[First stage in identifying traumatic profil inpatients hospitalised in psychiatry in Martinique]. / Premières identifications d'un profil traumatique chez des patients hospitalisés en psychiatrie en Martinique.

The population hospitalised in psychiatry seems more exposed to traumatic events than the French general population, with particularly more sexual aggressions. The aim of this study is to describe the population hospitalised in psychiatry and more precisely the traumatic history of these patients, their comorbidities (mental diseases and addictions), and socio economical level. This descriptive, cross sectional and retrospective study took place in the Crisis Center in the University Hospital in Martinique (French West Indies), from February to July 2013. A socio-demographic information, the Mini International Neuropsychiatric Interview 5.0, the Trauma History Questionnaire and the Impact Events Scale-Revised were realised with 49 of the 143 patients admitted during this period (34.3%). In this population, we found a mean of 6.5 (standart-deviation=4.2) different types of traumatic event, with 38.8% patients reporting a natural disaster, and 38.8% declaring at least one sexual aggression. In the 25 patients suffering from post-traumatic stress disorder, 66.7% underwent a sexual aggression, significatively during childhood (before 10 years old, P=0.01), and during adolescence (between 10 to 18 years old, P=0.01). These results underline the importance of a systematic screening of the traumatic profile: the characteristics of the traumatic events and its clinical impact.

Antihypertensive drugs in the stroke-prone spontaneously hypertensive rat.

The stroke-prone spontaneously hypertensive rat (SHR-SP) is an experimental model that has been widely used to investigate the potential preventive effects vs stroke and mortality of numerous antihypertensive agents. Among the latter, angiotensin I-converting enzyme inhibitors, angiotensin II AT1-receptor blockers and calcium antagonists have proven to be very effective. The mechanisms involved in their beneficial effects include limitation of the age-related alterations of large cerebral arteries' functional parameters, prevention of fibrinoid necrosis formation in cerebral arterioles and, to a lesser extent, limitation of the blood pressure rise.

Effects of losartan on cerebral arteries in stroke-prone spontaneously hypertensive rats.

OBJECTIVE: To investigate in young salt-loaded stroke-prone spontaneously hypertensive rats (SHR-SP) the effects of a long-term administration of the angiotensin II AT1 receptor antagonist losartan [1 mg/kg (L1) and 10 mg/kg (L10) per day, from 5 to 20 weeks of age] on the structural and functional characteristics of the middle cerebral artery. METHODS: Morphological measurements and isometric tension recordings (myograph, contractile responses to potassium chloride and serotonin, relaxant responses to bradykinin and sodium nitroprusside) were performed on isolated vessels from randomly selected control and losartan-treated SHR-SP and age-matched Wistar-Kyoto (WKY) rats killed at ages 6-7, 10-11 and 16-17 weeks. RESULTS: Whereas all control SHR-SP had died within 18 weeks of being born, losartan at both doses afforded full protection against stroke and mortality. Losartan limited malignant hypertension development dose-dependently. Age-related increases in cerebral arterial wall thickness and wall:lumen ratio were not affected (L1) or limited slightly (L10) by losartan. In control SHR-SP, contractile responses of cerebral arteries to agonists decreased with ageing and stroke occurrence and were significantly smaller than those of age-matched WKY rat arteries. Losartan limited the cerebrovascular contractility impairment dose-dependently in SHR-SP but did not affect the WKY rat cerebral artery contractility. In addition, losartan limited the age-related alteration of the endothelium-dependent relaxation of cerebral arteries observed in control SHR-SP dose-dependently. CONCLUSIONS: In SHR-SP, losartan prevented stroke and improved the cerebral artery's smooth muscle and endothelial cell functions, which are altered during ageing and impaired even more dramatically by stroke occurrence.

Mibefradil, a selective calcium T-channel blocker, in stroke-prone spontaneously hypertensive rats.

Several types of antihypertensive agents, including calcium antagonists, have been reported to prevent stroke and prolong survival in stroke-prone spontaneously hypertensive rats (SHR-SP). We investigated whether mibefradil, a new calcium antagonist acting selectively at the level of T-type calcium channels, would be able to (a) limit or prevent the structural and functional alterations that develop in the cerebral arteries of SHR-SP before stroke and (b) suppress stroke and prolong survival. Mibefradil (30 mg/kg/day) was given orally to young salt-loaded SHR-SP from age 5 weeks to age 20 weeks. Blood pressure (BP) (in conscious animals), diuresis, and proteinuria were determined weekly. After 1012 weeks of treatment, middle cerebral arteries and aortas were removed from randomly selected control and treated SHR-SP. Aortic media thickness and collagen density were evaluated by histomorphometry. Middle cerebral arteries were mounted in a myograph for wall thickness determination and isometric tension recordings. Mibefradil completely prevented stroke and mortality, significantly limited the increase in BP, and opposed the increases in diuresis and proteinuria observed in controls. Simultaneously, mibefradil abolished vascular fibrinoid necrosis formation in the brain and reduced arterial thickening in the cerebral artery as well as in the aorta. The maximal contractile responses of the cerebral arteries to potassium chloride and serotonin were greater in mibefradil-treated animals than in controls, as were the endothelium-dependent relaxant responses. Mibefradil, chronically administered to young SHRSP in a dose that limits the development of hypertension not only prevents stroke and mortality but also affords protection against the vascular structural alterations which develop with age in these animals and preserves or improves the cerebral artery's smooth muscle and endothelial cell functions.

