Midlife women's health consequences associated with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is one of the most common female endocrinopathies. Its symptoms may appear as early as adolescence and may include irregular menstrual periods, amenorrhea, hirsutism and obesity. Regardless of their phenotypic appearance, women with PCOS are metabolically obese. PCOS is associated with metabolic syndrome, type 2 diabetes, depression, cardiovascular disease and gynecological cancers. The metabolic disorders in obese women with PCOS are invariably due to insulin resistance, while inflammation, oxidative stress and possible interaction with environmental factors are among the features linking women with PCOS alone to metabolic disorders. The current review aims to highlight the relationship between PCOS and midlife women's health complications.

Insulin resistance in the control of body fat distribution: a new hypothesis.

Obesity causes insulin resistance, which is a prime etiological factor for type 2 diabetes, dyslipidemia, and cardiovascular disease. However, insulin resistance may be a normal physiological response to obesity that limits further fat deposition and which only has pathological effects at high levels. The current hypothesis suggests that in obesity the initial deposition of triglycerides occurs in subcutaneous adipose tissue and as this increases in size insulin resistance will rise and limit further subcutaneous lipid accumulation. Triglycerides will then be diverted to the visceral fat depot as well as to ectopic sites. This leads to a substantial rise in insulin resistance and the prevalence of its associated disorders. Evidence supporting this hypothesis includes studies showing that in lean subjects the prime determinant of insulin resistance is BMI, that is, subcutaneous fat whilst in overweight and obese subjects it is waist circumference and visceral adiposity. It has also been shown that the metabolic syndrome suddenly increases in prevalence at high levels of insulin resistance and we suggest that this is due to the diversion of lipids from the subcutaneous to the visceral depot. This system may have functioned in our evolutionary past to limit excessive adiposity by causing lipid deposition to occur at a site that has maximal effects on insulin resistance but involves minimal weight gain.

Vascular delay and intermittent stimulation: keys to successful latissimus dorsi muscle stimulation.

BACKGROUND: The goal of this study was to obtain physiologically significant increases in peak left ventricular (LV) systolic pressure and stroke volume with latissimus dorsi muscle (LDM) stimulation in cardiomyoplasty (CMP). We hypothesized that preserving LDM integrity by vascular delay and intermittent stimulation would significantly increase LDM cardiac assistance. METHODS: In 4 control dogs and 12 dogs that had undergone a vascular delay (VD) procedure, LV dysfunction was induced by intracoronary microsphere injections. Cardiomyoplasty surgery was performed 14 days later, followed by progressive LDM conditioning. In the control dogs and in 6 of the VD dogs, the LDM was stimulated 24 hours per day (VD plus constant stimulation [CS]). In the other 6 VD dogs, LDMs were stimulated on a daily schedule of 10 hours on and 14 hours off (VD plus interrupted stimulation [IS]). Latissimus dorsi muscle stimulated beats were compared with nonstimulated beats 9 weeks later. RESULTS: In the control dogs, LDM stimulation had minimal effects. In VD + CS and VD + IS, LDM stimulation increased peak LV pressure, stroke volume, stroke work, and stroke power (p < 0.05). However, these changes were greater in the VD + IS group, in which LDM stimulation increased peak aortic pressure by 17.6 +/- 1.7 mm Hg, peak LV pressure by 19.7 +/- 1.1 mm Hg, peak positive LV dp/dt by 398 +/- 144 mm Hg per second, stroke volume by 5.1 +/- 0.7 mL, stroke work by 10.9 +/- 0.9 gm.m, and stroke power by 122.7 +/- 11.6 gm.m per second (p < 0.05 compared with VD + CS). Quantitative morphometric analysis showed minimal LDM degeneration in the VD + IS group (7.5% +/- 1.1%), and VD + CS group (10.5% +/- 4.5%) compared with the control group (29.5% +/- 4.5%, p < 0.05). CONCLUSIONS: VD and IS considerably increased the LV assistance with LDM stimulation. Further studies of this combined approach to CMP should be planned.

Transthoracic ultrasonography is an alternative to subxyphoid ultrasonography for the diagnosis of hemopericardium in penetrating precordial trauma.

