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In 52 patients with acquired heart disease haemodynamic effects of 0,2 mg/kg and 1,0 mg/kg morphine were investigated during surgical procedures under neuroleptanalgesia. The following parameters were measured or calculated: heart rate (HR), arterial pressure (Part, Psyst, Pdiast), pulmonary artery pressure (PAP), right (PRA) and left atrial pressure (PLA), left ventricular pressure (PLV), left ventricular end-diastolic pressure (PLVED), left ventricular peak dp/dt (dp/dtmax), cardiac output (CO), cardiac index (CI), stroke volume (SV), stroke index (SI), total systemic resistance (TSR), total pulmonary resistance (TPR), work index of the right (RVWI) and left ventricle (LVWI). Myocardial oxygen consumption (EG) was calculated according to the method of Bretschneider. There was almost no change in cardiac index and stroke index. In comparison to a control group (n=36) morphine caused a dose-dependent decrease in arterial pressure and in arterial perfusion pressure during extracorporeal circulation. This, however, was mainly attributable to vasodilatation and not to a negative inotropic effect. In accordance with the changes in haemodynamics there was a remarkable decrease in myocardial oxygen consumption (EG: -21.1%; 1,0 mg/kg morphine).
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PMID:[Haemodynamic effects of morphine in man (author's transl)]. 728 4

The influence of Pb exposure on blood pressure was investigated in Wistar Kyoto, Sprague Dawley and stroke prone spontaneously hypertensive rats. In short-term experiments, a dose-dependent decrease of blood pressure was found with administration of Pb acetate in drinking fluid. This effect was more pronounced in young, male as compared to old, female animals. Pressor responses to noradrenaline and ANG II were decreased. In contrast, long-term Pb exposure of more than 1 year duration consistently caused hypertension. In SHR-sp a high proportion of animals died from cerebrovascular haemorrhage even before developing hypertension. Chronically Pb exposed hypertensive rats had increased plasma volume and total body sodium despite normal renal function. Plasma concentrations of catecholamines and PRA were normal. The results show a biphasic effect of Pb on blood pressure. An important role of renal sodium retention in chronic Pb-induced experimental hypertension is suggested.
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PMID:Chronic lead exposure in rats: effects on blood pressure. 837 62

A major variable in the cost of kidney transplants is the length of initial hospitalization. Using multivariate analysis, we studied risk factors for hospital stay > 10 d post-transplant. Between 1 January 1985 and 31 August 1995 a total of 1588 patients underwent first or second kidney transplants at the University of Minnesota. Antibody was used for 1 wk in cadaver donor recipients and for 2 wk in pediatric recipients (resulting in a long stay for all pediatric recipients). Adult living related donor recipients were immunosuppressed with triple therapy. Donor risk factors studied were age (< 15, 15-50, > 50 yr) and,- for cadaver recipients, preservation time (< 12, 12-18, 18-24, 24-30, > 30 h) and cause of death (trauma, cerebrovascular accident, or cardiac). Recipient risk factors studied were age (< 18, 18-55, > 55 yr); sex; transplant number; antigen mismatch; peak PRA; PRA at transplant (< 11, 11-50, > 50); diabetic status; pretransplant dialysis (vs. pre-emptive transplant); pretransplant cardiac, peripheral vascular, or respiratory disease; and delayed graft function (DGF) (dialysis in the first week vs. no dialysis). Risk factors were analyzed separately for living donor and cadaver donor recipients. For cadaver donor recipients, DGF was the major risk factor (p < 0.0001); others were age 55 yr (p = 0.03) and diabetes (p = 0.02). For living donor recipients, DGF was also a risk factor (p = 0.003); others were diabetes (p = 0.01), retransplant (p = 0.006), PRA at transplant > 50 (p < 0.0001), age > 55 yr (p = 0.02), pretransplant respiratory disease (p = 0.005), and pretransplant dialysis (p = 0.005). Because DGF was the major risk factor for a prolonged stay, we then studied risk factors for DGF using multivariate analysis. For cadaver donor recipients, risk factors were recipient weight > 90 kg (p = 0.004), preservation time 24 h (p = 0.03), PRA at transplant > 50 (p = 0.03), and donor age < 15 or > 50 yr (p = 0.002). For living donor recipients, risk factors were recipient age < 18 yr (p = 0.01), donor age > 50 yr (p = 0.03), female sex (p = 0.05), pretransplant respiratory disease (p = 0.1), pretransplant peripheral vascular disease (p = 0.05), and recipient weight > 90 kg (p = 0.1). From our data, a profile emerged of recipients likely to have a longer hospital stay. Important variables, either simultaneous with or related to DGF, include donor and recipient age, diabetes, pretransplant recipient weight, PRA at transplant, preservation time, and pretransplant respiratory or peripheral vascular disease.
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PMID:Risk factors for prolonged hospitalization after kidney transplants. 926 12

