity.

CO2 Has no Therapeutic Effect on Early Micro Vasospasm after Experimental Subarachnoid Hemorrhage

In addition to delayed vasospasm also early brain injury, which occurs during the first few days after subarachnoid hemorrhage (SAH) when large cerebral arteries are still fully functional, plays an important role for the outcome after SAH. In the current study, we investigated the hypothesis that carbon dioxide (CO2), a strong cerebral vasodilator, has a therapeutic potential against early posthemorrhagic microvasospasm. C57BL/6 mice ( n = 36) and Sprague-Dawley rats ( n = 23) were subjected to sham surgery or SAH by filament perforation. The pial microcirculation in the mice was visualized 3 and 24 hours after SAH using intravital fluorescence microscopy. Partial pressure of CO2 (PaCO2) was modulated by hyper- or hypoventilation or by inhalation of 10% CO2. In rats, CO2-mediated changes in cerebral blood flow (CBF) were measured at the same time points using laser Doppler fluxmetry. Increased PaCO2 caused vasodilatation in sham-operated animals. Following SAH, however, cerebral arterioles were nonreactive to CO2. This lack of microvascular CO2 reactivity was accompanied by a complete loss of CO2-induced hyperemia. Our data show that CO2 is not able to dilate spastic microvessels and to increase CBF early after SAH. Future therapeutic approaches will therefore need to address mechanisms beyond CO2.