Relating DSM-5 section III personality traits to section II personality disorder diagnoses.

BACKGROUND: The DSM-5 Personality and Personality Disorders Work Group formulated a hybrid dimensional/categorical model that represented personality disorders as combinations of core impairments in personality functioning with specific configurations of problematic personality traits. Specific clusters of traits were selected to serve as indicators for six DSM categorical diagnoses to be retained in this system - antisocial, avoidant, borderline, narcissistic, obsessive-compulsive and schizotypal personality disorders. The goal of the current study was to describe the empirical relationships between the DSM-5 section III pathological traits and DSM-IV/DSM-5 section II personality disorder diagnoses. METHOD: Data were obtained from a sample of 337 clinicians, each of whom rated one of his or her patients on all aspects of the DSM-IV and DSM-5 proposed alternative model. Regression models were constructed to examine trait-disorder relationships, and the incremental validity of core personality dysfunctions (i.e. criterion A features for each disorder) was examined in combination with the specified trait clusters. RESULTS: Findings suggested that the trait assignments specified by the Work Group tended to be substantially associated with corresponding DSM-IV concepts, and the criterion A features provided additional diagnostic information in all but one instance. CONCLUSIONS: Although the DSM-5 section III alternative model provided a substantially different taxonomic structure for personality disorders, the associations between this new approach and the traditional personality disorder concepts in DSM-5 section II make it possible to render traditional personality disorder concepts using alternative model traits in combination with core impairments in personality functioning.

In rabbits, landiolol, a new ultra-short-acting beta-blocker, exerts a more potent negative chronotropic effect and less effect on blood pressure than esmolol.

PURPOSE: To compare the cardiovascular and sympathetic effects of a new ultra-short-acting, highly cardioselective beta- blocker, landiolol, with esmolol, using an in vivo rabbit model. METHODS: Different bolus doses of landiolol (0.3, 1.0, 3.0 and 10.0 mg*kg(-1)) or esmolol (0.5, 1.5 and 5.0 mg*kg(-1)) were given intravenously, and the effects on heart rate (HR) mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were compared. RESULTS: Both landiolol and esmolol produced a dose-dependent decrease in HR. The maximum percent reductions of HR were similar with landiolol 3 mg*kg(-1) and esmolol 5 mg*kg(-1) (-14.0 +/- 0.9% and -13.9 +/- 1.4%, mean +/- SE, respectively). HR decreased more rapidly with landiolol than with esmolol. Esmolol produced a dose-dependent decrease in MAP that was not observed with landiolol. The percent maximum reduction of MAP was -38.2 +/- 3.2% with esmolol 5 mg*kg(-1). RSNA increased in a dose-dependent fashion with esmolol, but no changes were noted with landiolol. CONCLUSION: These results suggest that, in rabbits, landiolol has slightly more potent negative chronotropic action than esmolol with significantly less effects on blood pressure.

Hemodynamic and sympathetic effects of fenoldopam and sodium nitroprusside.

BACKGROUND: Fenoldopam is a novel dopamine-1 receptor selective agonist that can be used as a vasodilator perioperatively to treat hypertension and to produce induced hypotension. We were interested to find out whether there were any differences between fenoldopam (FM) and sodium nitroprusside (SNP), one of the most popular vasodilators, in their effects on hemodynamics and sympathetic outflow using not only neuraxis intact but also baro-denervated animal models. METHODS: A total of 60 New Zealand white rabbits were divided into two groups of 30 each: the neuraxis-intact group and the totally baro-denervated group. Each group was further divided into three groups of 10 each to receive SNP 10 microg x kg(-1), FM 10 microg x kg(-1) or FM 20 microg x kg(-1), respectively. Mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded before and after intravenous (i.v.) administration of each agent. In addition, cardiac and sympathetic baroreflex sensitivity were assessed in the neuraxis-intact animals. RESULTS: In the neuraxis-intact groups, although RSNA was increased to a similar extent in all three groups (P<0.01), the reduction of MAP with FM groups was significantly greater than with SNP (P<0.05). HR was increased only in the SNP group. Cardiac (HR) and sympathetic barosensitivity were significantly attenuated with FM 20 microg x kg(-1) as compared to the SNP group. In the baro-denervated groups, there were significant and similar degrees of reduction of MAP in all three group up to 1 min (P<0.01). MAP remained significantly decreased in the FM groups for 10 min (only 2 min with SNP) in both animal models. CONCLUSIONS: Unlike sodium nitroprusside, fenoldopam attenuates both cardiac (heart rate) and sympathetic baroreflex sensitivity, which may explain the lack of rebound hypertension with fenoldopam. The offset of hypotensive effects of fenoldopam is a significantly slower process as compared to nitroprusside, and this may be an unfavorable feature of fenoldopam should overshoot of hypotension occur.