1. GENERAL: Here we updated our analysis of the UNOS Kidney Registry for the compound effects of 26 transplantation factors on graft survival within 2 consecutive posttransplantation risk periods. During the early risk period, 83,867 kidney-only recipients were followed through one year, and, in the second (chronic) risk period, 66,358 recipients whose grafts survived beyond one year were followed for 5 years after transplantation. 2. SHORT-TERM EFFECTS: From the analysis, the top (< 2% of assignable variation) factors influencing one-year graft survival rates were ranked as follows: 1) living-related and living-unrelated donor transplants were preferred; 2) some transplant centers had outstanding results; 3) kidneys from stroke victims displayed poor results; 4) recipients with PRA > 80% demonstrated poor survival; 5) patients transplanted before 1991 had poor results; 6) increasing numbers of HLA-ABDR mismatches decreased survival; 7) cold ischemia times beyond 24 hours diminished survival; 8) kidneys from younger and older donors impaired survival; 9) regrafting was detrimental, 10) Asians and Hispanics enjoyed superior results; 11) recipients with restricted activities pretransplantation were at higher risk of early graft failure; and 12) high (> 30 kg/m2) body mass recipients demonstrated lowered rates. 3. LONG-TERM EFFECTS: Fewer net factors influenced graft survival beyond 1 year through 5 years. The following 9 factors, each explaining > 2% of the assignable variation in conditional 5-year graft survival, were ranked and yielded poor results: 1) older (> 65) donors; 2) Black recipients; 3) poor transplant centers; 4) male recipients; 5) kidneys from cadaver or living parental donors; 6) transplantation prior to 1991; 7) stroke donors; 8) non-zero HLA-AB mismatched transplants; and 9) teenage recipients. 4. IMPACT ON KIDNEY ALLOCATION: This UNOS data analysis combined with other recent multi-center studies suggest that the criteria for kidney allocation need contain just 2 components in order to maximize long-term survival-an immunologic factor (avoiding HLA mismatches) and a non-immunologic factor (a senior citizens pool to receive older donor organs).
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PMID:A multi-factor analysis of kidney graft outcomes at one and five years posttransplantation: 1996 UNOS Update. 928 81

