scholarly journals Characterization of the spontaneous degenerative mitral valve disease in FVB mice

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257022
Author(s):  
Estelle Ayme-Dietrich ◽  
Sylvia Da Silva ◽  
Ghina Alame Bouabout ◽  
Alizée Arnoux ◽  
Jérôme Guyonnet ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Weight ◽  
Mitral Valve ◽  
Whole Blood ◽  
Bleeding Time ◽  
Left Ventricular ◽  
Serotonergic System ◽  
Plasma Serotonin ◽  
Tgf Β1

Background The development of new non-surgical treatments dedicated to mitral valve degeneration is limited by the absence of relevant spontaneous and rapidly progressing animal experimental models. Animals We characterized the spontaneous mitral valve degeneration in two inbred FVB mouse strains compared to C57BL/6J and investigated a contribution of the serotonergic system. Methods Males and females FVB/NJ and FVB/NRj were compared to the putative C57BL/6J control at 12, 16, 20 and 24 weeks of age. Body weight, systolic blood pressure, heart rate, urinary 5-hydroxyindoleacetic acid (5-HIAA), whole blood and plasma serotonin, tail bleeding time, blood cell count, plasma TGF-β1 and plasma natriuretic peptide concentrations were measured. Myocardium and mitral valves were characterized by histology. mRNA mitral expression of 5-HT2A and 5-HT2B receptors was measured in the anterior leaflet. Cardiac anatomy and function were assessed by echocardiography. Results Compared to C57BL/6J, FVB mice strains did not significantly differ regarding body weight increase, arterial blood pressure and heart rate. A progressive augmentation of plasma pro-ANP was observed in FVB mice. Nevertheless, no cardiac hypertrophy or left-ventricular fibrosis were observed. Accordingly, plasma TGF-β1 was not different among the three strains. Conversely, FVB mice demonstrated a high prevalence of fibromyxoid highly cellularized and enriched in glycosaminoglycans lesions, inducing major mitral leaflets thickening without increase in length. The increased thickness was correlated with urinary 5-HIAA and blood platelet count. Whole blood serotonin concentration was similar in the two strains but, in FVB, a reduction of plasma serotonin was observed together with an increase of the bleeding time. Finally, echocardiography identified left atrial and left ventricular remodeling associated with thickening of both mitral leaflets and mitral insufficient in 30% of FVB mice but no systolic protrusion of mitral leaflets towards the atrium. Conclusion The FVB mouse strain is highly prone to spontaneous mitral myxomatous degeneration. A contribution of the peripheral serotonergic system is suggested.

HEART COMPLICATIONS IN HYPERTHYROIDISM

2011 ◽  
pp. 7-17
Author(s):  
Hai Thuy Nguyen ◽  
Anh Vu Nguyen
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Heart Rate ◽  
Heart Diseases ◽  
Systolic Dysfunction ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Cardiac Complications ◽  
Cardiac Symptoms

Thyroid hormone increases the force of the contraction and the amount of the heart muscle oxygen demand. It also increases the heart rate. Due to these reasons, the work of the heart is greatly increased in hyperthyroidism. Hyperthyroidism increases the amount of nitric oxide in the intima, lead them to be dilated and become less stiff. Cardiac symptoms can be seen in anybody with hyperthyroidism, but can be particularly dangerous in whom have underlying heart diseases. Common symptoms include: tachycardia and palpitations. Occult hyperthyroidism is a common cause of an increased heart rate at rest and with mild exertion. Hyperthyroidism can also produce a host of other arrhythmias such as PVCs, ventricular tachycardia and especially atrial fibrillation. Left ventricular diastolic dysfunction and systolic dysfunction, Mitral regurgitation and mitral valve prolapsed are heart complications of hyperthyroism could be detected by echocardiography. The forceful cardiac contraction increases the systolic blood pressure despite the increased relaxation in the blood vessels reduces the diastolic blood pressure. Atrial fibrillation, atrial enlargement and congestive heart failure are important cardiac complications of hyperthyroidism. An increased risks of stroke is common in patients with atrial fibrillation. Graves disease is linked to autoimmune complications, such as cardiac valve involvement, pulmonary arterial hypertension and specific cardiomyopathy. Worsening angina: Patients with coronary artery disease often experience a marked worsening in symptoms with hyperthyroidism. These can include an increase in chest pain (angina) or even a heart attack.