Early and late haemodynamic and morphological effects of angiotensin II subtype 1 receptor blockade during genetic hypertension development.

OBJECTIVE: To investigate the haemodynamic and morphological effects resulting from the chronic administration to young spontaneously hypertensive rats (SHR) of a new selective angiotensin II subtype 1 (AT1) receptor antagonist, SR 47436/BMS-186295 (SR/BMS) both during and after the treatment period. METHODS: SR/BMS (60 mg/kg per day, orally) or distilled water was chronically (from 4 to 20 weeks of age) administered to SHR. At age 8, 14, 20 and 28 weeks the effects of SR/BMS on the systemic and regional haemodynamic (radioactive microsphere technique) and the cardiac and vascular morphological parameters (automatic image analysis) were investigated. RESULTS: SR/BMS limited genetic hypertension development and opposed the age-related rises in total peripheral and regional vascular resistances. Simultaneously, it limited the age-related increases in heart weight, left ventricular cross-sectional area and collagen content. Age-related increases in aortic media thickness and amount of collagen were also significantly reduced, whereas aortic compliance was increased. Eight weeks after withdrawal of treatment the antihypertensive effect of SR/BMS, although attenuated, and the limitation of cardiac and vascular remodelling, persisted. CONCLUSIONS: Early AT1 receptor blockade in SHR opposes genetic hypertension development during the treatment period and persistently after its interruption. Prevention of genetic hypertension development during the treatment period can be accounted for by the limitation of the age-related development of the haemodynamic and morphological abnormalities, whereas the persistence of the antihypertensive effect observed after drug withdrawal is due mainly to a maintained prevention of the development of the cardiovascular morphological alterations.

Are vasopressin peripheral V1 receptors involved in the development of malignant hypertension and stroke in SHR-SPs?

The aim of this study was to determine whether activation of vasopressin (AVP) peripheral V1 receptors is involved in the development of malignant hypertension, stroke, and end-organ damage in stroke-prone spontaneously hypertensive rats (SHR-SPs). For this purpose, young salt-loaded SHR-SPs were treated orally daily from their 5th to 34th week of age, by a selective AVP V1 receptor antagonist, SR 49059, used in a dose (30 mg/kg) that achieved complete peripheral V1 receptor blockade. Untreated SHR-SPs served as controls. SR 49059 slightly and transiently (8th to 10th week of age) limited the rise in blood pressure, but thereafter systolic blood pressure values were similar in the two groups of SHR-SPs. Stroke-related mortality was not significantly different in SR 49059-treated and in control animals (65% vs 65% at 30 weeks, 65% vs 83% at 34 weeks). SR 49059 did not prevent the increases in fluid intake, diuresis and proteinuria seen in controls. Histological examination of the brain, kidneys and heart revealed that the development of fibrinoid necrosis and arterial thickening was not prevented by SR 49059, nor was that of malignant nephroangiosclerosis and of myocardial infarction and fibrosis. These data strongly suggest that AVP peripheral V1 receptor activation is not involved in the pathological processes that develop in SHR-SPs.

Trandolapril's protective effects in stroke-prone spontaneously hypertensive rats persist long after treatment withdrawal.

The effects of long-term oral administration of the angiotensin-converting enzyme (ACE) inhibitor trandolapril (0.01 mg/kg [T0.01] and 1 mg/kg [T1]) on the occurrence of stroke and on mortality were investigated in young salt-loaded stroke-prone spontaneously hypertensive rats during the treatment period (5-20 weeks of age) and up to 8 weeks thereafter. During the treatment period T1, but not T0.01, limited the increase in blood pressure. However, both doses of trandolapril prevented stroke and mortality and strongly opposed (T0.01) or abolished (T1) the increases in saline intake, diuresis, and proteinuria observed in control animals. Simultaneously, trandolapril markedly prevented (T0.01) or abolished (T1) vascular fibrinoid necrosis formation in the brain, kidney, and heart. Finally, trandolapril dose-dependently reduced arterial thickening and glomerular and tubulointerstitial lesions in the kidney, as well as arterial thickening, infarction, and fibrosis in the myocardium. At 8 weeks after treatment withdrawal, the antihypertensive effect of T1 had disappeared, but stroke-related mortality and fibrinoid necrosis remained completely suppressed. Further, no additional cerebral, renal, or cardiac lesions developed, and no increase in proteinuria occurred. In the T0.01 group, 17% of the animals died, fibrinoid necrosis tended to develop, organ lesions worsened, and proteinuria strongly increased. We conclude that (1) early ACE inhibition with trandolapril affords a long-lasting protection versus stroke and mortality both during and after the treatment period; and (2) that this beneficial effect is due to the suppression of fibrinoid necrosis formation and not to the drug's antihypertensive action. In contrast, both properties appear to contribute to trandolapril's renal and cardiac protective effects.

