angiotensin-i and Pulmonary-Edema

Topics: Acute Disease; Adrenergic beta-Antagonists; Aged; Analgesics, Opioid; Angioplasty, Balloon, Coronary; Angiotensin I; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Cardiac Glycosides; Defibrillators, Implantable; Diuretics; Emergencies; Furosemide; Heart Failure; Humans; Morphine; Myocardial Infarction; Nitrates; Nitroglycerin; Pacemaker, Artificial; Prognosis; Pulmonary Edema; Respiration, Artificial; Risk Factors; Shock, Cardiogenic; Time Factors; Vasodilator Agents; Ventricular Dysfunction, Right

Twenty-three patients with premature uterine contractions occurring between the 27th and 35th weeks of pregnancy were treated in a prospective and randomized study with intravenous ritodrine in a 0.1 wt/vol% solution of isotonic saline (N = 12) or isotonic glucose (N = 11). The aim of the study was to record the effects of these agents on the water-salt metabolism. In both the saline and the glucose groups there was a statistically significant fall in hemoglobin, hematocrit, and serum albumin (P less than .001). This fall correlated significantly with the dose of ritodrine (P less than .001). Serum renin and aldosterone levels revealed a statistically significant increase (P less than .0005). Seven of 12 patients in the saline group, but none in the glucose group, developed pulmonary congestion requiring treatment. The combination of ritodrine and saline should be used very cautiously, and the authors recommend accurate monitoring of the fluid balance during ritodrine treatment.

Topics: Aldosterone; Angiotensin I; Female; Glucose; Humans; Infusions, Parenteral; Obstetric Labor, Premature; Pregnancy; Propanolamines; Pulmonary Edema; Ritodrine; Sodium Chloride; Water-Electrolyte Balance

Acute pulmonary embolism (APE) has a very high mortality rate, especially at cardiac arrest and even after the return of spontaneous circulation (ROSC). This study investigated the protective effect of the angiotensin-converting enzyme (ACE) inhibitor captopril on postresuscitation hemodynamics, in a porcine model of cardiac arrest established by APE. Twenty-nine Beijing Landrace pigs were infused with an autologous thrombus leading to cardiac arrest and subjected to standard cardiopulmonary resuscitation and thrombolysis. Ten resuscitated pigs were randomly and equally apportioned to receive either captopril (22.22 mg/kg) infusion or the same volume saline, 30 min after ROSC. Hemodynamic changes and ACE-Ang II-angiotensin II type 1 receptor (AT1R) and ACE2/Ang-(1-7)/Mas receptor axis levels were determined. APE was associated with a decline in mean arterial pressure and a dramatic increase in pulmonary artery pressure and mean right ventricular pressure. After ROSC, captopril infusion was associated with significantly lower mean right ventricular pressure and systemic and pulmonary vascular resistance, faster heart rate, and higher Ang-(1-7) levels, ACE2/ACE, and Ang-(1-7)/Ang II, compared with the saline infusion. The ACE2/Ang-(1-7)/Mas pathway correlated negatively with external vascular lung water and pulmonary vascular permeability and positively with the right cardiac index. In conclusion, in a pig model of APE leading to cardiac arrest, captopril infusion was associated with less mean right ventricular pressure overload after resuscitation, compared with saline infusion. The reduction in systemic and pulmonary vascular resistance associated with captopril may be by inhibiting the ACE-Ang II-AT1R axis and activating the ACE2/Ang-(1-7)/Mas axis.

Topics: Angiotensin I; Angiotensin-Converting Enzyme 2; Angiotensin-Converting Enzyme Inhibitors; Animals; Arterial Pressure; Biomarkers; Capillary Permeability; Captopril; Cardiopulmonary Resuscitation; Disease Models, Animal; Enzyme Activation; Female; Heart Arrest; Hemodynamics; Male; Peptide Fragments; Peptidyl-Dipeptidase A; Proto-Oncogene Mas; Proto-Oncogene Proteins; Pulmonary Artery; Pulmonary Edema; Pulmonary Embolism; Receptors, G-Protein-Coupled; Renin-Angiotensin System; Signal Transduction; Sus scrofa; Thrombolytic Therapy; Time Factors; Vascular Resistance; Ventricular Function, Right; Ventricular Pressure

This study was performed to demonstrate an experimental procedure of pulmonary edema induced by angiotensin I (AT I) in rats and to elucidate the mechanism of hemodynamic pulmonary edema. In the previous pilot study, 20 microg/kg of AT I was found to be an adequate dose for inducing pulmonary edema. To elucidate the mechanism of AT I pulmonary edema and protective measures against it, we observed the effects of captopril (CAP, 5 and 10 mg/kg), an angiotensin converting enzyme inhibitor; losartan (LOS, 10 mg/kg), an angiotensin II (AT II)-receptor antagonist; and phentolamine (PHE, 10 mg/kg), an alpha-adrenergic receptor blocker, on AT I-induced pulmonary edema in rats. Similarly, we also observed the effects of CAP (10 and 20 mg/kg) on pulmonary edema induced by 25 microg/kg of adrenaline (ADR) in rats. The development of AT I-induced pulmonary edema was significantly suppressed by CAP and LOS, but was unaffected by PHE. In contrast, the development of ADR-induced pulmonary edema was not suppressed by CAP. These results suggest that AT I-induced pulmonary edema is developed via the AT II and a specific AT II-receptor, without the indirect action of adrenaline.

Topics: Adrenergic alpha-Antagonists; Angiotensin I; Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Blood Pressure; Captopril; Epinephrine; Losartan; Nitroglycerin; Phentolamine; Pulmonary Edema; Rats; Rats, Wistar; Receptors, Angiotensin; Regression Analysis; Respiration; Vasodilator Agents