scholarly journals Blood pressure reduction after gastric bypass surgery is explained by a decrease in cardiac output

2017 ◽  
Vol 122 (2) ◽  
pp. 223-229 ◽  
Author(s):  
Peter M. van Brussel ◽  
Bas van den Bogaard ◽  
Barbara A. de Weijer ◽  
Jasper Truijen ◽  
C.T. Paul Krediet ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gastric Bypass ◽  
Body Weight ◽  
Cardiac Output ◽  
Baroreflex Sensitivity ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility

Blood pressure (BP) decreases in the first weeks after Roux-and-Y gastric bypass surgery. Yet the pathophysiology of the BP-lowering effects observed after gastric bypass surgery is incompletely understood. We evaluated BP, systemic hemodynamics, and baroreflex sensitivity in 15 obese women[mean age 42 ± 7 standard deviation (SD) yr, body mass index 45 ± 6 kg/m2] 2 wk before and 6 wk following Roux-and-Y gastric bypass surgery. Six weeks after gastric bypass surgery, mean body weight decreased by 13 ± 5 kg (10%, P < 0.001). Office BP decreased from 137 ± 10/86 ± 6 to 128 ± 12/81 ± 9 mmHg ( P < 0.001, P < 0.01), while daytime ambulatory BP decreased from 128 ± 14/80 ± 9 to 114 ± 10/73 ± 6 mmHg ( P = 0.01, P = 0.05), whereas nighttime BP decreased from 111 ± 13/66 ± 7 to 102 ± 9/62 ± 7 mmHg ( P = 0.04, P < 0.01). The decrease in BP was associated with a 1.6 ± 1.2 l/min (20%, P < 0.01) decrease in cardiac output (CO), while systemic vascular resistance increased (153 ± 189 dyn·s·cm−5, 15%, P < 0.01). The maximal ascending slope in systolic blood pressure decreased (192 mmHg/s, 19%, P = 0.01), suggesting a reduction in left ventricular contractility. Baroreflex sensitivity increased from 9.0 [6.4–14.3] to 13.8 [8.5–19.0] ms/mmHg (median [interquartile range]; P < 0.01) and was inversely correlated with the reductions in heart rate ( R = −0.64, P = 0.02) and CO ( R = −0.61, P = 0.03). In contrast, changes in body weight were not correlated with changes in either BP or CO. The BP reduction following Roux-and-Y gastric bypass surgery is correlated with a decrease in CO independent of changes in body weight. The contribution of heart rate to the reduction in CO together with enhanced baroreflex sensitivity suggests a shift toward increased parasympathetic cardiovascular control. NEW & NOTEWORTHY The reason for the decrease in blood pressure (BP) in the first weeks after gastric bypass surgery remains to be elucidated. We show that the reduction in BP following surgery is caused by a decrease in cardiac output. In addition, the maximal ascending slope in systolic blood pressure decreased suggesting a reduction in left ventricular contractility and cardiac workload. These findings help to understand the physiological changes following gastric bypass surgery and are relevant in light of the increased risk of heart failure in these patients.

Abstract MP016: Innovation in Exercise: Increasing Capacity of Sedentary Obese Women with Cooling

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Stacy T Sims ◽  
Sandra Tsai ◽  
Marcia L Stefanick
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Weight ◽  
Waist Circumference ◽  
Body Mass ◽  
Exercise Tolerance ◽  
Thermal Strain ◽  
Walk Test ◽  
Obese Women ◽  
Thermal Discomfort