Adenosine triphosphate attenuates renal sympathetic nerve activity through left ventricular chemosensitive receptors.

We previously reported that ATP, but not adenosine, administered i.v. attenuates the baroreflex-mediated increase in sympathetic nerve activity in response to arterial hypotension by a vagal afferent mechanism. It was not elucidated in that study which vagal afferent endings are involved. Mongrel dogs were anesthetized with alpha-chloralose, thoracotomy was performed and a 27-gauge hypodermic needle was inserted into the left circumflex coronary artery. The left renal sympathetic nerves were isolated and placed on a bipolar silver electrode for measurement of renal sympathetic nerve activity (RSNA). Dose-response effects of intracoronary or i.v. infusion of ATP (100, 200 or 400 microg/kg/min) on RSNA and mean arterial pressure were studied in neuraxis-intact and cervically vagotomized dogs. RSNA was increased dose-dependently with decreasing mean arterial pressure during the i.v. ATP infusion. Elevation of RSNA was attenuated by higher intracoronary ATP infusion rates, despite the fact that mean arterial pressure was decreased dose-dependently. Left ventricular end-diastolic pressure, however, remained unchanged. This suppression of RSNA by the intracoronary ATP infusion was completely abolished by bilateral cervical vagotomy. Our data suggest that ATP attenuates reflex increases in sympathetic nerve activity by possibly stimulating ventricular chemoreceptors with cardiac vagal afferents.

Renal sympathetic nerve activity after dexmedetomidine in nerve-intact and baroreceptor-denervated rabbits.

To determine the effects of intravenous dexmedetomidine (DMED) on the sympathetic nervous system and to elucidate the mechanism of hypotension, we administered 3 micrograms/kg of DMED to nerve-intact and baroreceptor-denervated rabbits and compared the changes in renal sympathetic nerve activity (RSNA) and hemodynamic variables. In nerve-intact animals, mean arterial pressure (MAP) was increased briefly and then decreased significantly. Changes in RSNA were reciprocal to those of MAP. Heart rate decreased throughout the period of observation. In baroreceptor-denervated rabbits, both MAP and RSNA decreased significantly (-39.4% +/- 3.8% and -21.3% +/- 4.7%, respectively) after the initial increase of MAP. Twenty minutes after administration, hypotension had still continued (-21.1% +/- 3.2%) although RSNA returned to the baseline value. These results indicate that suppression of sympathetic nerve discharge is indeed one of the mechanisms of DMED-induced hypotension, although it may not be the principal one.

Attenuation of arterial baroreflex control of renal sympathetic nerve activity during lidocaine infusion in alpha-chloralose-anesthetized dogs.

The purpose of this study was to identify the relationship between sensitivity of arterial baroreflex and plasma concentrations of lidocaine. Using twelve mongrel dogs anesthetized with alpha-chloralose, the left kidney was exposed retroperitoneally, and renal sympathetic nerve activity was recorded continuously. Lidocaine was infused in four different doses: 2 mg.kg BW-1 bolus + 100 micrograms.BW-1 x min; 3 mg.kg BW-1 bolus + 200 micrograms.kg BW-1 x min; 6 mg.kg BW-1 bolus + 400 micrograms.kg BW-1 x min; and 12 mg.kg BW-1 + 800 micrograms.kg BW-1 x min. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after beginning lidocaine infusion. Plasma lidocaine concentrations determined by high performance liquid chromatography revealed that the steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at plasma concentrations of lidocaine below 5 micrograms.ml-1. However, cardiac and sympathetic baroreflex sensitivity were significantly attenuated (P < 0.01) when plasma lidocaine concentrations were well above human convulsion levels (10 micrograms.ml-1). The results indicate that hemodynamic derangement observed in the lidocaine-induced central nervous system toxicity is, at least in part, due to the attenuated arterial baroreflex.