BACKGROUND: Surgeon-performed ultrasonography is increasingly becoming part of the initial evaluation of patients after blunt or penetrating trauma. Currently, most institutions obtain a subxyphoid or subcostal view of the heart and pericardial space, and a three-view ultrasonogram of the abdomen to detect blood in the pericardial sac or in three dependent abdominal areas. METHODS: A left parastemal standard transverse transthoracic view is described in addition to the aforementioned views. This facilitates the visualization of the pericardial sac when a subxyphoid or subcostal view cannot be obtained because of anatomical reasons (narrow subxyphoid space) or local factors (pain, fractures, subcutaneous emphysema, or chest wall contusion). RESULTS: The transthoracic view can be useful in patients where the subxyphoid view is difficult to obtain through the conventional approach. In most patients an excellent view of the pericardial sac and ventricles can be obtained and, therefore, expedites the diagnosis and treatment of patients with hemopericardium. CONCLUSION: Surgeon-performed ultrasonography has become the diagnostic test of choice for patients suspected of having hemopericardium and cardiac tamponade. Transthoracic ultrasonography is an excellent alternative for those patients where a subxyphoid or subcostal view to visualize the pericardial sac and heart cannot be obtained owing to local or anatomical factors.

Vascular delay of the latissimus dorsi provides an early hemodynamic benefit in dynamic cardiomyoplasty.

OBJECTIVES: Dynamic cardiomyoplasty (CMP) as a surgical treatment for chronic heart failure improves functional class status for most patients. However, significant hemodynamic improvement with latissimus dorsi muscle (LDM) stimulation has not been consistent. The current protocols do not allow early LDM stimulation after CMP surgery. We hypothesized that vascular delay of LDM would increase myocardial assistance after CMP and allow early (48-h) LDM stimulation after CMP. METHODS: Mongrel dogs (n = 24) were divided in four groups: 1) controls (n = 6), single-stage CMP; 2) Group ES (n = 6), single-stage CMP with early LDM stimulation beginning 48 h, postoperatively; 3) Group VD (n = 6), vascular delay of the LDM followed by CMP without early LDM stimulation, and 4) Group VDES (n = 6), vascular delay of LDM (14-18 days), followed by CMP with early stimulation (48 h postoperatively). Two weeks after CMP, global cardiac dysfunction was induced by injecting microspheres into the left coronary artery. LDM-assisted (S) beats were compared with nonstimulated beats (NS) by measuring aortic pressure (AoP), LV pressure, aortic flow, and by calculating first derivative of LV contraction (+/-dP/dt), stroke volume (SV), and stroke work (SW). RESULTS: In ES, LDM stimulation had no effect on the hemodynamic parameters. In the other groups, LDM stimulation significantly (p < 0.05) increased AoP, LVP, dP/dt, SV, and SW. However, these increases were much larger in VD and VDES. In VD, LDM stimulation increased peak AoP by 21.5+/-3.8 mm Hg, LVP by 22.1+/-4.1 mm Hg, dP/dt by 512+/-163 mm Hg/sec, SV by 10.4+/-2.3 mL, and SW by 22.1+/-5.4 g/m(-1). Similarly, in VDES, LDM stimulation increased peak AoP by 24.1+/-4.7 mm Hg, LVP by 26.2+/-4.3 mm Hg, dP/dt by 619+/-47 mm Hg/sec, SV by 6.5+/-0.7 mL, and SW by 16.7+/-4.1 g/m(-1). CONCLUSIONS: In dogs with global LV dysfunction, CMP after vascular delay resulted in a significant improvement in hemodynamic function measured 2 weeks after surgery. This improvement was not provided by single-stage CMP with or without early stimulation. Vascular delay of the LDM before surgery may play an important role for early benefit after CMP, shorten the overall muscle training period, as well as increase hemodynamic response to LDM stimulation.

Gastric protection against cold restraint stress-induced lesions by amoxycillin in rats.

AIMS: Recent investigations have shown that amoxycillin possesses gastric protection properties in addition to its known antimicrobial effects. Therefore, this study was undertaken to investigate the potential gastric protection effects of amoxycillin and to determine its possible mechanism(s) of action in rats. METHODS: The cold restraint stress model was used to produce gastric mucosal lesions. The gastric secretion studies were undertaken by using Shay's pylorus ligation technique. The antioxidant effect was studied by luminol dependent chemiluminescence technique in vitro. RESULTS: Amoxycillin dose-dependently prevented cold restraint stress-induced mucus depletion and afforded protection. It inhibited indomethacin-stimulated gastric acid secretion with a high dose without affecting basal secretion. Furthermore, amoxycillin dose-dependently inhibited the phorbol myristate acetate-stimulated luminol-dependent chemiluminescence responses of isolated human poylmorphonuclear leukocytes in vitro. CONCLUSIONS: These results suggest that mechanisms of gastric protection effects of amoxycillin may include inhibition of stimulated acid secretion, prevention of depletion of mucus and antioxidant properties.

