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Biomedical subjects

Y Shapira

Publications and source records attributed to Y Shapira.

At least 73 records · Page 4Linked to original sources
PubMed1999

Albumin or hetastarch improves neurological outcome and decreases volume of brain tissue necrosis but not brain edema following closed-head trauma in rats.

The present study examined whether hemodilution with 20% human serum albumin (HSA) or 10% hydroxyethyl starch (HES) improved the outcome from closed-head trauma (CHT) in rats. Rats anesthetized with halothane were given one of three hemodilution solutions (i.e., 20% HSA, 10% HES, or control [0.9% saline]) after CHT or sham surgery. CHT was delivered using a weight drop impact of 0.5 J onto the closed cranium. The hemodilution solution (volume = 1% of body weight) was given just after determining the neurological severity score (NSS) at 1 hour following CHT. The NSS was determined again at 24, 48, and 72 hours following CHT. At 72 hours, brains were removed, and brain edema and brain tissue necrosis volume were determined. Solutions of 20% HSA and 10% HES significantly improved brain tissue necrosis volume (143 +/- 72 mm3 and 104 +/- 53 mm3 as compared to 271 +/- 65 mm3 in controls, mean +/- SD) and NSS (12 +/- 2 and 9 +/- 2 as compared to 15 +/- 2 in controls at 72 hours, median +/- range) but not brain edema. The hematocrit decreased similarly in all groups during hemodilution. Hemodilution with 20% HSA and 10% HES following CHT in rats did not decrease brain edema but did decrease brain tissue necrosis volume and NSS (improved neurological function), suggesting that the beneficial effect of hemodilution resulted not from decreased edema formation but rather from effects not measured in this study such as improved perfusion of the salvageable brain tissue surrounding the core injury.

Animals↗
PubMed1999

Tricuspid regurgitation late after mitral valve replacement: clinical and echocardiographic evaluation.

BACKGROUND AND AIM OF THE STUDY: Significant tricuspid regurgitation (TR) can contribute to increased morbidity and mortality in patients after mitral valve replacement (MVR), both in the immediate and late postoperative period. The aim of this study was to evaluate the prevalence and the clinical importance of TR late after MVR, as assessed both clinically and echocardiographically. METHODS: The study group comprised 65 patients (39 women, 26 men; mean age 61+/-12 years) with rheumatic heart disease who had undergone MVR without tricuspid valve surgery between one and 30 years (mean 11.3+/-8 years) before their last clinical examination. All patients underwent a complete color-Doppler echocardiographic examination. The predominant presurgical mitral lesion was stenosis in 44 patients and regurgitation in 21. The severity of the tricuspid valve disease was assessed echocardiographically using color-Doppler flow images and flow direction in the inferior vena cava or hepatic veins, and by clinical evaluation. RESULTS: Echocardiography revealed significant late TR in 44 patients (67%), which was moderate in 16 and severe in 28, and evident on physical examination in 24 cases (37%). Age (relative risk (RR) = 1.1; C.I. 1-1.1) and female sex (RR = 1.8; C.I. = 1.0-3.2) were identified as statistically significant predictors for late clinical TR development, but only age was found as a statistically significant predictor for echocardiographic TR development. An elevated RR for organic TR and predominant mitral regurgitation was found. In contrast, pre- and postoperative pulmonary artery pressure, predominant mitral lesion, prosthetic valve gradient and regurgitation were similar in patients with and without late TR. CONCLUSIONS: Significant TR diagnosed by echocardiography late after MVR is common, and clinically evident in more than one-third of patients. Therefore, a lower threshold for tricuspid valve repair should be considered when mitral valve surgery is carried out.

Aged↗
PubMed1998

Mitral annular calcium detected by transthoracic echocardiography is a marker for high prevalence and severity of coronary artery disease in patients undergoing coronary angiography.