Background: Barriers to physical activity for obese women include overheating, sweating, fatigue, exhaustion, and rapid heart rate. Adipose tissue acts as a thermal insulator, promoting a greater heat load on the nonfat tissues, reducing heat tolerance; exercise causes a rise in body temperature with an inability to dissipate heat contributing to reduced exercise tolerance. With difficulties of thermoregulation in the sedentary obese population, the aspect of attenuating the discomfort thus associated may encourage continuation of exercise. A heat sink applied to palmar surfaces extracts heat and cools the venous blood, reducing thermal strain by enhancing the volume of cooled venous return. We hypothesized that palmar cooling using a rapid thermal exchange device (RTX) during exercise would attenuate the thermal discomfort of exercise of sedentary obese women, improving exercise tolerance. Methods: To examine whether palmar cooling would impact exercise tolerance in obese women, 24 healthy women aged 30–45 years, with no history of long term structured exercise, a body mass of 120–135% above ideal and/or BMI between 30 and 34.9 were recruited. Women were randomized into a cooling (RXT with 16°C water circulating) or a control (RTX with 37°C water circulating) group and attended 3 exercise sessions a week for 3-months (12 weeks). Each session was comprised of 10 min body weight exercises, 25–45 min treadmill walking at 70–85% HRR with the RTX device, and 10 min of core strengthening exercises. The performance marker was a 1.5 mi walk for time; conducted on the first and last days of the intervention. Mixed models were used to model each of the outcomes as a function of thermal strain, time and treatment with covariates of speed, heart rate, distance, and the interaction of the main effects included in the model. Results: Groups were matched at baseline for key variables (time for 1.5 mile walk test, resting and exercising heart rate [HR], blood pressure [BP], waist circumference [WC], body weight, body mass index [BMI]). Among the cooling group, time to complete the 1.5mile walk test was significantly faster (31.6 ± 2.3 vs. 24.6 ± 2.5 min, pre vs. post, P< 0.01). A greater average exercising HR was observed (136 vs. 154 bpm, pre vs. post, P <0.001), with a significant reduction in WC (41.8 ± 3.1 vs. 39.1 ± 2.2 inches, pre vs. post, P< 0.01) and resting BP (139/84 ± 124/70 mmHg, pre vs. post, P < 0.025). There were no significant differences observed in the control group. Conclusion: Results indicate that exercise tolerance in obese women improved with cooling during exercise, more so than those women who did not have cooling. An improvement in blood pressure, heart rate, waist circumference, and overall aerobic fitness was observed. These findings suggest that by reducing thermal discomfort during exercise, tolerance increases, thus improving cardiovascular parameters of obese women.

Hypoxic pressor response, cardiac size, and natriuretic peptides are modified by long-term intermittent hypoxia

1999 ◽  
Vol 87 (6) ◽  
pp. 2025-2031 ◽  
Author(s):  
Holger Kraiczi ◽  
Jarkko Magga ◽  
Xiang Ying Sun ◽  
Heikki Ruskoaho ◽  
Xiaohe Zhao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Weight ◽  
Atrial Natriuretic Peptide ◽  
Right Ventricular ◽  
Natriuretic Peptide ◽  
Intermittent Hypoxia ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

We investigated whether the effect of long-term intermittent hypoxia (LTIH) on cardiovascular function may be modified by preexisting genetic traits. To induce LTIH experimentally, cycles of 90-s hypoxia (nadir 6%) followed by 90-s normoxia were applied to six Wistar-Kyoto and six spontaneously hypertensive rats during 8 h daily. Comparison with the same number of control animals after 70 days revealed no alteration of intra-arterial blood pressure or heart rate. Blood pressure responsiveness to a brief hypoxic stimulus was enhanced in the LTIH animals, regardless of strain, whereas the hypoxia-induced increase in heart rate was abolished. In the spontaneously hypertensive but not the Wistar-Kyoto rats, LTIH increased left ventricular weight-to-body weight ratio and content of atrial natriuretic peptide mRNA. Expression of B-type natriuretic peptide was unchanged (Northern blot). Slightly increased right ventricular weight-to-body weight ratios in the LTIH animals were associated with higher right ventricular atrial natriuretic peptide and B-type natriuretic peptide mRNA amounts. Consequently, the effects of LTIH on different components of cardiovascular function appear incompletely related to each other and differentially influenced by constitutional traits.