Preconditioning of the latissimus dorsi muscle in cardiomyoplasty: vascular delay or chronic electrical stimulation.

OBJECTIVES: In standard single stage cardiomyoplasty (CMP), the latissimus dorsi muscle (LDM) is not preconditioned prior to surgery. We hypothesized that latissimus dorsi preconditioning by vascular delay or by chronic electrical stimulation would result in an improved LV hemodynamic function early (14 days) after CMP. METHODS: Mongrel dogs had preconditioning of the latissimus dorsi by a vascular delay procedure followed by CMP 14-18 days later (group I VD). Dogs in group II underwent 4 weeks of chronic stimulation (CS) of the latissimus dorsi (2 V/30 Hz, six bursts/min) followed by CMP. The latissimus dorsi muscle was fully stimulated from 48 h after cardiomyoplasty in both groups (2 V/30 Hz, three bursts/min). Two weeks after myoplasty, injecting 2.0-3.0 x 10(5) 90 microm latex microspheres in the left main coronary artery induced global cardiac dysfunction. Hemodynamic function was then evaluated for latissimus dorsi muscle assisted (S) beats and non-stimulated beats (NS) in each group by measuring peak systolic aortic pressure (AOP), left ventricular pressure (LVP) and end diastolic pressure (LVEDP), and by calculating maximum and minimum dP/dt. RESULTS: Dogs with vascular delay of the latissimus dorsi showed a marked increase for all hemodynamic indices (AOP: 23.9+/-2.5%, LVP: 23.5+/-2.2%, max dP/dt: 49.4+/-3.3%) for LDM assisted (S) beats compared to non-stimulated beats (P < 0.001). Animals with chronic electrical training did not demonstrate a significant increase in any hemodynamic parameter with LDM stimulation. CONCLUSION: Preconditioning the LDM may play an important role in providing early cardiac assistance in CMP. Preconditioning the LDM with vascular delay resulted in improving performance of the LDM with consistent increases in LV hemodynamics. This was not observed after preconditioning with chronic electrical stimulation. Vascular delay of the latissimus dorsi can significantly improve muscle performance in CMP and could provide hemodynamic assistance early after surgery.

Effect of ablation of capsaicin-sensitive neurons on gastric protection by honey and sucralfate.

BACKGROUND/AIMS: Accumulating evidence indicates that capsaicin-sensitive afferent neurons play a pivotal role in acute gastroprotection by liberating vasodilator substances. The mechanism of gastric protection by honey and sucralfate has been shown to be mediated through the vasodilator nitric oxide and cytoprotective sulphydryl-sensitive pathways in the stomach. The aim of the present study was to investigate the role of capsaicin-sensitive afferent neurons in the protective mechanism of honey and sucralfate against ethanol-induced gastric lesions. METHODOLOGY: Ablation of capsaicin-sensitive afferent neurons was carried out by treating rats with neurotoxic doses of capsaicin (50 + 50 mg/kg subcutaneously over 2 consecutive days). The control groups received equal volumes of the vehicle (10% ethanol + 10% Tween 80 + 80% normal saline). The non-protein sulphydryl level was determined spectrophotometrically. RESULTS: Afferent sensory nerve ablation significantly aggravated ethanol-induced gastric lesions and caused a greater depletion of non-protein sulphydryl levels. Pretreatment with honey (0.078-0.625 g/kg, orally) or sucralfate (0.062-0.250 g/kg, orally) 30 min before administration of the ethanol prevented ethanol-induced gastric lesions and the depletion of non-protein sulphydryls in vehicle-treated rats. However, honey failed to afford protection or reverse non-protein sulphydryl depletion, while sucralfate was effective in the capsaicin-treated animals. The protective effect of sucralfate was lost in both groups following pretreatment with indomethacin (10 mg/kg, subcutaneously), while honey-induced protection was unaffected. CONCLUSIONS: These results suggest that the gastric protection by honey is solely dependent on the presence of intact afferent sensory neurons, whereas sucralfate-induced gastroprotection is mediated through the afferent sensory neuron and prostaglandin systems. It seems that the non-protein sulphydryl level is affected by the ablation of sensory neurons and plays an important regulatory role in gastric protection.