This study tests the hypothesis that mitral annular calcium (MAC) detected by transthoracic echocardiography (TTE) is a marker for high prevalence and severity of coronary artery disease (CAD) in patients undergoing coronary angiography. Pathological studies have suggested that there is an association between MAC and calcific deposits in coronary arteries; however, there are no clinical data to support this association. One hundred sixty-five patients with MAC (101 women and 64 men; mean age 71 +/- 8 years) who underwent cardiac catheterization with coronary angiography for various reasons were compared with 147 age-matched controls without MAC who underwent coronary angiography for the same indications during the same period. MAC was defined as a dense, localized, highly reflective area at the base of the posterior mitral leaflet detected by TTE. Obstructive CAD was defined as either > or = 50% reduction of the internal diameter of the left main coronary artery or > or = 70% reduction of the internal diameter of the left anterior descending, right coronary, or left circumflex artery distribution. Compared with controls, the MAC group had a significantly higher prevalence of CAD (89% vs 75%, p = 0.001) and higher rates of 3-vessel disease (45% vs 24%, p = 0.001) and left main CAD (13% vs 5%, p = 0.009). Nonsignificant CAD was more common in the control group (25% vs 11%, p = 0.001). Multivariate analysis identified MAC (p = 0.0002), indications for cardiac angiography (p = 0.02), sex (p = 0.03), and diabetes mellitus (p = 0.03) as independent predictors for the presence and severity of obstructive CAD. MAC detected by TTE may be a marker for high prevalence and severity of CAD in patients undergoing coronary angiography.

Adult↗
PubMed1998

SMA type 2 unrelated to chromosome 5q13.

We describe two brothers with clinical and histological findings of type 2 spinal muscular atrophy (SMA) associated with small head circumference (<2%) and normal cognitive development. No survival motor neuron (SMN) or neuronal apoptosis-inhibitory protein (NAIP) deletions were detected in these sibs, and they were discordant for the haplotypes determined by DNA markers flanking the 5q13 SMA locus. These findings support the presence of a distinct anterior horn disease unrelated to 5q13. This entity may have either autosomal recessive or X-linked inheritance.

Child, Preschool↗
PubMed1998

Labetalol-induced hypotension decreases blood loss during uncontrolled hemorrhage.

In a model of uncontrolled hemorrhagic hypotension (UCHH) in rats, we examined whether blood loss or blood chemistry were affected by (1) deliberate, controlled hypotension induced with labetalol (L) or sodium nitroprusside (SNP) and (2) intravenous (iv) fluid therapy. Two hours of UCHH was induced by resecting the distal 25% of the tail. L or SNP was infused with the aim of decreasing MAP to 50 mmHg. In the groups receiving iv fluid, 3 ml of 0.9% saline was given for each 1 ml of blood loss. L decreased blood loss (2.8+/-2.0 and 3.0+/-1.9 ml, respectively, in the groups not receiving and receiving iv fluid) compared to the groups not given hypotensive drugs (6.3+/-4.1 and 13.5+/-6.6 ml). SNP did not decrease blood loss (5.7+/-4.7 and 11.0+/-6.2 ml), increased serum potassium (5.0+/-0.6 and 5.8+/-0.4 mEq l(-1)), and with accompanying iv fluid administration decreased hematocrit, worsened acidosis, and increased mortality. In this model of 2 h of UCHH in rats, hypotension to MAP of 50 mmHg with L but not with SNP decreased blood loss.

Animals↗
PubMed1998

Evaluation of tricuspid regurgitation severity: echocardiographic and clinical correlation.

The correlation between 19 echocardiographic markers of tricuspid regurgitation (TR) severity and findings on physical examination was studied in 66 consecutive patients (age 63 +/- 12 years) with moderate or severe TR. Clinical TR was defined by two or more of the following: prominent jugular venous pulse V waves, pulsating liver, and sea-saw parasternal movement. Thirty-eight patients (57.6%) had clinical TR, whereas 28 patients (42.4%) did not. In a univariate analysis, the most powerful predictors of clinical TR (p < 0.01) were jet area > or =9 cm2, right atrial area > or =30 cm2, jet width at origin > or =0.8 cm, systolic flow reversal in the hepatic veins, paradoxical septal movement, diastolic septal flattening, inferior vena cava diameter > or =2.1 cm, and lack of inferior vena cava respiratory variation. Regurgitant index was a weaker predictor. Multivariate analysis showed that the only independent echocardiographic predictor of clinical TR was systolic flow reversal (positive and negative predictive values 91.2% and 78.1%, respectively). Significant echocardiographic TR can be subclinical in a substantial number of patients.

