Model of reentrant ventricular tachycardia based on infarct border zone geometry predicts reentrant circuit features as determined by activation mapping

BACKGROUND: Infarct border zone (IBZ) geometry likely affects inducibility and characteristics of postinfarction reentrant ventricular tachycardia, but the connection has not been established. OBJECTIVE: The purpose of this study was to determine characteristics of postinfarction ventricular tachycardia in the IBZ. METHODS: A geometric model describing the relationship between IBZ geometry and wavefront propagation in reentrant circuits was developed. Based on the formulation, slow conduction and block were expected to coincide with areas where IBZ thickness (T) is minimal and the local spatial gradient in thickness (DeltaT) is maximal, so that the degree of wavefront curvature rho proportional, variant DeltaT/T is maximal. Regions of fastest conduction velocity were predicted to coincide with areas of minimum DeltaT. In seven arrhythmogenic postinfarction canine heart experiments, tachycardia was induced by programmed stimulation, and activation maps were constructed from multichannel recordings. IBZ thickness was measured in excised hearts from histologic analysis or magnetic resonance imaging. Reentrant circuit properties were predicted from IBZ geometry and compared with ventricular activation maps after tachycardia induction. RESULTS: Mean IBZ thickness was 231 +/- 140 microm at the reentry isthmus and 1440 +/- 770 microm in the outer pathway (P <0.001). Mean curvature rho was 1.63 +/- 0.45 mm(-1) at functional block line locations, 0.71 +/- 0.18 mm(-1) at isthmus entrance-exit points, and 0.33 +/- 0.13 mm(-1) in the outer reentrant circuit pathway. The mean conduction velocity about the circuit during reentrant tachycardia was 0.32 +/- 0.04 mm/ms at entrance-exit points, 0.42 +/- 0.13 mm/ms for the entire outer pathway, and 0.64 +/- 0.16 mm/ms at outer pathway regions with minimum DeltaT. Model sensitivity and specificity to detect isthmus location was 75.0% and 97.2%. CONCLUSIONS: Reentrant circuit features as determined by activation mapping can be predicted on the basis of IBZ geometrical relationships.     

Intravenous Lidocaine Infusion Facilitates Acute Rehabilitation after Laparoscopic Colectomy

Background: Intravenous infusion of lidocaine decreases postoperative pain and speeds the return of bowel function. The authors therefore tested the hypothesis that perioperative lidocaine infusion facilitates acute rehabilitation protocol in patients undergoing laparoscopic colectomy.

Methods: Forty patients scheduled to undergo laparoscopic colectomy were randomly allocated to receive intravenous lidocaine (bolus injection of 1.5 mg/kg lidocaine at induction of anesthesia, then a continuous infusion of 2 mg [middle dot] kg-1 [middle dot] h-1 intraoperatively and 1.33 mg [middle dot] kg-1 [middle dot] h-1 for 24 h postoperatively) or an equal volume of saline. All patients received similar intensive postoperative rehabilitation. Postoperative pain scores, opioid consumption, and fatigue scores were measured. Times to first flatus, defecation, and hospital discharge were recorded. Postoperative endocrine (cortisol and catecholamines) and metabolic (leukocytes, C-reactive protein, and glucose) responses were measured for 48 h. Data (presented as median [25-75% interquartile range], lidocaine vs. saline groups) were analyzed using Mann-Whitney tests. P < 0.05 was considered statistically significant.

Results: Patient demographics were similar in the two groups. Times to first flatus (17 [11-24] vs. 28 [25-33] h; P < 0.001), defecation (28 [24-37] vs. 51 [41-70] h; P = 0.001), and hospital discharge (2 [2-3] vs. 3 [3-4] days; P = 0.001) were significantly shorter in patients who received lidocaine. Lidocaine significantly reduced opioid consumption (8 [5-18] vs. 22 [14-36] mg; P = 0.005) and postoperative pain and fatigue scores. In contrast, endocrine and metabolic responses were similar in the two groups.     

The interferon antagonist sarcolectin in the progress of HIV-1 infection and in AIDS.

Sarcolectin (SCL) is a nonspecific stimulator of cellular DNA synthesis that was found in all animal sera tested to date. It inhibits the established interferon (IFN)-dependent antiviral state, restoring cells to their normal status. In this study, we examined the excretion/secretion of the IFN antagonist SCL in sera from healthy donors and in sera collected during different periods of human immunodeficiency virus type 1 (HIV-1) infection. We followed HIV-1-infected patients during all stages of development (seroconversion, initial and advanced phases of AIDS) and found a significant increase in SCL in sera of HIV-infected patients compared with seronegative subjects used as controls. This increase was established during seroconversion, and then the titers leveled off. In the final stage of the disease, the SCL titer increased again very significantly. We attribute this rapid rise to the virus-dependent destruction of T cells that can no longer be repaired. The high SCL level observed at this final stage, which is most predictive of the disease's progression, suggests that the action, rather than the production, of IFN is impaired.     