Effects of calcium chloride on verapamil- and diltiazem-pretreated isolated rat hearts.

The effects of calcium chloride on cardiac responses to verapamil and diltiazem were investigated using isolated and perfused rat hearts with a Langendorff technique. Ionized calcium concentrations were increased approximately from 0.5 mM to 2.2 mM when the hearts were pretreated with 0.2 mg/L of verapamil or 0.28 mg/L of diltiazem, or were untreated with calcium blockers. Calcium significantly counteracted the negative inotropic effect produced by diltiazem and verapamil. In contrast, the negative chronotropic effects of both diltiazem and verapamil were potentiated by increasing concentrations of ionized calcium, and this potentiation was not eliminated by 1.0 mg/L of atropine. An atrioventricular block was induced by both verapamil and diltiazem when ionized calcium concentrations were lower than normal. It is suggested from this study that, although calcium chloride counteracts the negative inotropic effects of verapamil and diltiazem, abruptly increased ionized calcium may cause severe bradycardia clinically.

Effects of fentanyl, diazepam, and the combination of both on arterial baroreflex and sympathetic nerve activity in intact and baro-denervated dogs.

The combination of fentanyl and diazepam significantly decreases systemic vascular resistance and blood pressure. We attempted to elucidate the reason the combination of these drugs can reduce blood pressure. In alpha-chloralose-anesthetized dogs, we investigated the effects of fentanyl and diazepam on mean arterial pressure (MAP) and arterial baroreflex control of renal sympathetic nerve activity (RSNA) in both intact (Study 1) and baroreflex-denervated dogs (Study 2). Study 1 included five dogs that received fentanyl 10 micrograms/kg followed by diazepam 0.4 mg/kg after a 10-min interval. Five more received both drugs in reversed sequence. The arterial baroreflex depressor test was performed with sodium nitroprusside before and after administration of each drug. Sensitivity of arterial baroreflex was examined by using the ratio of maximum increase of RSNA to maximum decrease of MAP (delta RSNA/delta MAP). RSNA and MAP significantly decreased only after both drugs had been administered (P < 0.05). Fentanyl alone did not attenuate arterial baroreflex sensitivity. Diazepam after fentanyl and diazepam alone attenuated baroreflex sensitivity to the same extent (P < 0.05). Study 2 comprised 14 dogs that underwent further surgical preparation of bilateral carotid sinus, aortic, and vagal nerve denervations. Seven received fentanyl, 5 and 10 micrograms/kg, and the other seven received diazepam, a total of 0.4 mg/kg. Fentanyl decreased both RSNA and MAP. Diazepam decreased only MAP significantly. The results indicate that fentanyl decreases mainly sympathetic outflow, whereas diazepam attenuates arterial baroreflex. We conclude that these combined effects of fentanyl and diazepam significantly decrease arterial blood pressure.

Arterial baroreflex attenuation during and after continuous propofol infusion.