Abstract 608: Uric Acid Potentially Interacts With Parathyroid Hormone To Promote Left Ventricular Diastolic Dysfunction In Mice Fed A Western Diet

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Guanghong Jia ◽  
Brian P Bostick ◽  
Javad Habibi ◽  
Annayya R. Aroor ◽  
Vincent G. DeMarco ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Uric Acid ◽  
Parathyroid Hormone ◽  
Diastolic Dysfunction ◽  
Cardiac Mri ◽  
Left Ventricular ◽  
Western Diet ◽  
P Value ◽  
Lv Diastolic Dysfunction

Hyperuricemia is frequently observed in obese people and rising obesity rates parallel increased consumption of a high-fat/high-fructose western diet (WD). Epidemiologic and clinical data suggest that serum uric acid (UA) is positively associated with serum parathyroid hormone (PTH) and may be linked with left ventricular (LV) hypertrophy and LV diastolic dysfunction. Accordingly, we hypothesized that allopurinol, a potent xanthine oxidase (XO) inhibitor, would prevent development of LV diastolic dysfunction, independent of blood pressure, by reducing the levels of UA and PTH. Four week-old C57BL6/J male mice were fed a WD and water with 125mg/L allopurinol. After 16 weeks, we assessed levels of UA, XO activity, PTH, as well as diastolic function by cardiac MRI and cardiac ultrastructure by transmission electron microscopy (TEM). Body weight and fat composition were obtained along with HOMA -IR testing for insulin resistance. Allopurinol has been show to exert no effect on blood pressure. High resolution cardiac MRI revealed diastolic dysfunction with WD feeding that was prevented by allopurinol (LV diastolic relaxation time 35.3 ms for WD, 25.4 ms for CD and 27.7 ms for WD+ allopurinol, p value <0.01; Initial filling rate 0. 28 μl/ms for WD, 0.43 μl/ms for CD and 0.42 μl/ms for WD+ allopurinol, p value <0.05). Body weight, fat mass, and HOMA-IR were increased by WD feeding but not significantly improved by allopurinol. However, allopurinol markedly decreased the WD-induced increase in heart weight associated with activation of translational S6 kinase. TEM examination of myocardial ultrastructure revealed that WD induced remodeling changes with large mitochondria with disordered cristae and increased lysosomes. The ultrastructural changes were improved with treatment by allopurinol. Furthermore, allopurinol significantly inhibited both of plasma and urine UA levels and cardiac XO activity caused by WD. Interestingly , WD increased PTH levels which were decreased in parallel with reductions in uric acid with allopurinol. These findings support the notion that increased plasma levels of UA, in concert with elevated PTH, may play a key role in LV hypertrophy and associated LV diastolic dysfunction that result from consuming a WD high in fructose and fat.

Abstract 13421: Ventricular and Arterial Elastance During Isometric Handgrip Exercise and Post-exercise Circulatory Arrest in Heart Failure With and Without Preserved Ejection Fraction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Naoki Fujimoto ◽  
Keishi Moriwaki ◽  
Issei Kameda ◽  
Masaki Ishiyama ◽  
Taku Omori ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Circulatory Arrest ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Isometric Handgrip ◽  
Arterial Elastance ◽  
Post Exercise