Ventrolateral medullary neurons projecting to the medial preoptic/anterior hypothalamic area through the medial forebrain bundle: an electrophysiological study in the rat

Summary A total of 152 ventrolateral medullary neurons was antidromically stimulated from both the medial preoptic/anterior hypothalamic area (MPOAH) and the medial forebrain bundle (MFB) in urethane anesthetized rats. These neurons were located primarily dorsal to the lateral reticular nucleus and could be readily classified in at least two groups, type I and type II cells on the basis of electrophysiological properties. The action potentials of type I cells had a shorter duration, and their conduction velocities ranged from 0.45 to 3.1 m/s. By contrast, type II cells, most predominantly observed, were characterized by a longer duration and an unusual shape of their action potential, and the antidromic propagation into the somatodendritic complex was often blocked. The conduction velocity (mean = 0.21 m/s) and absolute refractory period (mean = 2.63 ms) of type II cells are consistent with them having fine non-myelinated axons. Injection of 6-hydroxydopamine (6-OHDA), but not 5,7-dihydroxytryptamine, directly into the MFB blocked antidromic responses of 57% of type II cells tested. The residual type II cells whose antidromic responses were not affected by 6-OHDA were located significantly rostral to the 6-OHDA sensitive cells. Neither antidromic response of type I cells tested, on the other hand, was affected by 6-OHDA. The majority of type I cells were dramatically activated by noxious pinches of the tail, whereas the noxious stimuli produced no detectable change in the firing of type II cells. These data demonstrate that ventrolateral medullary neurons projecting to the MPOAH through the MFB are comprised of at least three distinct populations: 6-OHDA resistant fast conducting cells with somatic afferents, 6-OHDA sensitive and resistant slow conducting cells.     

Subfornical organ neurons act to enhance the activity of paraventricular vasopressin neurons in response to intravenous angiotensin II

The effects of pretreatment of the angiotensin II (ANGII) antagonist, saralasin (Sar), in the subfornical organ (SFO) on intravenous ANGII-induced responses of the activity of phasically firing paraventricular nucleus (PVN) neurons (n = 23) antidromically identified as projecting to the posterior pituitary were examined in urethane-anesthetized rats. The activity of the majority (n = 18) of identified PVN neurons was excited by intravenously administered ANGII, whereas the remaining neurons (n = 5) were not affected. The excitatory responses (n = 13) to ANGII were prevented by pretreatment with Sar, but not by isotonic saline (n = 3), in the SFO. These results suggest that ANGII-sensitive SFO neurons may act to enhance the excitability of putative vasopressin (VP)-secreting neurons in the PVN in response to circulating ANGII.     

Neurosteroid modulation of dendrodendritic inhibition in the mouse olfactory bulb

The present report describes neurosteroid modulation of olfactory bulb function by examining the effects of intrabulbar infusion of dehydroepiandrosterone sulfate (DHEAS), a neurohormone discovered in rat brain, on field potentials in the granule cell layer evoked by paired-pulse stimulation of the mouse lateral olfactory tract. Infusion of DHEAS (5 nmol) significantly decreased the test response without affecting the conditioning response. As a consequence, DHEAS selectively potentiated paired-pulse depression, which is believed to be due to granule cell-mediated inhibition of the mitral/tufted cells. The granule-to-mitral/tufted dendrodendritic synapse is GABAergic. Taken together, these results suggest that DHEAS potentiates the GABAergic dendrodendritic inhibition exerted by the granule cells on the mitral/tufted cells.     

Oestrogen infusions into the amygdala potentiate excitatory transmission from the accessory olfactory bulb to tuberoinfundibular arcuate neurones in the mouse.

We have previously shown that oestrogen increases the percentage of tuberoinfundibular (TI) arcuate neurones that respond to electrical stimulation of the accessory olfactory bulb (AOB). This study focuses on the amygdala as a possible site for the hormonal modulation of AOB input to TI arcuate neurones. Local infusions of 17 beta-oestradiol (30 pmol) into the amygdala of ovariectomized female mice significantly potentiated excitatory responses of TI arcuate neurones to AOB stimulation. This effect appeared rapidly (less than 10 min) after infusion. The inactive oestrogen isomer, 17 alpha-oestradiol, infused in the same manner, was without effect. These results suggest that oestrogen acts directly on amygdala neurones, thereby modulating olfactory information relayed along the vomeronasal pathway to TI arcuate neurones.     

Subfornical organ and hypothalamic paraventricular nucleus connections with median preoptic nucleus neurons: an electrophysiological study in the rat

Summary The role of pathways from the subfornical organ (SFO) to the hypothalamic paraventricular nucleus (PVN) through the median preoptic nucleus (MnPO) in regulating the activity of putative vasopressin (VP)-secreting neurons in the PVN was examined in urethane-anesthetized male rats. The activity of the majority (79%) of SFO neurons antidromically identified as projecting to the MnPO was excited by microiontophoretically (MIPh) applied angiotensin II (ANG II) and the effect was blocked by MIPh-applied saralasin (Sar), an ANG II antagonist. Identified SFO neurons that were excited by MIPh-applied ANG II were also excited by intravenously administered ANG II. Electrical stimulation of the SFO produced orthodromic excitation (48%) or inhibition (24%) of the activity of MnPO neurons antidromically identified as projecting to the PVN. Identified MnPO neurons that were excited by SFO stimulation were also excited by MIPh-applied ANG II, while the remaining neurons were not affected. The excitatory responses to SFO stimulation and to MIPh-applied ANG II were both blocked by MIPh-applied Sar, whereas the inhibitory responses to SFO stimulation were not affected. ANG II injected into the region of the SFO produced either an excitation (55%) or no effect (45%) on the activity of identified MnPO neurons. Electrical stimulation of the MnPO produced orthodromic excitation (27%) or inhibition (23%) of the activity of putative VP-secreting PVN neurons. ANG II injected into the region of the MnPO produced either an excitation (31%) or no effect (69%) on the activity of putative VP-secreting PVN neurons. These observations reveal some possible interconnections between three brain regions and suggest that circulating ANG II excites a population of neurons projecting from the SFO to the MnPO, and that these neurons themselves release ANG II as an excitatory transmitter on part of MnPO neurons projecting to the PVN, thereby causing enhanced activity of putative VP-secreting PVN neurons.