Guillain-Barré Syndrome and Chronic Inflammatory Demyelinating Polyradiculoneuropathy in Pregnancy

Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are both immune-mediated diseases of the peripheral nervous system that typically present with symmetric, progressive muscle weakness, areflexia, and sensory symptoms or signs. GBS evolves rapidly with a nadir at 2–4 weeks usually with an antecedent viral illness, while CIDP progresses more slowly over months to years. GBS is sometimes complicated by life-threatening respiratory failure or dysautonomia. Onset of GBS and relapse of CIDP can occur during pregnancy or postpartum. But with appropriate supportive care and immunotherapy, maternal and fetal outcome in both conditions is typically excellent. The exception is fetal outcome in GBS triggered by maternal CMV or Zika infection transmitted to the fetus. Full-term vaginal delivery and regional anesthesia are preferred in maternal GBS and CIDP, but if C-section and general anesthesia are indicated, non-depolarizing agents such as succinylcholine should be avoided.

Pregnancy restores insulin secretion from pancreatic islets in cafeteria diet-induced obese rats

Insulin resistance during pregnancy is counteracted by enhanced insulin secretion. This condition is aggravated by obesity, which increases the risk of gestational diabetes. Therefore, pancreatic islet functionality was investigated in control nonpregnant (C) and pregnant (CP), and cafeteria diet-fed nonpregnant (Caf), and pregnant (CafP) obese rats. Isolated islets were used for measurements of insulin secretion (RIA), NAD(P)H production (MTS), glucose oxidation (14CO2 production), intracellular Ca2+ levels (fura-2 AM), and gene expression (real-time PCR). Impaired glucose tolerance was clearly established in Caf and CafP rats at the 14th wk on a diet. Insulin secretion induced by direct depolarizing agents such as KCl and tolbutamide and increasing concentrations of glucose was significantly reduced in Caf, compared with C islets. This reduction was not observed in islets from CP and CafP rats. Accordingly, the glucose oxidation and production of reduced equivalents were increased in CafP islets. The glucose-induced Ca2+ increase was significantly lower in Caf and higher in CafP, compared with all other groups. CP and CafP islets demonstrated an increased Ca2+ oscillation frequency, compared with both C and Caf islets, and the amplitude of oscillations was augmented in CafP, compared with Caf islets. In addition, Cavα1.2 and SERCA2a mRNA levels were reduced in Caf islets. Cavα1.2, but not SERCA2a, mRNA was normalized in CafP islets. In conclusion, cafeteria diet-induced obesity impairs insulin secretion. This alteration is related to the impairment of Ca2+ handling in pancreatic islets, in especial Ca2+ influx, a defect that is reversed during pregnancy allowing normalization of insulin secretion.

Hypertension attenuates cell-to-cell communication in hamster retractor muscle feed arteries

This study examined whether hypertension attenuated cell-to-cell communication in skeletal muscle resistance arteries. Briefly, arteries feeding the retractor muscle of normotensive and hypertensive hamsters were cannulated, pressurized, and superfused with a physiological saline solution. Cell-to-cell communication was functionally assessed by application of vasoactive stimuli (via micropipette) to a small portion of a feed artery while diameter at sites distal to the point of agent application was monitored. In keeping with past observations, discrete application of a smooth muscle depolarizing agent (phenylephrine or KCl) elicited a localized vasoconstriction that conducted poorly along feed arteries from normotensive hamsters. In contrast, acetylcholine, an agent known to hyperpolarize endothelial cells, elicited a vasodilation in normotensive feed arteries that conducted with little decay. Whereas smooth muscle depolarizing agents continued to elicit a localized response, conduction of endothelium-dependent vasodilation was attenuated in hypertensive hamsters. This decrease occurred in the absence of changes in vessel reactivity to intravascular pressure or to global application of phenylephrine, U-46619, or acetylcholine. We propose, on the basis of these physiological observations, quantitative mRNA measurements of connexins 37, 40, 43, and 45, and analysis of the literature, that an increase in endothelial-to-endothelial or smooth muscle-to-endothelial coupling resistance is likely responsible for hypertension-induced impairment in vascular communication. We hypothesize that this attenuation could contribute to the rise in total peripheral resistance characteristically observed in hypertension.