BackgroundPostural tachycardia syndrome (POTS) is a heterogeneous condition. We stratified patients previously evaluated for POTS on the basis of supine resting cardiac output (CO) or with the complaint of platypnea or “shortness of breath” during orthostasis. We hypothesize that postural hyperventilation is one cause of POTS and that hyperventilation‐associated POTS occurs when initial reduction in CO is sufficiently large. We also propose that circulatory abnormalities normalize with restoration of CO 2.Methods and ResultsFifty‐eight enrollees with POTS were compared with 16 healthy volunteer controls. Low CO in POTS was defined by a resting supine CO <4 L/min. Patients with shortness of breath had hyperventilation with end tidal CO 2 <30 Torr during head‐up tilt table testing. There were no differences in height or weight between control patients and patients with POTS or differences between the POTS groups. Beat‐to‐beat blood pressure was measured by photoplethysmography, and CO was measured by ModelFlow. Systemic vascular resistance was defined as mean arterial blood pressure/CO. End tidal CO 2 and cerebral blood flow velocity of the middle cerebral artery were only reduced during head‐up tilt in the hyperventilation group, whereas blood pressure was increased compared with control. We corrected the reduced end tidal CO 2 in hyperventilation by addition of exogenous CO 2 into a rebreathing apparatus. With added CO 2, heart rate, blood pressure, CO, and systemic vascular resistance in hyperventilation became similar to control.ConclusionsWe conclude that all POTS is related to decreased CO, decreased central blood volume, and increased systemic vascular resistance and that a variant of POTS is consequent to postural hyperventilation.

Osmotic minipumps containing 400 micrograms ovine LH installed subcutaneously on day 1 (oestrus) of the cycle in the hamster induced superovulation of 30.0 +/- 2.1 ova (n = 5) at the next expected oestrus. Controls ovulated 12.0 +/- 0.8 ova (n = 6). Bovine LH, human LH, porcine LH, human chorionic gonadotrophin and pregnant mare serum gonadotrophin were effective in approximately doubling the number of ova spontaneously shed in the hamster. Ovine FSH (200 micrograms/pump) was most effective in increasing the number of ova spontaneously shed (55 +/- 6, n = 5) in the hamster. Infusion of ovine LH on days 1-4 prevented the reduction of the number of antral follicles that occurs normally between days 3 and 4 of the 4-day cycle. Since this reduction in follicular numbers in control cyclic hamsters is due to atresia, the exogenous LH might prevent atresia of the developing follicles. In the hamster, exogenous ovine LH significantly increased the serum concentrations of androstenedione, oestradiol and LH but not of FSH. Hamsters were hypophysectomized on the day of oestrus, given immediate LH (400 micrograms) or FSH (200 micrograms) replacement therapy and autopsied on day 4. Ovarian histology revealed that immediate LH treatment after hypophysectomy sustained development of histologically normal preovulatory follicles but had no effect on the number of smaller sizes of follicles. Immediate FSH treatment after hypophysectomy increased only the number of smaller sized follicles. Since LH did not increase the smaller sized follicles, no 'FSH-like' effect on follicular development was observed. In the hamster, the ability of various preparations of LH to induce superovulation did not correlate with their ability to displace 125I-labelled ovine FSH from its ovarian binding sites. The superovulatory action of LH required the presence of the pituitary gland, indicating that LH might synergize with FSH and/or prolactin (or hamster LH) for spontaneous superovulation and it appears that exogenous LH might induce superovulation by prevention of atresia. Infusion of LH into the guinea-pig beginning on day 12 of the cycle (day 1 is the day of ovulation) doubled the ovulation rate whereas in the cyclic rat and mouse LH treatment throughout the cycle was ineffective in increasing the number of ova shed.

