Neurotransmitter-Mediated Changes in the Electrophysiological Properties of Pituicytes

Intracellular recordings were obtained from pituicytes in the neural lobe of the isolated rat pituitary. Like other glia, pituicytes lacked action potentials in response to depolarizing current injection, but they tended to have more positive resting membrane potentials and higher input resistances than astrocytes in other preparations. Dye-coupling typical of astrocytes was also demonstrated amongst pituicytes, and their morphologies were similar to those of pituicytes stained for glial fibrillary acidic protein. Action potentials, anode-break spikes or barium spikes were not observed in pituicytes, even under conditions that maximized the elicitation of Ca²⁺-dependent responses. This suggests that pituicytes either have no or a very low density of Ca²⁺ channels or Ca²⁺ currents that are too small to generate action potentials. Dynorphin A (1–13), a kappa-opioid agonist, produced long-lasting increases in pituicyte input resistance with no significant changes in resting membrane potential. Dynorphin's action was concentration-dependent and was blocked by the opioid antagonist naloxone. This is consistent with previous reports demonstrating kappa-opioid receptors on pituicytes in the neurohypophysis. The β-adrenergic agonist isoproterenol (100 μM) reversed the increases in pituicyte input resistance produced by opioid application, with no significant changes in resting membrane potential. The fact that pituicytes responded to neurotransmitters suggests a functional link between pituicytes and neurosecretory nerve fibres.     

Creating empowering meaning: an interactive process of promoting health with chronically ill older Canadians

Many health promotion approaches afford education about disease prevention and enhancement of one's health status. But strategies for enabling older people with chronic illness to better mobilize their resources for everyday living still require development. This practical action research study explored the experiences of 13 purposefully selected older persons who participated in a health promotion intervention premised on the adult education theory of perspective transformation. Findings illuminate health promotion through a holistic interactive process in which professional and chronically ill older person together evolved a caring relationship and enhanced conscious awareness of life and health experiences. Five health-promoting strategies were identified: building trust and meaning; connecting; caring; mutual knowing; and mutual creating. Researchers suggest several important directions to refine professional practice approaches and health care delivery systems in order to promote the health of older persons with chronic conditions.     

颈内动脉接近完全闭塞时的处理

目的由于卒中风险随着狭窄严重程度的增加而升高，因此认为颈内动脉（ICA）接近闭塞患者的卒中风险很高。在现有的随机试验中，还没有专门针对这种情况进行探讨，因此其处理尚存在争汶。方法：对相关文献进行系统评价。结果：对ICA接近闭塞患者的处理还存在争议：一些学者支持进行干预，而另一些学者则认为存在风险或没有益处而反对进行干预。在ICA接近闭塞的有症状患者中进行一项比较外科治疗与最佳内科治疗的多中心前瞻性随机试验似乎非常困难，因为这类研究需要大量的患者。尽管如此，基于目前的证据，似乎很难拒绝手术治疗。结论：由于目前对ICA接近闭塞患者的最佳处理方案仍存在着争议，因此需要前瞻性观察性研究以证实其在有症状和无症状人群中的患病率以及相关的卒中风险。基于目前的证据，大多数医疗中心选择手术治疗，但它相对干内科治疗的特粱尚右待证章．     

Prevention of arginine-vasopressin-induced motor disturbances by a potent vasopressor antagonist

The antivasopressor analog d(CH2)5Tyr(Me) arginine-vasopressin completely blocked the convulsive-like behavior and other severe motor disturbances which are normally observed following a second central arginine-vasopressin injection. This vasopressor antagonist appears to be selective for arginine-vasopressin-induced motor disturbances, in that the convulsive and motor effects of pentylenetetrazol and somatostatin were not altered significantly by pretreatment with the central antagonist. Results suggest that arginine-vasopressin-induced motor disturbances are mediated via central receptors. The classic antidiuretic (V2) type of arginine-vasopressin receptor does not appear to be involved, since the agonist 1-desamino-8-D-arginine-vasopressin did not elicit convulsive-like behavior or other severe motor disturbances 2 days following a first ('priming') injection of arginine-vasopressin.     