The reduction of arterial blood pressure produced by propofol may be, in part, attributable to impaired baroreflex integrity. The purpose of this study was to investigate arterial baroreflex sensitivity during and after continuous propofol infusion. In urethane anaesthetized rabbits, left renal sympathetic nerves were exposed and placed on a bipolar silver electrode to record renal sympathetic nerve activity (RSNA). Mean arterial pressure (MAP) via a femoral artery and heart rate (HR) by electrocardiogram were continuously recorded. The rabbits were divided into two groups of eight each: Group 1, propofol 5 mg.kg-1 bolus followed by infusion 0.5 mg.kg-1 x min-1; Group 2, propofol 2 mg.kg-1 bolus followed by 0.2 mg.kg-1 x min-1. Phenylephrine pressor and sodium nitroprusside (SNP) depressor tests were carried out before propofol was started (control), at 15 and 30 min during 30 min infusion, and at 15, 30 and 60 min after its discontinuation. The change of RSNA was plotted with respect to every 5 mmHg increment and decrement of MAP to construct sympathetic baroreflex sigmoid curves, and to evaluate baroreflex sensitivity. The baroreflex sensitivity was also evaluated by calculating the ratio of maximum increase of RSNA or HR to SNP-induced maximum decrease of MAP (delta RSNA/delta MAP, delta HR/delta MAP). Despite the same decreases or increases in MAP, RSNA was attenuated after 15 and 30 min of propofol infusion in both groups compared with control (P < 0.05). Decreased delta RSNA/delta MAP gradually returned to the control level 60 min after discontinuation of propofol in Group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of flumazenil on intravenous lidocaine-induced convulsions and anticonvulsant property of diazepam in rats.

We investigated the effect of flumazenil on intravenous (IV) lidocaine-induced convulsions with and without diazepam pretreatment in rats. Wistar rats (200-250 g) were divided into four groups of seven each and were pretreated with IV diazepam or normal saline solution at 6 min and flumazenil or normal saline solution at 3 min before lidocaine infusion. The control group received normal saline solution; the diazepam group received 0.2 mg/kg of diazepam and normal saline solution; the diazepam+flumazenil group received 0.2 mg/kg of diazepam and 0.1 mg/kg of flumazenil; and the flumazenil group received normal saline solution and 0.1 mg/kg of flumazenil. After surgical preparation and recovery from anesthesia, all groups received a continuous IV infusion of lidocaine (15 mg/mL) at a rate of 4 mg.kg-1.min-1 until tonic/clonic convulsions occurred. The values of pH and blood gases were maintained within physiologic ranges. Heart rate was significantly decreased after 5 min of lidocaine infusion, but arterial blood pressure did not change until convulsions occurred in all groups. Pretreatment with diazepam alone increased both cumulative convulsant doses and plasma concentrations of lidocaine at the onset of convulsions. Flumazenil reversed these effects of diazepam. Pretreatment with flumazenil alone changed neither cumulative convulsant doses nor plasma concentrations of lidocaine at the onset of convulsions. Our data show that IV flumazenil reverses the anticonvulsant property of IV diazepam against lidocaine-induced convulsions and that flumazenil itself has no effect on lidocaine-induced convulsions in rats.

Mixtures of sodium nitroprusside and trimethaphan for induction of hypotension.

A mixture of sodium nitroprusside (SNP) and trimethaphan, empirical 1:10 weight ratio, has been advocated to decrease untoward side effects of SNP when used to induce hypotension during anesthesia and operation. The purpose of this study was to investigate the effects of various ratios of mixtures of SNP and trimethaphan on heart rate (HR), renal sympathetic nerve activity (RSNA), and renal artery blood flow to find the best ratio of SNP and trimethaphan for producing induced hypotension. Five mixtures with different ratios of SNP and trimethaphan, as well as each drug alone, were given intravenously to mongrel dogs in amounts adequate to achieve a stable mean arterial blood pressure of 75 +/- 5 mm Hg. Sodium nitroprusside alone significantly increased HR (163% +/- 14.5%) and RSNA (222% +/- 24%). Trimethaphan alone significantly decreased RSNA (11.6% +/- 4.5%). There were significant positive correlations between SNP-to-trimethaphan ratios and percent changes in HR (r2 = 0.301, P less than 0.01) and in RSNA (r2 = 0.648, P less than 0.01). Renal artery blood flow was well maintained with all ratios. Sodium nitroprusside and trimethaphan interacted synergistically to produce hypotension. However, they antagonize each other in their effects on arterial baroreflex-mediated changes in HR and RSNA. According to linear regression lines, HR changed least with a SNP-to-trimethaphan ratio of 1:5, and RSNA changed least with SNP-to-trimethaphan ratios of 1:2.5 and 1:5. Our results indicate that mixtures of SNP and trimethaphan in ratios of approximately 1:2.5 to 1:5 may produce induced hypotension with stable reflex sympathetic nerve activity.