Adult↗
PubMed1998

Uprighting mesially impacted mandibular permanent second molars.

Impaction of permanent teeth is a relatively common occurrence and can involve any tooth in the dental arch. Impacted mandibular second molars are relatively rare, but when they occur they may present a clinical problem for the orthodontist and oral surgeon. A typical case of bilaterally impacted mandibular second molars is illustrated, with orthodontic and surgical treatment options presented. Emphasis is placed on early diagnosis and initiation of corrective orthodontic therapy.

Child↗
PubMed1998

0.45% saline and 5% dextrose in water, but not 0.9% saline or 5% dextrose in 0.9% saline, worsen brain edema two hours after closed head trauma in rats.

UNLABELLED: In this study, we examined the effect of four i.v. fluids (250 mL/kg) on blood glucose and osmolality and brain tissue specific gravity after closed head trauma (CHT) in rats. CHT was delivered at Time 0; blood was sampled at 60 min; fluid infusion began at 75 min and ended at 105 min. Blood was again sampled at 105 and 120 min, and brain tissue specific gravity was determined at 120 min. Five groups (one control and four fluid-treated groups) received CHT, and five other groups (one control and four fluid-treated) did not (n = 9 in each group). 0.45% saline (1/2 NS) and 5% dextrose in water (D5W) accentuated the decrease of brain tissue specific gravity (1.0366 +/- 0.0025 and 1.0368 +/- 0.0028, respectively; mean +/- SD) caused by CHT (1.0395 +/- 0.0036), but 5% dextrose in 0.9% saline (D5NS) and 0.9% saline (NS) did not (1.0431 +/- 0.0042 and 1.0389 +/- 0.0049, respectively). In addition, 1/2 NS decreased blood osmolality (248 +/- 6 mOsm/L), D5W increased blood glucose (1095 +/- 173 mg/dL), D5NS increased blood osmolality (350 +/- 5 mOsm/L) and glucose (1695 +/- 76 mg/dL), and NS caused no significant change. We conclude that administering hypoosmolar i.v. fluids after CHT causes a significant worsening of cerebral edema 2 h after CHT. IMPLICATIONS: We previously reported worse neurological outcome and/or mortality after closed head trauma in rats when 5% dextrose in water or 0.45% saline was given i.v. compared with 0.9% saline or 5% dextrose in 0.9% saline. The present results and our previous findings indicate that worsening of outcome after closed head trauma in rats may be caused more by edema formation than by hyperglycemia.

Analysis of Variance↗
PubMed1998

Ketamine attenuates the interleukin-6 response after cardiopulmonary bypass.

UNLABELLED: Cardiopulmonary bypass (CPB) has been proposed as a model for studying the inflammatory cascade associated with the systemic inflammatory response syndrome. Serum interleukin-6 (IL-6) concentration seems to be a good indicator of activation of the inflammatory cascade and predictor of subsequent organ dysfunction and death. Prolonged increases of circulating IL-6 are associated with morbidity and mortality after cardiac operations. In the present study, we compared the effects of adding ketamine 0.25 mg/kg to general anesthesia on serum IL-6 levels during and after elective coronary artery bypass grafting (CABG). Thirty-one patients undergoing elective CABG were randomized to one of two groups and prospectively studied in a double-blind manner. The patients received either ketamine 0.25 mg/kg or a similar volume of isotonic sodium chloride solution in addition to large-dose fentanyl anesthesia. Blood samples for analysis of serum IL-6 levels were drawn before the operation; after CPB; 4, 24, and 48 h after surgery; and daily for 6 days beginning the third day postoperatively. Ketamine suppressed the serum IL-6 response immediately after CPB and 4, 24, and 48 h postoperatively (P < 0.05). During the first 7 days after surgery, the serum IL-6 levels in the ketamine group were significantly lower than those in the control group (P < 0.05). On Day 8 after surgery, IL-6 levels were no different from baseline values in both groups. A single dose of ketamine 0.25 mg/kg administered before CPB suppresses the increase of serum IL-6 during and after CABG. IMPLICATIONS: In this randomized, double-blind, prospective study of patients during and after coronary artery bypass surgery, we examined whether small-dose ketamine added to general anesthesia before cardiopulmonary bypass suppresses the increase of the serum interleukin-6 (IL-6) concentration. Serum IL-6 levels correlate with the patient's clinical course during and after coronary artery bypass. Ketamine suppresses the increase of serum IL-6 during and after coronary artery bypass surgery.