Introduction: Isometric handgrip (IHG) training at 30% maximal voluntary contraction (MVC) lowers blood pressure in hypertensive patients. Impacts of IHG exercise and post-exercise circulatory arrest (PECA), which isolates metaboreflex control, have been unclear in heart failure (HF). Purpose: To investigate the impacts of IHG exercise and PECA on ventricular-arterial stiffness and left ventricular (LV) relaxation in HF with preserved (HFpEF) and reduced ejection fraction (HFrEF). Methods: We invasively obtained LV pressure-volume (PV) loops in 20 patients (10 HFpEF, 10 HFrEF) using conductance catheter with microtip-manometer during 3 minutes of IHG at 30%MVC and 3 minutes of PECA. Hemodynamics and LV-arterial function including LV end-systolic elastance (Ees) by the single-beat method, effective arterial elastance (Ea), and time constant of LV relaxation (Tau) were evaluated every minute. Results: At rest, HFpEF had higher LV end-systolic pressure (ESP) and lower heart rate than HFrEF with similar LV end-diastolic pressure (EDP). The coupling ratio (Ees/Ea) was greater in HFpEF than HFrEF (1.0±0.3 vs. 0.6±0.3, p<0.01). IHG for 3minutes similarly increased heart rate in HFpEF (by 10±8 bpm) and HFrEF (by 14±6 bpm). IHG also increased end-diastolic and LVESP (134±21 vs. 158±30 mmHg and 113±25 vs. 139±25 mmHg) in both groups (groupхtime effect p≥0.25). In HFpEF, Ees, Ea and Ees/Ea (1.0±0.3 vs. 1.1±0.4) were unaffected during IHG. In HFrEF, IHG induced variable increases in Ea. LV end-systolic volume and the ESPV volume-axis intercept were larger, and Ees at IHG 3 rd min was greater (1.30±0.7 vs. 3.1±2.1 mmHg/ml, p<0.01) than baseline, resulting in unchanged Ees/Ea at IHG 3 rd min (0.6±0.3 vs. 0.8±0.4, p≥0.37). Tau was prolonged only in HFrEF during IHG and was returned to the baseline value during PECA. During the first 2 minutes of PECA, LVESP was lower than that at IHG 3 rd min only in HFpEF, suggesting less metaboreflex control of blood pressure in HFpEF during IHG. Conclusions: IHG exercise at 30%MVC induced modest increases in LV end-systolic and end-diastolic pressures in HFpEF and HFrEF. Although the prolongation of LV relaxation was observed only in HFrEF, the ventricular and arterial coupling was maintained throughout the IHG exercise in both groups.

Enhanced brain natriuretic peptide response to peak exercise in heart transplant recipients

1998 ◽  
Vol 85 (6) ◽  
pp. 2270-2276 ◽  
Author(s):  
Bernard Geny ◽  
Anne Charloux ◽  
Eliane Lampert ◽  
Jean Lonsdorfer ◽  
Pascal Haberey ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Transplantation ◽  
Left Ventricular Mass ◽  
Heart Transplant ◽  
Left Ventricular Mass Index ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Transplant Recipients ◽  
Heart Transplant Recipients

We investigated the atrial (ANP) and brain natriuretic peptides (BNP), catecholamines, heart rate, and blood pressure responses to graded upright maximal cycling exercise of eight matched healthy subjects and cardiac-denervated heart transplant recipients (HTR). Baseline heart rate and diastolic blood pressure, together with ANP (15.2 ± 3.7 vs. 4.4 ± 0.8 pmol/l; P < 0.01) and BNP (14.3 ± 2.6 vs. 7.4 ± 0.6 pmol/l; P< 0.01), were elevated in HTR, but catecholamine levels were similar in both groups. Peak exercise O2uptake and heart rate were lower in HTR. Exercise-induced maximal ANP increase was similar in both groups (167 ± 34 vs. 216 ± 47%). Enhanced BNP increase was significant only in HTR (37 ± 8 vs. 16 ± 8%; P < 0.05). Similar norepinephrine but lower peak epinephrine levels were observed in HTR. ANP and heart rate changes from rest to 75% peak exercise were negatively correlated ( r = −0.76, P < 0.05), and BNP increase was correlated with left ventricular mass index ( r = 0.83, P < 0.01) after heart transplantation. Although ANP increase was not exaggerated, these data support the idea that the chronotropic limitation secondary to sinus node denervation might stimulate ANP release during early exercise in HTR. Furthermore, the BNP response to maximal exercise, which is related to the left ventricular mass index of HTR, is enhanced after heart transplantation.