Release of benzalkonium chloride from a heparin-bonded umbilical catheter with resultant factitious hypernatremia and hyperkalemia

Elevated serum sodium and potassium levels were recently observed when sampled through a heparin-bonded umbilical catheter and measured with certain ion-selective electrodes. The cationic surfactant, benzalkonium chloride (BZC), is known to falsely elevate those cations in serum. Inasmuch as most heparin-bonded umbilical catheters use BZC during the bonding process, an in vitro study was performed to estimate the quantity of BZC released and the duration of sodium and potassium elevations during pooled sera infusion. Three heparin-bonded umbilical catheters and 3 silastic umbilical catheters were first flushed with 0.3 mL of normal saline and then perfused with pooled sera (sodium, 142 mEq/L; potassium, 4.6 mEq/L) at 2.5 microL/h. Effluent samples were collected from 0 to 8 hours and analyzed by ion-selective electrodes. Elevated serum sodium concentrations from 160 to greater than or equal to 250 mEq/L and potassium concentrations from 6.0 to greater than or equal to 9.6 mEq/L were observed. The BZC concentration in the catheter effluent was measured by mass spectrometry, with peak values of 10 micrograms/mL detected by this method. When varying concentrations of BZC (1 to 100 micrograms/mL) were added directly to pooled serum, a dose-dependent increase in serum sodium was observed. These data demonstrate that BZC released from heparin-bonded umbilical catheters elevates serum electrolyte values measured with some ion-selective electrodes. The observed increase in sodium and potassium concentrations may lead to clinical errors in management. Benzalkonium chloride is associated with myriad of linical symptomatology. Whether this amount of BZC is toxic in the small premature neonate is presently unknown.     

Estimation of red cell flow microvessels: consequences of the Baker-Wayland spatial averaging model

The dual sensor cross-correlation method of H. Wayland and P.C. Johnson [1967), J. Appl. Physiol. 22, 333-337) has become a standard technique for determining the velocity of red blood cells (RBCs) in glass tubes and blood vessels. M. Baker and H. Wayland [1974), Microvasc. Res. 7, 131-143) found that under a variety of conditions the ratio of dual sensor velocity at the centerline of a glass tube to the blood velocity averaged over the lumen was close to 1.6. They provided an explanation of this factor based on spatial averaging of RBC velocity vertically through the tube as well as laterally across the face of the sensor. Their spatial averaging model could also account for the apparent blunting of RBC velocity profiles determined with the dual sensor technique. We used Baker and Wayland's spatial averaging model to calculate how the above velocity ratio depends on sensor size. A nonlinear relation between the velocity ratio and sensor size was found such that the velocity ratio varied from 1.6 to 1.33 as the ratio of sensor width to vessel or tube diameter was varied from 0 to 1. These results also hold for vessels or tubes of elliptic cross section. Some investigators have found that the velocity of red cells near the walls of blood vessels can be a substantial fraction of centerline velocity which suggests that RBC velocity distributions can be blunter than a Poiseuille distribution. We repeated the above calculation for blunted parabolic profiles and we found that the velocity ratio ranged from 1 for plug flow to 1.6 for Poiseuille flow. These calculations show that reliable estimates of RBC flow from dual sensor centerline velocity measurements require one to take into account the relative size of the sensor and blood vessel diameter as well as the bluntness of the RBC velocity distribution.     

Neuropeptide Y action in the rat hippocampal slice: site and mechanism of presynaptic inhibition

Neuropeptide Y (NPY), the most abundant peptide in mammalian CNS, has been shown to inhibit excitatory neurotransmission presynaptically at the stratum radiatum-CA1 synapse in the in vitro rat hippocampal slice. We examined the site and mechanism of this inhibition in a series of in vitro intra- and extracellular recordings in areas CA1 and CA3, the source of much of the excitatory synaptic input to the CA1 neurons. NPY's inhibitory action at the stratum radiatum-CA1 synapse was unaffected by high concentrations of the antagonists bicuculline, theophylline, or atropine, suggesting that it does not act by stimulating the release of the known presynaptic inhibitory transmitters GABA, adenosine, or ACh, respectively. Bath application of 10(-6) NPY, a concentration that strongly inhibited the stratum radiatum-CA1 synapse had no effect on CA3 neuron resting potential, input resistance or action potential amplitude, threshold, or duration. NPY also does not alter the amplitude or duration of the prolonged CA3 action potentials evoked in the presence of TTX, tetraethyl-ammonium, and elevated external Ca2+ or those evoked in the presence of TTX and Ba2+ ions. NPY therefore does not alter the passive or active properties of the somata of the presynaptic CA3 neurons. Neither the afferent fiber volley of the Schaffer collaterals in stratum radiatum of area CA1 nor the excitability of the CA3 terminals in CA1 was affected by NPY application. However, application of the transient K+ current blocker, 4-aminopyridine (4-AP) at concentrations of 10 and 50 microM, completely abolished the action of 10(-6) M NPY on the stratum radiatum-CA1 excitatory synaptic potentials. This action of 4-AP could be reversed by reducing extracellular Ca2+ concentrations from a control level of 1.5 to 0.7 mM (in 10 microM 4-AP) and to 0.5 mM (in 50 microM 4-AP). The evidence suggests that NPY inhibits excitatory synaptic transmission at the Schaffer collateral-CA1 synapse by acting directly at the terminal to reduce a Ca2+ influx.