Upright hyperventilation occurs in approximately 25% of our patients with postural tachycardia syndrome (POTS). Poikilocapnic hyperventilation alone causes tachycardia. Here we examined changes in respiration and hemodynamics comprising cardiac output (CO), systemic vascular resistance (SVR) and blood pressure (BP) measured during head-up tilt (HUT) in 3 groups: patients with POTS and hyperventilation (POTS-HV), patients with Panic Disorder who hyperventilate (Panic), and healthy controls performing voluntary upright hyperpnea (Voluntary-HV). Though all were comparably tachycardic during hyperventilation, POTS-HV manifested hyperpnea, decreased CO, increased SVR and increased BP during HUT; Panic patients showed both hyperpnea and tachypnea, increased CO and increased SVR as BP increased during HUT; and Voluntary-HV were hyperneic by design and had increased CO, decreased SVR, and decreased BP during upright hyperventilation. Mechanisms of hyperventilation and hemodynamic changes differed among POTS-HV, Panic and Voluntary-HV subjects. We hypothesize that the hyperventilation in POTS is caused by a mechanism involving peripheral chemoreflex sensitization by intermittent ischemic hypoxia.

Treatment of immature female rats with 100 micrograms 2-bromo-alpha-ergocryptine mesylate (CB-154) per ml drinking water beginning on Day 30 of age until vaginal opening delayed puberty by 6 days. Rats treated with CB-154 exhibited vaginal opening at 43.3 +/- 0.6 days whereas controls exhibited vaginal opening at 37.9 +/- 0.8 days. Most interestingly, serum levels of luteinizing hormone (LH) and prolactin (PRL) on Days 31-35, determined by a homologous radioimmunoassay were significantly lower in treated rats than in controls. The ovarian concentrations of progesterone (P) and androstenedione (A) were lower in rats treated with CB-154 than in controls; ovarian estradiol (E2) concentrations were low in both groups. Serum levels of P (but not A and E2) were reduced on Days 31-35 of the treatment period. Cessation of the CB-154 treatment on the morning of Day 35 returned the onset of puberty to normal values; steroid and gonadotropin levels also returned to normal values within 2 days after removal of the CB-154 from the drinking water. Near the time of onset of puberty, serum levels of LH in rats treated with CB-154 returned to control values. These data indicate that in the female rat the delay in puberty induced by CB-154 might be due to a reduction in the secretion of LH, especially since the onset of delayed puberty in rats treated with CB-154 correlates with an increase in the serum level of LH. Further studies are needed to elucidate the specific effects of hypoprolactinemia on ovarian function and the onset of puberty in the rat.

BackgroundIntradialytic hypotension is a serious complication during renal replacement therapy in critically ill patients. Early prediction of intradialytic hypotension could allow adequate prophylactic measures. In this study we evaluated the ability of peripheral perfusion index (PPI) and heart rate variability (HRV) to predict intradialytic hypotension.MethodsA prospective observational study included 36 critically ill patients with acute kidney injury during their first session of intermittent hemodialysis. In addition to basic vital signs, PPI was measured using Radical-7 (Masimo) device. Electrical cardiometry (ICON) device was used for measuring cardiac output, systemic vascular resistance, and HRV. All hemodynamic values were recorded at the following time points: 30 min before the hemodialysis session, 15 min before the start of hemodialysis session, every 5 min during the session, and 15 min after the conclusion of the session. The ability of all variables to predict intradialytic hypotension was assessed through area under receiver operating characteristic (AUROC) curve calculation.ResultsTwenty-three patients (64%) had intradialytic hypotension. Patients with pulmonary oedema showed higher risk for development of intradialytic hypotension {Odds ratio (95% CI): 13.75(1.4–136)}. Each of baseline HRV, and baseline PPI showed good predictive properties for intradialytic hypotension {AUROC (95% CI): 0.761(0.59–0.88)}, and 0.721(0.547–0.857)} respectively.ConclusionsEach of low PPI, low HRV, and the presence of pulmonary oedema are good predictors of intradialytic hypotension.