P3835Improvement of myocardial energetic efficiency during treatment in hypertensive patients: the life study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M A Losi ◽  
C Mancusi ◽  
E Gerdts ◽  
K Wachtell ◽  
S E Kjeldsen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Energetic Efficiency ◽  
Stroke Work ◽  
Hypertensive Patients ◽  
Life Study ◽  
Over Time

Abstract Background Myocardial energetic efficiency (MEE) per unit of left ventricular (LV) mass significantly predicts composite of cardiovascular (CV) events in treated hypertensive patients and specifically heart failure in an event-free population-based cohort with normal ejection fraction, independently of LV hypertrophy (LVH). Purpose To investigate whether MEEi changes over time in treated hypertensive patients, and whether different treatments have different effects. Methods From the Losartan Intervention For Endpoint study (LIFE Echo Sub-study) we selected 744 hypertensive patients (age 66±7 years; 45% women) with LVH at ECG, without atrial fibrillation, previous or incident myocardial infarction and with normal echocardiographic ejection fraction (>50%). MEE was estimated as the ratio of stroke work to the “double” product of heart rate times systolic blood pressure (BP), simplified as the ratio of stroke volume to heart rate, as previously reported. MEE was normalized for LVM (MEEi) and analyzed in quartiles at baseline and at the end treatment, according to an “intention-to-treat” protocol. Results Age and proportion of women were not significantly different from the highest to the lowest quartiles (from 65±7 to 66±7 years, p for trend=0.352; from 45% to 42%, p=0.946, respectively), whereas diastolic blood pressure (from 97±8 to 100±9 mmHg, p=0.006), prevalence of obesity (from 14 to 31%, p=0.001) and diabetes (from 4 to 14%, 0.004) progressively increased. Prevalence of concentric LV geometry and echocardiographic LVH also progressively increased from the highest to the lowest quartile (from 14 to 70%, and 61 to 90%, both p<0.0001). MEEi increased over time (p<0.007), independently of initial diastolic BP, diabetes and obesity, significantly more in patients treated with atenolol than with losartan (p<0.0001) (Figure), due to both increased stroke volume and decreased heart rate (both p<0.0001). Figure 1 Conclusions In a randomized clinical study, MEEi improves with anti-hypertensive therapy. Improvement is more evident in patients with atenolol than with losartan-based treatment, possibly providing pathophysiologic explanation of the comparable performance in prevention of ischemic heart disease previously reported in the LIFE study.

Effects of isoproterenol on the cardiovascular system of fetal sheep exposed to long-term high-altitude hypoxemia

1995 ◽  
Vol 78 (5) ◽  
pp. 1793-1799 ◽  
Author(s):  
M. Kamitomo ◽  
T. Ohtsuka ◽  
R. D. Gilbert
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Right Ventricular ◽  
High Altitude ◽  
Arterial Blood Pressure ◽  
Left Ventricular ◽  
Arterial Blood ◽  
Isoproterenol Infusion

We exposed fetuses to high-altitude (3,820 m) hypoxemia from 30 to 130 days gestation, when we measured fetal heart rate, right and left ventricular outputs with electromagnetic flow probes, and arterial blood pressure during an isoproterenol dose-response infusion. We also measured the distribution of cardiac output with radiolabeled microspheres during the maximal isoproterenol dose. Baseline fetal arterial blood pressure was higher in long-term hypoxemic fetuses (50.1 +/- 1.3 vs. 43.4 +/- 1.0 mmHg) but fell during the isoproterenol infusion to 41.3 +/- 1.4 and 37.5 +/- 1.4 mmHg, respectively, at the highest dose. Heart rate was the same in both groups and did not differ during isoproterenol infusion. Baseline fetal cardiac output was lower in the hypoxemic group (339 +/- 18 vs. 436 +/- 19 ml.min-1.kg-1) due mainly to a reduction in right ventricular output. During the isoproterenol infusion, right ventricular output increased to the same extent in both hypoxemic and normoxic fetuses (approximately 35%); however, left ventricular output increased only approximately 15% in the hypoxemic group compared with approximately 40% in the normoxic group. The percent change in individual organ blood flows during isoproterenol infusion in the hypoxemic groups was not significantly different from the normoxic group. All of the mechanisms that might be responsible for the differential response of the fetal left and right ventricles to long-term hypoxia are not understood and need further exploration.

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