Evidence for improved cerebral function after minimally invasive bypass surgery.

BACKGROUND: Neurological impairment is a major cause of morbidity after cardiac surgery and may be associated with occurrence of cerebral microemboli generated during cardiopulmonary bypass (CPB). This study evaluates cerebral dysfunction following coronary artery surgery on-pump and off-pump. METHODS: Neurological outcome was evaluated in 322 patients with a coronary artery bypass graft (CABG). Conventional CPB was used (on-pump) in 305 patients and in 17 patients no CPB was used (off-pump). Intraoperatively, a pulsed-wave transcranial Doppler with a 2-MHZ probe measured high-intensity transient signals (HITS) by ultrasonic insonnation of the middle cerebral artery indicating the presence of emboli within the vessel lumen. Transcranial near-infrared spectroscopy measured cerebral venous oxygen saturation for adequate perfusion. Postoperatively, all patients were subjected to the antisaccadic eye movement (ASEM) test, a sensitive indicator of neurocognitive deficits secondary to frontal lobe dysfunction. RESULTS: While there was no significant difference in O2 saturation, the number of microemboli HITS generated was significantly higher in the on-pump group than the off-pump group. In the off-pump group, 16 (94%) of 17 patients had perfect scores on the ASEM test, while only 108 (35.4%) of 305 patients achieved a perfect score in the on-pump group (p < 0.01). Furthermore, while all patients in the off-pump group achieved at least 90%, 28% (86/305) in the on-pump group scored "zero" on the ASEM test. CONCLUSION: Cerebral dysfunction as evidenced by ASEM errors is common following coronary bypass on-pump, but rare with off-pump bypass surgery. Cerebral microemboli generated during CPB may account for this difference.

The role of non-protein sulphydryls in the protective effects of antioxidants against ethanol-induced vascular permeability changes in the rat stomach.

Increased vascular permeability has been reported to preceed the development of ethanol-induced gastric lesions. Both generation of oxygen-derived free radicals and depletion of non-protein sulphydryls may be involved in the ethanol-induced vascular permeability. Thus, this study aimed to examine the effect of antioxidants, allopurinol and dimethylsulphoxide, and a sulphydryl blocker, N-ethylmaleimide, on ethanol-induced vascular permeability changes and to evaluate the possible interactions between antioxidants and endogenous sulphydryls. Extravasation of intravenously administered Evans blue into the stomach of rats following 30 min exposure to ethanol was used as an indicator of vascular permeability. The glandular non-protein sulphydryl and extravasated Evans blue were determined spectrophotometrically. Increased vascular permeability and a significant depletion of non-protein sulphydryl contents of the gastric mucosa were observed following 30 min exposure to 50% ethanol. Treatment with N-ethylmaleimide (50 mg/kg subcutaneously) caused enhancement of ethanol-induced vascular permeability and further depletion of non-protein sulphydryls. Intraperitoneal pretreatment with either allopurinol (12.5-50 mg/kg) or dimethylsulphoxide (20-40 mg/kg) attenuated ethanol-induced vascular permeability changes and restored the non-protein sulphydryl levels towards control. In contrast, treatment with N-ethylmaleimide before allopurinol (50 mg/kg) or dimethylsulphoxide (40 mg/kg) reduced the protective effect of both and are also associated with corresponding depletion of non-protein sulphydryl contents. These results suggest that oxygen-derived free radicals may be involved in the pathogenesis of ethanol-induced vascular permeability changes and endogenous sulphydryls may facilitate and mediate beneficial effects of antioxidants.

Cardiomyoplasty: hemodynamic benefit to normal and depressed canine left ventricular function.