Vagal involvement in the action of exogenous adenosine triphosphate on reflex renal sympathetic nerve activity.

The reason why adenine compounds when used as hypotensive agents are devoid of significant reflex sympathetic activity, such as rebound hypertension and tachycardia, is not clearly understood. This study, performed on alpha-chloralose-anesthetized dogs, examined, first, the effects of adenosine triphosphate (ATP) and adenosine as compared with those of sodium nitroprusside on efferent renal sympathetic nerve activity (RSNA), as an indicator of general reflex sympathetic activity, and second, whether vagal involvement could be demonstrated in the action of ATP and adenosine on RSNA. Renal sympathetic nerve activity increased progressively with increasing doses of sodium nitroprusside (5, 10, and 20 micrograms/kg) and adenosine (0.5, 2.0, and 4.0 mg/kg), whereas ATP suppressed RSNA at 2.0 and 4.0 mg/kg. High doses of ATP and adenosine (4.0 mg/kg) were injected into intact (n = 7) and vagotomized dogs (n = 7). Both ATP and adenosine induced rapid onset of hypotension without rebound hypertension and tachycardia. After vagotomy, the attenuation of RSNA by ATP was completely abolished and rebound hypertension and tachycardia were observed. Vagotomy did not alter the effect of adenosine on RSNA. It is concluded that ATP-induced hypotension is associated with attenuation of sympathetic efferent nerve activity mediated through vagal afferent pathways. Vagal afferent impulses are thought to be one of the mechanisms that inhibit reflex sympathetic activities, such as rebound hypertension after ATP-induced hypotension. The mechanisms by which adenosine inhibits reflex sympathetic activity are not, however, secondary to vagal afferent involvement and must be multifactorial.

Attenuation of arterial baroreceptor reflex response to acute hypovolemia during induced hypotension.

Preservation of the arterial baroreflex response is important to restore cardiac output and blood pressure by reflex sympathetic nerve activation in the event of sudden hypotension caused by acute blood loss during surgery. However, the arterial baroreflex may be significantly attenuated by both anesthetics and hypotensive agents. In isoflurane-anesthetized dogs, the authors investigated the arterial baroreflex response 1) to bolus injections of sodium nitroprusside (SNP), prostaglandin E1 (PGE1) and trimethaphan (TM); and 2) to rapid blood loss (5 ml/kg) before and during induced hypotension with SNP, PGE1, and TM by measuring mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA). Hypotension produced by both SNP and PGE1 was accompanied by an increase in RSNA and HR. The increase in RSNA and HR following the SNP bolus injection was significantly greater than that following injection of PGE1 (P less than 0.05). Trimethaphan was associated with a decrease in RSNA and HR. Rapid blood loss resulted in the same degree of MAP reduction (20 +/- 2 mmHg) before and during induced hypotension. Sensitivities of baroreflex, as evaluated by ratios of maximum changes in RSNA or HR to MAP (delta RSNA/delta MAP, delta HR/delta MAP), in response to rapid blood loss, were significantly suppressed during continuously induced hypotension, as compared with responses before induced hypotension. Despite the same degree of induced hypotension (70 +/- 5 mmHg of MAP), delta RSNA/delta MAP and delta HR/delta MAP in response to rapid blood loss were significantly greater with PGE1 than those with SNP (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

[Baroreceptor reflex response to acute blood loss during induced hypotension--a comparison of sodium nitroprusside, prostaglandin E1 and trimethaphan].