In familial hyperaldosteronism type I (FH-I), inheritance of a hybrid 11beta-hydroxylase/aldosterone synthase gene causes ACTH-regulated aldosterone overproduction. In an attempt to understand the marked variability in hypertension severity in FH-I, we compared clinical and biochemical characteristics of 9 affected individuals with mild hypertension (normotensive or onset of hypertension after 15 yr, blood pressure never >160/100 mm Hg, < or = 1 medication required to control hypertension, no history of stroke, age >18 yr when studied) with those of 17 subjects with severe hypertension (onset before 15 yr, or systolic blood pressure >180 mm Hg or diastolic blood pressure >120 mm Hg at least once, or > or = 2 medications, or history of stroke). Severe hypertension was more frequent in males (11 of 13 males vs. 6 of 13 females; P < 0.05). All 4 subjects still normotensive after age 18 yr were females. Of 10 other affected, deceased individuals (7 males and 3 females) from a single family, all six who died before 60 yr of age (4 by stroke) were males. Biochemical studies were conducted in 6 mild and 16 severe subjects. The 2 groups were similar in terms of urinary sodium excretion. Mild subjects tended, although not significantly, to have lower urinary 18-oxo-cortisol (mean +/- SD, 27.4 +/- 9.0 vs. 35.2 +/- 12.9 nmol/mmol creatinine x day), higher plasma potassium (4.0 +/- 0.3 vs. 3.6 +/- 0.4 mmol/L), and lower recumbent (0800 h after overnight recumbency) plasma aldosterone levels (498 +/- 279 vs. 744 +/- 290 pmol/L). Upright (midmorning after 2-3 h of upright posture) plasma aldosterone levels were similar (mild, 485 +/- 150; severe, 474 +/- 188 pmol/L). In 1 normotensive female, upright PRA was much higher, and the upright aldosterone/PRA ratio was much lower than that in the other subjects. The remaining mild subjects had similar upright PRA levels (mild, 2.8 +/- 1.4; severe, 3.7 +/- 3.2 pmol/ L x min) and aldosterone/PRA ratios (mild, 199.5 +/- 133.4; severe, 200.6 +/- 150.9) as severe subjects. During angiotensin II (AII) infusion studies (n = 6 mild and 10 severe), performed during recumbency, aldosterone levels were lower in the mild group both basally (404 +/- 144 vs. 843 +/- 498 pmol/L; P < 0.05) and after 60 min AII (2 ng/kg x min; 261 +/- 130 vs. 520 +/- 330 pmol/L; P < 0.05). Aldosterone was unresponsive (rose by <50%) to AII in all subjects. Day curve studies (blood collected every 2 h for 24 h; n = 2 mild and 7 severe) demonstrated abnormal regulation of aldosterone by ACTH rather than by AII in both groups. In conclusion, in this series of patients with FH-I, males had more severe hypertension, and the degree of hybrid gene-induced aldosterone overproduction may have contributed to the severity of hypertension.
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PMID:Severity of hypertension in familial hyperaldosteronism type I: relationship to gender and degree of biochemical disturbance. 1085 45

The aim of this study was to evaluate the cardiac effects of transjugular intrahepatic portosystemic shunts (TIPS) in cirrhotic patients with different effective blood volume. Two-dimensional echocardiography was performed before and 7 and 28 days after TIPS insertion in 7 cirrhotic patients with PRA <4 ng/mL/h (group A, normal effective blood volume) and 15 with PRA >4 ng/mL/h (group B, reduced effective blood volume). Before TIPS, most cirrhotic patients showed diastolic dysfunction as indicated by reduced early maximal ventricular filling velocity (E)/late filling velocity (A) ratio. Patients of group B differed from patients of group A because of smaller left ventricular volumes and stroke volume, indicating central underfilling. After TIPS insertion, portal decompression was associated with a significant increase of cardiac output (CO) and a decrease of peripheral resistances. The most important changes were recorded in patients of group B, who showed a significant increase of both the end-diastolic left ventricular volumes and the E/A ratio and a significant decrease of PRA. In conclusion, these results show that the hemodynamic effects of TIPS differ according to the pre-TIPS effective blood volume. Furthermore, TIPS improves the diastolic cardiac function of cirrhotic patients with effective hypovolemia. This result is likely due to a TIPS-related improvement of the fullness of central blood volume.
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PMID:Humoral and cardiac effects of TIPS in cirrhotic patients with different "effective" blood volume. 1464 47

Primary aldosteronism (PA) is the most common cause of mineralocorticoid hypertension. Different studies, using the plasma aldosterone concentration to plasma renin activity ratio (PAC/PRA) for the screening of patients with hypertension, have shown a marked increase in the detection rate of PA. Idiopathic bilateral adrenal hyperplasia (IHA) and aldosterone-producing adrenal adenoma (APA), are the leading causes of primary aldosteronism. Glucocorticoid-remediable aldosteronism (GRA), also called familial hyperaldosteronism type I, familial hyperaldosteronism type II and carcinomas are rare causes of PA. Patients with hypertension and hypokalemia, those with a family history of hypertension and stroke at an early age, or patients with medication-resistant hypertension should be screened for PA using the PAC/PRA ratio. If a high ratio is found, a sodium loading test or a captopril test is warranted to confirm the diagnosis. Adrenal gland imaging is important in subtype differentiation (APA vs IHA). Adrenal venous sampling should be used when other tests prove inconclusive. Genetic testing has facilitated detection of GRA. Surgery is considered the treatment of choice for patients with APA, while bilateral hyperplasia subtypes are treated medically. Normalization of aldosterone levels or aldosterone receptor blockade are necessary to prevent the morbidity and mortality associated with hypertension, hypokalemia, and cardiovascular damage.
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PMID:Detecting and treating primary aldosteronism: primary aldosteronism. 1742 5