This study examined the effects of cardiomyoplasty with vascular delay on canine normal and depressed left ventricular (LV) function. To improve viability of the latissimus dorsi muscle (LDM), vascular delay was performed 2 weeks before cardiomyoplasty in 10 mongrel dogs. Two weeks after cardiomyoplasty, LV function was evaluated by simultaneously measuring LV and aortic pressure, and aortic flow. The LDM was stimulated at a ratio of 1:4-1:7 synchronously with ventricular systole. Microspheres (90 mu) were sequentially injected into the left coronary artery to depress LV function. Data were acquired and analyzed on a beat to beat basis. Results were as follows: LDM stimulation significantly augmented LV systolic pressure (LVSP) from 138 +/- 2 to 161 +/- 2* mmHg, the peak rate of change of LV pressure (+dP/dt) from 1888 +/- 46 to 2584 +/- 43* mmHg/sec, aortic systolic pressure (AoSP) from 140 +/- 2 to 159 +/- 2* mmHg, stroke volume (SV) from 11.2 +/- 0.3 to 13.3 +/- 0.3* ml, stroke work (SW) from 19 +/- 1 to 26 +/- 1* gm.m, peak aortic flow (P Qa) from 5542 +/- 142 to 7190 +/- 161* ml/min, and decreased -dP/dt from -1683 +/- 31 to -1689 +/- 49* mmHg/sec (* = p < 0.05). Microsphere injections depressed LV function, but did not affect the magnitude of the net changes between stimulated and nonstimulated beats. However, the percent changes significantly increased. Preconditioning of LDM with vascular delay augments cardiac function in LDM assisted beats. This improved performance was present in both normal as well as depressed LV function groups. Thus, investigations of cardiomyoplasty may not necessarily require a model of severe myocardial dysfunction. Vascular delay offers an important preconditioning method of LDM to augment cardiac function in cardiomyoplasty.

Preventing gastroepiploic artery spasm: papaverine vs calcium channel blockade.

UNLABELLED: The gastroepiploic artery (GEA) is a highly vasoactive artery gaining wider acceptance as a conduit for coronary artery bypass surgery. A variety of agents are used to dilate the GEA prior to grafting; however, little is known about the duration of their effect in the immediate postoperative period. This study evaluated three calcium channel blockers and papaverine in preventing graft spasm. METHODS: Porcine GEA segments (10-12 cm in length) were connected to a computer-controlled perfusion system with a constant in-flow pressure and distal resistance to simulate bypass flow (80-100 ml/min). Norepinephrine (NE; 10(-9) to 10(-5) M) was given in incremental doses at baseline before the vasodilator, immediately after (0 hr), and again at 2 hr after the vasodilator. Changes in flow and ED50 were recorded. Group INT (N = 25) received papaverine (PAP), diltiazem, nifedipine (NFP), or verapamil (VPL) intraluminally, while group EXT (N = 25) received the same dilators externally. RESULTS: All arteries showed dose-dependent vasoconstriction to NE prior to treatment. Immediately after receiving the vasodilator, arteries in both groups (INT and EXT) showed initial protection against NE-induced spasm with the exception of arteries receiving NFD externally. However, at 2 hr, for group INT, only VPL and NFD prevented NE-induced graft spasm (VPL: 40.4 +/- 6.8 ml/min vs 17.9 +/- 3.3 ml/min and NFD: 27.0 +/- 6.5 ml/min vs 13.1 +/- 0.9 ml/min, P < 0.02). In group EXT, after 2 hr, only VPL- and PAP-treated grafts showed resistance to NE-induced vasospasm (VPL: 35.6 +/- 7.3 ml/min vs 15.0 +/- 6.9 ml/min and PAP: 47.4 +/- 15.1 ml/min vs 8.0 +/- 2.0 ml/min, P < 0.001). CONCLUSIONS: Papaverine, a lipophilic vasodilator, when given externally on the perivascular fat of the GEA, prevented graft spasm for up to 2 hr. In contrast, intraluminally applied papaverine did not show graft protection against NE-induced spasm. Nifedipine prevented NE-induced spasm only when given intraluminally. Verapamil proved to be the most potent and versatile vasodilator with effective graft protection of up to 2 hr whether applied externally or internally and was the preferred agent for protecting against GEA spasm.

Sucralfate attenuates gastric mucosal lesions and increased vascular permeability induced by ischaemia and reperfusion in rats.