This experiment was designed to evaluate the reflexive heart rate (HR) response to acute blood loss during sodium nitroprusside (SNP), prostaglandin E1 (PGE1) and trimethaphan (TM) induced-hypotension in isoflurane anesthetized dogs. Reflexive increase in HR to acute blood loss was significantly greater during PGE1 induced-hypotension than during that with SNP. TM inhibited the reflexive HR response to acute blood loss. These results suggest that PGE1 induced-hypotension provides a safer margin than that with SNP and TM when rapid bleeding occurs during anesthesia and surgery.

Efficacy of high-frequency jet ventilation in cardiac tamponade.

To evaluate the effects of high-frequency jet ventilation (HFJV) (f = 60, 120 breaths/min) and conventional mechanical ventilation (CMV) (f = 10, 20) during equivalent conditions of cardiac tamponade, stroke index (SI), intrapericardial pressure (IPP), airway pressure (P(aw)), and cardiac pressures were measured in anesthetized, paralyzed, chest-closed dogs with the same levels of PaCO2. Cardiac tamponade was produced by infusing normal saline into the intrapericardial space to increase IPP to either 8 mm Hg (group 1, n = 8) or 12 mm Hg (group 2, n = 8). Stroke index in group 1 was 7.3 +/- 0.8 during CMV (f = 10), 8.1 +/- 0.7 during CMV (f = 20), 10.9 +/- 1.4 during HFJV (f = 60), and 10.7 +/- 1.2 (mL.beat-1.m-2) during HFJV (f = 120). Stroke index in group 2 was 4.1 +/- 0.7, 5.1 +/- 0.5, 7.2 +/- 0.5, and 6.7 +/- 0.5 (mL.beat-1.m-2), respectively. In both IPP groups, stroke index values during HFJV were significantly higher than during CMV; however, there were no significant differences in mean left and right atrial transmural pressures between HFJV and CMV. Peak IPP, mean P(aw), and peak P(aw) during HFJV were significantly lower than those during CMV. The results indicate that HFJV with lower mean and peak Paw, and with lower mean and peak IPP, can result in higher cardiac output than CMV in cardiac tamponade. Thus, HFJV may be superior to CMV in the clinical management of cardiac tamponade.

Activated partial thromboplastin time-protamine dose relation in the presence and absence of heparin.

A protamine titration is one of the methods to determine the protamine dose necessary to neutralize heparin. The protamine dose response was studied with the activated partial thromboplastin time (APTT) in the presence of a known amount of heparin and in the absence of heparin, using freshly prepared human plasma. When heparin was present in the plasma, APTT values plateaued between a minimal neutralizing dose of protamine and a protamine dose five times greater. At doses above the APTT plateau, protamine exerted its own anticoagulant action as evidenced by an increase in APTT values. In the absence of heparin, APTT did not change until the protamine concentration reached 50 micrograms/mL. Then the APTT began to increase above this critical concentration. The increases in APTT values caused by an increase of 50 micrograms/mL of protamine were significantly greater without heparin than they were in the presence of heparin. These results suggest that protamine has a wide safety range when neutralizing heparin without exerting its own anticoagulant action. Although the mechanisms are under speculation, the heparin-protamine complex may inhibit the anticoagulant action of protamine in vitro.

Alteration of red cell deformability during extracorporeal bypass: membrane v bubble oxygenator.

Red cell deformability is essential for normal microcirculation, since the red cell is greater in diameter than the caliber of small capillaries. Red cell filtration rate (RFR) was measured using a 5 microns nucleopore polycarbonate filter as an index of red cell deformability before, during, and after two hours of extracorporeal circulation for coronary artery bypass surgery, with a bubble oxygenator (eight patients) or a hollow fiber membrane oxygenator (14 patients). RFR decreased steadily and significantly during bypass in the bubble oxygenator group. After the start of bypass, RFR was significantly higher at all measurement intervals in the membrane oxygenator group as compared with the bubble oxygenator group. It can be postulated that significantly impaired red cell deformability caused by the bubble oxygenator is attributed to mechanical damage secondary to a huge blood-gas interface, and possibly to neutrophil-mediated oxygen free radical formation due to complement activation. Results indicate that the hollow fiber membrane oxygenator is superior to the bubble oxygenator in maintaining red cell deformability.