Vascular control of the CO2/H+ dependent drive to breathe

Respiratory chemoreceptors regulate breathing in response to changes in tissue CO2/H+. Blood flow is a fundamental determinant of tissue CO2/H+, yet little is known regarding how regulation of vascular tone in chemoreceptor regions contributes to respiratory behavior. Previously, we showed in rat that CO2/H+-vasoconstriction in the retrotrapezoid nucleus (RTN) supports chemoreception by a purinergic-dependent mechanism (Hawkins et al. 2017). Here, we show in mice that CO2/H+ dilates arterioles in other chemoreceptor regions, thus demonstrating CO2/H+ vascular reactivity in the RTN is unique. We also identify P2Y2 receptors in RTN smooth muscle cells as the substrate responsible for this response. Specifically, pharmacological blockade or genetic deletion of P2Y2 from smooth muscle cells blunted the ventilatory response to CO2, and re-expression of P2Y2 receptors only in RTN smooth muscle cells fully rescued the CO2/H+ chemoreflex. These results identify P2Y2 receptors in RTN smooth muscle cells as requisite determinants of respiratory chemoreception.Significance StatementDisruption of vascular control as occurs in cardiovascular disease leads to compromised chemoreceptor function and unstable breathing. Despite this, virtually nothing is known regarding how regulation of vascular tone in chemoreceptor regions contributes to respiratory behavior. Here, we identify P2Y2 receptors in RTN vascular smooth muscle cells as a novel vascular element of respiratory chemoreception. Identification of this mechanism may facilitate development of treatments for breathing problems including those associated with cardiovascular disease.

Safety and effectiveness of microvascular decompression for treatment of hemifacial spasm through mini craniotomy

Background: The hemifacial spasm (HFS) defined as involuntary intermittent twitching of the muscles of the face (usually unilateral). The spasms characteristically begin around the eye and then extend to affect other muscles of the ipsilateral face. It is caused by vascular element compressing the facial nerve that may be either the anterior or the posterior inferior cerebellar arteries in most cases. Objective of our work: to describe the operative technique (pearls and common mistakes), the efficacy and morbidity of microvascular decompression technique for hemifacial spasm through mini craniotomy, determine the prognostic factors affecting success rate of the surgery. Material & method: A retrospective study of 23 cases of hemifacial spasm treated by mini craniotomy retro sigmoid approach and microvascular decompression at neurosurgery dept., Mansoura University Hospital in last 10 years was investigated. This include Epidemiological, clinical and imaging details, selected treatment options and patients’ outcome. Results: complete resolving of symptoms was conducted in 19 cases 82.6% while reoperated in 2 cases with improvement in one case. Facial palsy appeared postoperative in 6 cases 4 of them improved in 3 months, transient hearing loss in 4 cases17.4% which improved later, cerebrospinal fluid leak appeared in 3 cases 13% which managed conservatively. Conclusions: MVD relieves symptoms of HFS in about 80% of patients while recurrence still in low percentage. The study reported low permanent Complications and generally transient.

A role for the rice homeobox gene Oshox1 in provascular cell fate commitment

The vascular tissues of plants form a network of interconnected cell files throughout the plant body. The transition from a genetically totipotent meristematic precursor to different stages of a committed procambial cell, and its subsequent differentiation into a mature vascular element, involves developmental events whose molecular nature is still mostly unknown. The rice protein Oshox1 is a member of the homeodomain leucine zipper family of transcription factors. Here we show that the strikingly precise onset of Oshox1 gene expression marks critical, early stages of provascular ontogenesis in which the developmental fate of procambial cells is specified but not yet stably determined. This suggests that the Oshox1 gene may be involved in the establishment of the conditions required to restrict the developmental potential of procambial cells. In support of this hypothesis, ectopic expression of Oshox1 in provascular cells that normally do not yet express this gene results in anticipation of procambial cell fate commitment, eventually culminating in premature vascular differentiation. Oshox1 represents the first example of a transcription factor whose function can be linked to specification events mediating provascular cell fate commitment.