Recent evidence suggests that oxygen-derived free radicals are involved in mediating gastric microvascular and parenchymal cell injuries induced by ischaemia and reperfusion. Therefore, the effect of the locally acting anti-ulcer drug, sucralfate, was studied on ischaemia and reperfusion (e.g. induced gastric lesions, intraluminal bleeding, changes in vascular permeability and non-protein sulfhydryl levels in the rat stomach). Allopurinol was used as a known standard antioxidant drug. Rats were subjected to 30 min of gastric ischaemia in the presence of 100 mmol/L hydrochloric acid and reperfusion periods of 15, 30 or 60 min duration. The gastric lesions were assessed microscopically under an inverted microscope. The vascular permeability was quantified by measuring the extravasated Evans blue in the stomach. There were significantly greater numbers of gastric lesions, intraluminal bleeding and leakage of Evans blue during all reperfusion periods as compared with those of ischaemia, with maximum effects occurring at 60 min following reperfusion. Pretreatment with sucralfate (31.25-250 mg/kg, p.o.) or allopurinol (12.5-50 mg/kg, i.p.) 30 min before the procedure, dose-dependently reduced the gastric lesions, intraluminal bleeding, and decreased the vascular permeability induced by ischaemia and reperfusion. Furthermore, sucralfate dose-dependently reverses the ischaemia and reperfusion-induced depletion of mucosal non-protein sulfhydryl levels and inhibited the superoxide radical production in both cell-free xanthine-xanthine oxidase and in the stimulated polymorphonuclear cellular systems. These results suggest that the protection produced by sucralfate against gastric injury may be due to its antioxidant effects.

Natural honey prevents ethanol-induced increased vascular permeability changes in the rat stomach.

The effect of honey on ethanol-induced increased vascular permeability changes was studied in the rat stomach. Sucralfate and allopurinol were used as standard gastroprotective and antioxidant drugs, respectively. Extravasation of intravenously administered Evans blue dye into the stomach following 30 min exposure to ethanol was used as an indicator of vascular permeability. The amounts of the extravasated dye were quantified spectrophotometrically. Ethanol produced concentration and time-dependent increase in the extravasation of Evans blue. Oral administration of honey (0.078-0.625 g/kg) 30 min before ethanol dose-dependently attenuated ethanol-induced increased vascular permeability. Pretreatment with a sulfhydryl blocker, N-ethylmaleimide (0.050 g/kg, subcutaneously), caused enhancement of ethanol-induced vascular permeability changes. Treatment with N-ethylmaleimide before honey reduced the protective effects of honey. Similarly, sucralfate (0.031-0.250 g/kg) orally and allopurinol (0.025-0.050 g/kg) intravenously inhibited vascular permeability caused by ethanol and treatment with N-ethylmaleimide before sucralfate or allopurinol reduced their inhibitory effects. These results suggest that the protective effect of honey may be mediated through sulfhydryl-sensitive processes and it may also possess antioxidant properties. It is also suggested that endogenous sulfhydryl may facilate and mediate beneficial effects of gastroprotective and antioxidant drugs.

Enhancement of anti-inflammatory effects of calcium channel blockers by allopurinol and dimethylsulphoxide.

The effects of the calcium channel blockers, nifedipine, verapamil and flunarizine, and the antioxidants, allopurinol and dimethylsulphoxide, were investigated on carrageenan-induced rat paw oedema and changes in vascular permeability. Paw volume was measured by using a plethysmometer and vascular permeability was quantified by measuring the extravasated Evans blue dye 3 h after injecting the phlogistic agent. Intraperitoneal administration of nifedipine (1,2 and 4 mg/kg), verapamil (5, 10 and 20 mg/kg), flunarizine (2.5, 5 and 10 mg/kg), allopurinol (6.25, 12.5 and 25 mg/kg) and dimethylsulphoxide (20, 40 and 80 mg/kg) 30 min before carrageenan, dose dependently inhibited oedema formation and increased vascular permeability. Co-administration of the lowest doses of calcium channel blockers with the lowest doses of antioxidants produced synergistic inhibitory effects. These results indicate that both calcium influx and oxygen-derived free radicals are involved in carrageenan-induced inflammatory responses. Thus, the synergistic effects of their combination may be due to the blockade of calcium entry and reduction in the generation of oxygen-derived free radicals.

Selenium protects against ischemia-reperfusion-induced gastric lesions in rats.

