cyclic-gmp and Rheumatic-Heart-Disease

Pulmonary arterial hypertension [PAH] and cardiopulmonary bypass [CPB] induce systemic inflammatory cytokines that are critical factors related to postoperative mortality of open heart surgery. We studied the expression of proinflammatory cytokines and cyclic guanosine monophosphate [cGMP] in patients suffering from PAH after CPB.. Seventy-six patients who underwent valve replacement surgery were recruited and divided into two groups according to their pulmonary arterial pressure [< 50 mmHg for Group A and > or = 50 mmHg for Group B]. Blood samples were taken to measure the concentrations of interleukin-1 beta [IL-1 beta], tumour necrosis factor alpha [TNF-alpha], interleukin-10 [IL-10] and cGMP.. IL-1 beta and TNF-alpha were significantly higher in Group B [28.6 +/- 9.1 mmHg] than in Group A [65.8 +/- 10.2 mmHg] at baseline. After CPB, IL-1 beta of both groups rose significantly, while only TNF-alpha of Group B rose significantly higher. There were significant differences between the two groups after CPB. IL-10 and cGMP in Group B were lower than in Group A at baseline. They all decreased significantly after CPB. Significant differences were seen between the groups after CPB.. Patients suffering from PAH had different levels of proinflammatory and anti-inflammatory cytokines compared to normal patients. PAH aggravates the production of IL-1 beta and TNF-alpha, while it decreases the production of IL-10 and cGMP after CPB.

Topics: Adult; Cardiopulmonary Bypass; Cyclic GMP; Female; Humans; Hypertension, Pulmonary; Interleukin-1; Interleukin-10; Male; Middle Aged; Pulmonary Artery; Rheumatic Heart Disease; Tumor Necrosis Factor-alpha

Pulmonary hypertension following cardiac surgery is an important factor affecting postoperative mortality, and its mechanism has not been thoroughly clarified. Cardiopulmonary bypass (CPB) can destroy pulmonary endothelium and aggravate pulmonary hypertension. This study is designed to investigate the impacts of CPB on vascular endothelium-dependent relaxation, and the relations of CPB to pulmonary hypertension. Forty patients undergoing valve surgery were involved. According to their preoperative pulmonary arterial pressure (PAP), these patients were divided into pulmonary hypertension group (H group) and normal group (N group). The concentrations of cyclic guanosine monophosphate (cGMP) were measured at baseline conditions, after acetylcholine (Ach) injection, and during nitric oxide (NO) inhalation. Samples were taken before sternotomy and after weaning from CPB, 4 and 12 hours post-CPB. At baseline, the level of cGMP in the H group was lower than that of the N group by 33.9% before CPB. After initiating the CPB, although the level of cGMP continuously decreased in both groups until weaning from CPB (the N group decreased 33.3%, and the H group decreased 59%). At that point cGMP was higher in N group than in the H group (p < .01). The level of cGMP of both groups tended to recover 4 hours after CPB, but only the N group returned to baseline 12 hours after CPB. After injection of Ach, the level of cGMP of both groups followed the same change as in the baseline, except with different numeric value. The level of cGMP in N group rose ranging from 160.0-197.3%, while it rose ranging from 87.7-168.1% in H group. The levels of cGMP were higher in N group than those in H group at all times following injection of Ach (61.4, 173.3, 202.7, and 188.0%) (p < .01). After inhalation of NO, the level of cGMP of both groups followed the same change as the baseline. The level of cGMP in N group rose ranging from 194.8-320.5%. Although the levels of cGMP were higher in N group than those in H group (6.9, 25.3, 23.3, and 16.6%), significant differences were achieved at the 4 and 12 hour post-CPB periods (p < .05 or p < .01, respectively). It was concluded that the injury of vascular endothelial function caused by CPB was more critical in pulmonary hypertension patients.

Topics: Acetylcholine; Administration, Inhalation; Adult; Analysis of Variance; Cardiac Surgical Procedures; Cardiopulmonary Bypass; Case-Control Studies; Cyclic GMP; Female; Humans; Hypertension, Pulmonary; Injections, Intravenous; Male; Middle Aged; Nitric Oxide; Rheumatic Heart Disease; Time Factors

We examined the histologic, hemodynamic and metabolic factors associated with rheumatic mitral stenosis. Eighteen patients comprised three groups: Group I - 7 patients in sinus rhythm; Group II - 5 patients in intermittent atrial fibrillation; Group III - 6 patients in chronic atrial fibrillation. The left atrial dimension was determined by echocardiography. Left atrial pressure, mitral valve gradient, mitral valve area and the presence or absence of calcium in the mitral valve were determined at catheterization. The left atrial appendage was removed during open heart surgery and the tissue was analyzed for cell size, percent fibrosis and content of cyclic AMP and GMP. There was no difference between the groups in pulmonary capillary wedge pressure, mitral valve gradient, mitral valve area or the presence of calcium. The Group I left atrial dimension (51 +/- 2 mm, means +/- SE) was significantly smaller than that of Group III (56 +/- 2 mm, P less than 0.05). Group II was not different from Groups I or III. Although the concentration of cyclic AMP did not differ among the groups, the cyclic GMP was significantly depressed in Group III (0.15 +/- 0.02 fmol/microgram protein) when compared to Group I (0.24 +/- 0.05 fmol/microgram protein, P less than 0.01). Group II had intermediate values which did not differ from Groups I or III. The percent fibrosis was greatest in Group III (34.8 +/- 1.8%) and least in Group I (27.2 +/- 2.8%, P less than 0.05). There was no difference in cell size among the groups. Although atrial fibrillation may lead to some of these irregularities, a depressed cyclic GMP, increased fibrosis and increased left atrial dimension may play a role in the pathogenesis of irreversible atrial fibrillation.

Topics: Adult; Atrial Fibrillation; Calcium; Cyclic AMP; Cyclic GMP; Echocardiography; Heart Atria; Hemodynamics; Humans; Male; Middle Aged; Mitral Valve; Mitral Valve Stenosis; Rheumatic Heart Disease