Quinapril prevents stroke both during and after the treatment period in stroke-prone spontaneously hypertensive rats.

The effects of long-term oral administration of quinapril on the occurrence of stroke and on mortality were investigated in young salt-loaded stroke-prone spontaneously hypertensive rats (SHR-SPs) during the treatment period (8th-34th week of age) and up to 6 weeks thereafter. Simultaneously, blood pressure, saline intake, diuresis, and proteinuria were investigated at regular intervals, and cerebrovascular, renal, and cardiac lesions were assessed after death. Untreated SHR-SPs served as controls. Quinapril completely suppressed stroke and mortality, afforded only limited protection v blood pressure rise, and prevented any increase in saline intake, diuresis, and proteinuria both during and after the treatment period. Quinapril long-lastingly prevented vascular fibrinoid necrosis development at the cerebral, but also at the renal and cardiac levels. In the kidneys, vascular intimal and medial hyperplasia were strongly reduced, as were the glomerular and tubulo-interstitial lesions. At the cardiac level, intimal and medial hyperplasia were slightly reduced but infarction and fibrosis were hardly affected. As the renin-angiotensin system is highly stimulated in SHR-SPs and as angiotensin II (AII) is responsible for fibrinoid necrosis formation, vessel obstruction, and stroke in these animals, we conclude that the long-lasting protection afforded by quinapril v stroke and mortality in SHR-SPs both during and after the treatment period is mostly due to the drug-induced interruption of the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)

Losartan's protective effects in stroke-prone spontaneously hypertensive rats persist durably after treatment withdrawal.

The effects of long-term oral administration of losartan on the occurrence of stroke and on mortality were investigated in young salt-loaded stroke-prone spontaneously hypertensive rats (SHR-SPs) during the treatment period (5-20 weeks of age) and up to 8 weeks thereafter. Two doses of losartan, 1 and 10 mg/kg/day, were investigated, which afforded no and only moderate antihypertensive effects, respectively. During the treatment period, losartan at both doses completely suppressed stroke and mortality and strongly opposed (low dose) or abolished (high dose) the increases in saline intake, diuresis, and proteinuria observed in controls. It markedly limited (low dose) or abolished (high dose) vascular fibrinoid necrosis formation in the brain, kidneys, and heart. Finally, losartan, especially at the high dose, reduced arterial thickening and glomerular and tubulo-interstitial lesions in the kidneys, as well as arterial thickening, infarction, and fibrosis in the heart. Eight weeks after treatment discontinuation, all animals but one (low dose) were still alive. Vascular fibrinoid necrosis development remained strongly prevented (low dose) or fully suppressed (high dose) in all investigated organs. Finally, cardiac and renal lesions tended to worsen, and proteinuria was noted only in the low-dose group. We conclude that in SHR-SPs, angiotensin II, through AT1 receptor stimulation, most likely plays a major role in fibrinoid necrosis formation, vascular proliferative changes, and stroke occurrence and that losartan, most likely independently of its effect on blood pressure, affords a full and long-lasting protection against stroke and mortality both during and after the treatment period.

Continuous spinal anesthesia: does low-dose plain or hyperbaric bupivacaine allow the performance of hip surgery in the elderly?

OBJECTIVES: This study was designed to assess the predictability of 5 mg bupivacaine to give a T10 sensory level when injected subarachnoid in elderly patients. METHODS: Sixty-five patients aged 75 years or more, scheduled to undergo elective hip surgery, participated in the study. Patients were randomized to receive either 5 mg plain bupivacaine without epinephrine (isobaric group), or 5 mg hyperbaric bupivacaine (hyperbaric group). A 19-gauge catheter was inserted at the L3-4 interspace and threaded 4 cm cephalad in the subarachnoid space. Patients were placed in supine horizontal position and sensory level was assessed every 5 minutes over 20 minutes. Increments of 2.5 mg bupivacaine were given when sensory level did not reach T10 at the 20th minute. RESULTS: After 20 minutes, the mean sensory level was T8.8 +/- 3.2 in the isobaric group and T7.2 +/- 4.3 in the hyperbaric group without significant difference. Hypotension, defined as greater than a 25% drop in mean arterial pressure, was not significantly different in the two groups: 37.5% and 42.4%, respectively. However, patients who developed hypotension were older (84.3 +/- 7.8 years) than the others (80.3 +/- 5.9 years), and cephalad spread of sensory anesthesia was higher in patients who developed a hypotension (T5.3 +/- 1.4 versus T9.5 +/- 4). In each group, sensory levels did not reach T10 in five patients after initial dose. Five had a sensory block that was too low in spite of incremental doses with the patient in the horizontal position. For the last three, an unintentional sacral placement of the catheter was proved radiologically. CONCLUSIONS: The authors conclude that 5 mg bupivacaine is too high a dose in the elderly to limit the sensory blockade at T10 and avoid hypotension. In elderly patients, this dose allowed surgery to be performed, provided that the sensory level reached T10. When the initial dose only affects lumbar dermatomes, a caudal direction of the catheter must be evoked, and changing position must be preferred to incremental injections to reach thoracic levels.