Recent studies have shown that selenium afforded protection against ethanol and stress-induced gastric lesions in rats. The present study was undertaken to investigate the effect of selenium on ischemia-reperfusion-induced gastric injuries in which rats were subjected to 30 minutes of ischemia in the presence of 100 mM HCI and a reperfusion for 60 minutes duration. Intraluminal bleeding was assessed macroscopically and gastric lesions were graded microscopically under an inverted microscope. Nonprotein sulphydryl levels were measured spectrophotometrically. The severity of gastric lesions, intraluminal bleeding as well as the depletion of nonprotein sulphydryls during the reperfusion periods was significantly different from that of control. Pretreatment with selenium (0.125-2.0 mg/kg, intraperitoneally) 30 minutes before the ischemia-reperfusion, dose-dependently attenuated the gastric lesions, reduced the severity of intraluminal bleeding and prevented the depletion of nonprotein sulphydryls in the stomach. These results suggest that the gastric protection effect of selenium may be due to its antioxidant properties. Furthermore, endogenous nonprotein sulphydryls may play a significant role in the protective mechanisms of selenium.

Natural honey prevents ischaemia-reperfusion-induced gastric mucosal lesions and increased vascular permeability in rats.

OBJECTIVE: It has been proposed that natural honey may contain a 'sucralfate-like' substance. Recent studies have shown that sucralfate affords protection against ischaemia-reperfusion-induced injuries in the rat stomach. Therefore, the effect of honey was studied on ischaemia-reperfusion-induced gastric lesions, intraluminal bleeding, vascular permeability and non-protein sulphhydryls (NP-SH) in the rat stomach. METHODS: Rats were subjected to 30 min of gastric ischaemia in the presence of 100 mM HCl and reperfusion period of 60 min. Intraluminal bleeding was assessed macroscopically and the gastric lesions were graded microscopically under an inverted microscope. Vascular permeability was quantified by measuring spectrophotometrically the extravasated Evans blue dye in the stomach. NP-SH levels were measured spectrophotometrically. A luminol-dependent chemiluminescence method was used to assess antioxidant effects of honey in vitro. RESULTS: There were significantly more gastric lesions, more severe intraluminal bleeding, more leakage of Evans blue and depletion of NP-SH during the reperfusion period as compared to controls. Pre-treatment with honey (0.078-0.625 g/kg, orally) or dimethyl sulphoxide (0.02-0.08 g/kg, intraperitoneally) 30 min before the ischaemia-reperfusion dose-dependently reduced the gastric lesions and intraluminal bleeding and decreased the vascular permeability. Furthermore, honey reversed the ischaemia-reperfusion-induced depletion of NP-SH levels and inhibited the luminol-dependent chemiluminescence induced in a cell-free xanthine-xanthine oxidase system. CONCLUSION: These results suggest that gastric protection by honey may be a result of its antioxidant effect. It is suggested that this property of honey may be due to the presence of a 'sucralfate-like' substance.

Variable effects of cardiomyoplasty on left ventricular function.

Cardiomyoplasty (CMP) has been considered as a possible treatment for patients with heart failure. Symptomatic improvements occur almost uniformly among survivors with CMP, but changes in left peak ventricular systolic pressure (PVSP) and stroke volume vary in patients. This study examined whether there is variability present shortly after cardiomyoplasty surgery. Cardiomyoplasty was performed in 11 mongrel dogs with normal ventricular function. Nine to twelve days after CMP, left ventricular (LV) function was evaluated by simultaneously measuring LV volume (conductance catheter) and pressure (Millar catheter). The latissimus dorsi muscle (LDM) was stimulated synchronously with ventricular systole in a ratio of 1:4 to 1:7 to avoid muscle fatigue. Data were analyzed on a beat by beat basis. The PVSP, and maximum dP/dt (+dP/dt) increased, but the absolute value of minimum dP/dt (-dP/dt) decreased in stimulated beats in 7 dogs while 4 dogs did not respond. The net changes in stimulated beats versus nonstimulated beats of PVSP were 6.1 +/- 1.8 mm Hg (4.3%), of stroke work was 4.5 +/- 1.9 gm x m (29.5%), of +dP/dt was 185 +/- 47 mm Hg/s (8%), and of -dP/dt was 168 +/- 43 mm Hg/s (7.8%) (p < 0.05) for all these net changes in the responding group while these variations were not significant in the nonresponding group. From the results of our study, active LDM assist improves left ventricular systolic function, occurring in only 7 of 11 experiments. This improvement is inconsistent and varied individually. The integrity of the LDM, tightness of wrapping, and adhesions might contribute to the variability which is present early after surgery and before the LDM is converted into a fatigue resistance muscle.