Prospective study of the changes in left ventricular mass and geometry patterns in hypertensive patients During 5 years of follow-up.

BACKGROUND: Left ventricular hypertrophy (LVH), as well as the geometry pattern of the left ventricle, is believed to be an independent risk factor for hypertension. The present study investigated the changes in left ventricular mass, diastolic function and geometry in hypertensive patients in a prospective 5-year follow-up in conjunction with an evaluation of the regularity and effectiveness of treatment. METHODS AND RESULTS: One hundred hypertensive patients older than 18 years were examined according to the study protocol, which included registration of weight, height, vital signs, and echocardiography. After 5 years a repeat examination was performed. Patients were divided into 3 groups according to blood pressure (BP) control: group 1 (n=32), no regular medication; group 2 (n=44), regular treatment but no target BP levels; group 3 (n=14), regular effective treatment. In group 1 an increase in LVH and worsening of diastolic function were observed; in group 2 LVH and isovolumetric relaxation time remained unchanged, while the early peak velocity/atrial peak velocity ratio decreased; in group 3 there was a significant decrease in LVH. The geometry pattern only changed in 21 (23%) patients. CONCLUSIONS: LVH can be successfully reversed in only hypertensive with adequate BP control. The remodeling pattern appears to be a stable characteristic of the patient and transformation of one pattern into another is infrequent.     

A purinergic component of the excitatory postsynaptic current mediated by P2X receptors in the CA1 neurons of the rat hippocampus

The pyramidal neurons in the CA1 area of hippocampal slices from 17- to 19-day-old rats have been investigated by means of patch clamp. Excitatory postsynaptic currents (EPSCs) were elicited by stimulating the Schaffer collateral at a frequency below 0.2 Hz. It was found that inhibition of glutamatergic transmission by 20 μm 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 100 μm 2-amino-5-phosphonovaleric acid (D-APV) left a small component of the EPSC uninhibited. The amplitude of this residual EPSC (rEPSC) comprised 25 ± 11% of the total EPSC when measured at a holding potential of ?50 mV. The rEPSC was blocked by selective P2 blocker pyridoxal phosphate-6-azophenyl-2′-4′-disulphonic acid (PPADS) 10 μm and bath incubation with non-hydrolysable ATP analogues, ATP-γ-S and α,β-methylene-ATP at 50 and 20 μm , respectively. The rEPSC was dramatically potentiated by external Zn²⁺ (10 μm ). In another series of experiments exogenous ATP was applied to the CA1 neurons in situ. An inward current evoked by ATP was inhibited by PPADS to the same extent as the rEPSC. It is concluded that, depending on membrane voltage, about one-fifth to one-quarter of the EPSC generated by the excitatory synaptic input to the hippocampal CA1 neurons of rat is due to the activity of P2X receptors.     

Postoperative complications of laparoscopic adjustable gastric banding

Background: The primary aim was to determine the rate and nature of late postoperative complications in relation to the type of band used and the route through which it encircled the stomach in a retrospective review of postoperative complications that necessitated reoperation in 500 consecutive cases of laparoscopic adjustable gastric banding (LAGB) conducted over the past 48 months. Methods: The four study groups were: (A) Lap‐Band^® perigastric route, 186 cases; (B) Lap‐Band^® pars flaccida route 73 cases; (C) SAGB perigastric 70 cases, and (D) SAGB pars flaccida, 171 cases. There were 414 women and 86 men. The mean age was 39.2 ± 11.0 years (17–68). The mean weight was 126 kg, and mean BMI was 43.4 kg/m² prior to operation. Results: There were 32 cases of slippage (17%) in group A and five cases (7%) in Group B (P < 0.05). In group C there were 15 cases (21%) of slippage and in group D six cases (3%) (P < 0.05). There were no significant differences between Groups A and C or Groups B and D. Except for one case of band erosion in Group C, erosion, tube disconnection and aneurysmatic balloon dilatation occurred only in groups A and B. Band erosion occurred in 2% each in groups A and B, tube disconnection in 3% and 4%, respectively, and balloon dilatation in 2% in each of groups A and B. Conclusions: Slippage was primarily route dependent. Erosion, tube disconnection and aneurysmatic dilatation of the balloon were encountered almost exclusively in the high‐pressure system. We conclude that the pars flaccida route with the low‐pressure system is more effective in reducing the rate of complications necessitating reoperation.     