The purpose of this investigation was to assess the effects of acute hypoxia on left (LV) and right ventricular (RV) contractility in clinically stable chronic obstructive pulmonary disease (COPD) patients. Eleven male patients (mean age 52.4 +/- 12.6 years) who were diagnosed to have COPD were included into the study. All of the patients underwent left and right heart catheterization. RV contractility was measured according to the method of Ferlinz and LV contractility according to the method of Kennedy and colleagues using indirect digital substraction angiography. Mean pulmonary artery pressures (Mean PPA) and oxygen saturation of the pulmonary artery (SaO2) were measured before and at each stage of graded hypoxic exposure 14%, 12%, and 10% of O2. Right atrial pressures (PRA,syst, PRA,diast, PRA,mean), RV pressures (PRV,syst, PRV,diast, PRV,mean, PRV,end-diast), RV and LV end-diastolic volume index (EDVI), end-systolic volume index (ESVI), stroke volume index (SVI), cardiac index (CI), ejection fraction (EF), and heart rate (HR) were calculated before and after breathing a hypoxic mixture of 10% of O2 for 30 minutes. Acute hypoxia induced significant elevation of mean PPA, PRA,syst, PRA,diast, PRA,mean, PRV,syst, PRV,mean, PRV,end-diast, RV EDVI, RV ESVI, LV EDVI, LV ESVI, confidence interval, and HR (p < 0.05). Whereas SaO2 decreased significantly after acute hypoxia (p < 0.05). These findings suggest that the systolic performance of the right and left ventricles were well-maintained during acute hypoxia in patients with COPD.
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PMID:Effects of acute hypoxia on left and right ventricular contractility in chronic obstructive pulmonary disease. 1804 69

Obstructive sleep apnoea (OSA) is a sleep disorder characterized by recurrent episodes of oxygen desaturation during sleep, representing an independent risk factor for cardiovascular disease, such as myocardial infarction, stroke, congestive heart failure and resistant hypertension. Several neurohormonal mechanisms have been suggested to account for blood pressure increases, such as sympathetic nervous system hyperactivity, oxidative stress, renin-angiotensin-aldosterone system (RAAS) activation, endothelin system activation, and endothelial dysfunction. The aim of this study was to evaluate the behaviour of RAAS and the presence of primary aldosteronism (PA) in these patients and possible correlations between RAAS and the severity of OSA. From October 2007 to November 2008 we studied 325 consecutive newly diagnosed hypertensive patients; 71 patients (21.8%) presented with clinical signs of sleep disorders, evaluated also through a specific questionnaire (Epworth Sleepiness Scale). In hypertensive patients with sleep disorders, 53 patients were affected by OSA; in this group 18 patients were affected by PA (five with aldosterone-producing adenoma (APA) and 13 with bilateral hyperplasia (IHA)); obesity was also demonstrated (BMI > 30 kg/m(2)). Overall, in patients with OSA PRA levels correlated positively with apnoea/hypopnoea index (AHI; r = 0.35; p<0.01), and in all groups the waist circumference and the neck circumference were correlated positively with AHI (r = 0.3 p<0.02 and r = 0.3 p<0.03, respectively). We revealed a high prevalence of PA in patients with OSA, and we can conclude that patients with hypertension and OSA, especially those who are newly diagnosed, must be evaluated for PA.
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PMID:Renin-angiotensin-aldosterone system in patients with sleep apnoea: prevalence of primary aldosteronism. 2048 24


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