Aged↗
PubMed1998

Phenylephrine-induced hypertension does not improve outcome after closed head trauma in rats.

UNLABELLED: Phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) is reported to increase cerebral perfusion pressure and collateral flow to ischemic areas of the brain in a rat model of focal cerebral ischemia. In the present study, we examined whether phenylephrine-induced hypertension of similar magnitude and duration was beneficial in a rat model of closed head trauma (CHT). Forty-eight rats were randomized into four experimental conditions: CHT at time 0 min (yes/no), plus phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) at 65 min (yes/no). CHT was delivered using a weight-drop device (0.5 J). Outcome measures were neurological severity score (NSS) at 1, 4, and 24 h, and brain tissue specific gravity (microgravimetry) and injury volume (2,3,5-triphenyltetrazoium chloride) at 24 h. After CHT, NSS at 24 h (median +/- range) and brain tissue specific gravity (mean +/- SD, injured hemisphere) were 7+/-2 and 1.033+/-0.007 without phenylephrine and 8+/-2 and 1.035+/-0.005 with phenylephrine (P = 0.43), respectively. Tissue injury volume (mean +/- SD) was 335+/-92 mm3 without phenylephrine and 357+/-154 mm3 with phenylephrine (P > 0.62). The results of our study indicate that postinjury treatment with 15 min of phenylephrine-induced hypertension does not attenuate brain edema, reduce tissue injury volume, or improve neurological outcome after CHT in rats. IMPLICATIONS: Phenylephrine-induced hypertension is reported to increase cerebral perfusion pressure and blood flow in a rat model of focal cerebral ischemia. In our study, phenylephrine-induced hypertension did not decrease brain edema or tissue injury volume or improve neurological outcome in a rat model of closed head trauma.

Animals↗
PubMed1998

Effects of closed head trauma and lipopolysaccharide on body temperature, brain tissue water content, and PGE2 production in rats.

Closed head trauma (CHT) increases brain tissue prostaglandin E2 (PGE2) concentration, and that increase is associated with cerebral edema formation and worsening of the neurologic severity score (NSS). Injection of the bacterial endotoxin lipopolysacharride (LPS) increases cerebral and hypothalamic PGE2, and the hypothalamic increase is associated with increased body temperature. The present study determined (a) whether LPS-induced increase of PGE2 causes brain edema or worsens NSS and (b) whether CHT increases hypothalamic PGE2 and thereby increases body temperature. Halothane-anesthetized rats were divided into four groups: group 1 = surgery with no CHT and no LPS (n = 8); group 2 = surgery with LPS and no CHT (n = 8); group 3 = surgery with CHT and no LPS (n = 8); and group 4 = surgery with CHT plus LPS (n = 8). NSS was determined at 1 and 24 h after injury, and brain tissue PGE2 and edema were determined when animals were killed 24 h after injury. As compared with group 1, LPS alone, but not CHT or CHT plus LPS, increased rectal temperature. CHT and CHT plus LPS, but not LPS alone increased brain water content and worsened NSS. LPS, CHT, and CHT plus LPS all increased hypothalamic and cerebral PGE2 production. We conclude that although LPS and CHT increased PGE2 levels, LPS alone did not affect neurologic status or brain edema, CHT did not increase rectal temperature, and addition of LPS to CHT did not aggravate the sequelae of CHT.

Animals↗