Expandable metal stent application in obstructing carcinoma of the proximal colon

PURPOSE: The increased mortality of emergency vs. elective colonic surgery applies equally to the right and left colon. Recent interest has surrounded the application of expandable metal stenting in acute obstruction but has been confined to the left colon. We describe successful application of stenting in the right colon, allowing postponement of a particularly high-risk laparotomy. METHODS: A patient with acute bilateral iliofemoral thromboses simultaneously developed complete obstruction of the proximal transverse colon. After heparinization and under fluoroscopic control, a 10-cm-long, self-expanding Wallstent ^® (Schneider, Bulach, Switzerland), 22 mm in diameter, was manipulated across the obstruction. RESULTS: Immediate decompression with symptomatic relief ensued. The stent prevented obstruction during a 10-week period of anticoagulation, and repeat duplex scanning showed resolution of iliac thrombus. An elective right hemicolectomy was then performed. Postoperative course was uncomplicated, and histopathology confirmed a Dukes B carcinoma. CONCLUSIONS: This case, in which a potentially hazardous laparotomy was delayed until the operative risk improved, defines a new role for stenting in colonic obstruction and demonstrates an extension of its applicability to the right colon. Literature review found no other report of stent application in the right colon.     

MECHANISMS OF MYOCARDIAL PROTECTION BY AMINO ACIDS: FACTS AND HYPOTHESES

1. Positive inotropic effect of taurine and improvement of cardiac performance of failing heart are mediated through the modulation of Ca²⁺ movement through the sarcolemma. 2. Cardioprotection with glutamate and aspartate is related to enhanced anaerobic energy formation in mitochondria coupled with succinate formation and, probably, with the relieving of glycolytic flux. During reperfusion, both amino acids replenish the malate-aspartate shuttle reactants, thereby facilitating glucose oxidation. 3. Increased intracellular concentrations of branched chain amino acids (leucine, valine and isoleusine) stimulate formation of acetyl-coenzyme (CoA) and succinyl-CoA and, thus, recovery of oxidative metabolism. 4. Methionine and cysteine enhance force of contraction by N-methylation of membrane phospholipids of the sarcolemma and sarcoplasmic reticulum. Methionine and, to a lesser extent, cysteine may reduce myocardial damage by oxygen radical species. 5. Histidine exerts antioxidant properties as a scavenger of singlet oxygen and OH’ radicals. High concentrations of histidine provide intracellular buffering to stimulate anaerobic energy formation.     

Direct Activation of ENaC by Angiotensin II: Recent Advances and New Insights

Angiotensin II (Ang II) is the principal effector of the renin–angiotensin–aldosterone system (RAAS). It initiates myriad processes in multiple organs integrated to increase circulating volume and elevate systemic blood pressure. In the kidney, Ang II stimulates renal tubular water and salt reabsorption causing antinatriuresis and antidiuresis. Activation of the RAAS is known to enhance activity of the epithelial Na⁺ channel (ENaC) in the aldosterone-sensitive distal nephron. In addition to its well described stimulatory actions on aldosterone secretion, Ang II is also capable of directly increasing ENaC activity. In this brief review, we discuss recent findings about non-classical Ang II actions on ENaC and speculate about its relevance for renal sodium handling.     

Leptin-stimulated KATP channel trafficking

Insulin secretion from pancreatic β-cells is initiated by the closure of ATP-sensitive K⁺ channels (K_ATP) in response to high concentrations of glucose, and this action of glucose is counteracted by the hormone leptin, an adipokine that signals through the Ob-R_b receptor to increase K_ATP channel activity. Despite intensive investigations, the molecular basis for K_ATP channel regulation remains uncertain, particularly from the standpoint of whether fluctuations in plasma membrane K_ATP channel content underlie alterations of K_ATP channel activity in response to glucose or leptin. Surprisingly, newly published findings reveal that leptin stimulates AMP-activated protein kinase (AMPK) in order to promote trafficking of K_ATP channels from cytosolic vesicles to the plasma membrane of β-cells. This action of leptin is mimicked by low concentrations of glucose that also activate AMPK and that inhibit insulin secretion. Thus, a new paradigm for β-cell stimulus-secretion coupling is suggested in which leptin exerts a tonic inhibitory effect on β-cell excitability by virtue of its ability to increase plasma membrane K_ATP channel density and whole-cell K_ATP channel current. One important issue that remains unresolved is whether high concentrations of glucose suppress AMPK activity in order to shift the balance of membrane cycling so that K_ATP channel endocytosis predominates over vesicular K_ATP channel insertion into the plasma membrane. If so, high concentrations of glucose might transiently reduce K_ATP channel density/current, thereby favoring β-cell depolarization and insulin secretion. Such an AMPK-dependent action of glucose would complement its established ability to generate an increase of ATP/ADP concentration ratio that directly closes K_ATP channels in the plasma membrane.