Chikao Kotake

Atrial natriuretic peptide as a preload depressor in acute renal failure secondary to congestive heart failure

The present study was undertaken to verify the hypothesis that infusion of atrial natriuretic peptide (ANP) might lower preload and be beneficial in the treatment of pulmonary congestion even without a diuresis in patients with acute renal failure (ARF) secondary to severe congestive heart failure (CHF). We studied 22 patients with ARF secondary to CHF. The mean age of the patients (14 men and 8 women) was 72 years (range 36 to 85 years). Seven of the patients had dilated cardiomyopathy, ten had ischemic heart disease, and five had valvular heart disease. ANP was infused intravenously and the following data before and 1 hour after the start of ANP infusion were recorded; urinary output, systemic blood pressure (SBP), pulmonary blood pressure (PBP), right atrial pressure (RAP), cardiac index (CI), heart rate (HR), and arterial blood oxygen partial pressure. Diastolic PBP were employed as pulmonary capillary wedge pressure. Urinary output did not change. Mean SBP decreased from 92 to 85 mmHg (p < 0.05), and mean PBP decreased from 34 to 28 mmHg (p < 0.01). Mean RAP decreased from 11 to 9 mmHg (p < 0.01) and diastolic PBP decreased from 25 to 19 mmHg (p < 0.01). HR did not change significantly and CI increased 2.4 to 2.5 mi/min/m2 (p < 0.05). Arterial blood oxygen partial pressure increased significantly from 71 to 82 mmHg (p < 0.05). In conclusion, ANP decreased preload and improved arterial blood oxygen partial pressure, though diuretic response to ANP is attenuated in ARF secondary to CHE. Infusion of ANP will be very beneficial in cases in which dyspnea and pulmonary edema due to elevation of preload are the principal clinical problems.

Protective effect of coenzyme Q10 on thyrotoxic heart in rabbits

SummaryAn excess of thyroid hormone is known to produce cardiac dysfunction and failure, i.e., thyrotoxic heart. We studied the protective effect of coenzyme Q10 (CoQ10) on the thyrotoxic heart in 29 rabbits. A group treated with 1-thyroxine sodium salt (T4; 167 µg/kg) for 3 weeks showed marked decreases in the myocardial content of norepinephrine (NE) and ATP (0.5±0.2 µg/g wet weight,P<0.05 and 31.1±2.6 nmol/mg protein,P<0.05, respectively) as compared with a group treated with CoQ10 solvent (2 ml/kg) for 3 weeks (1.1±0.1 µg/g wet weight and 45.7±4.7 nmol/mg protein). The mitochondrial Ca2+ content of the T4 group showed significant increases (21.3 ± 0.6 nmol/mg protein,P<0.05) compared with the solvent group (18.2±0.8 nmol/mg protein), while the total tissue Ca2+ content of the T4 group was unchanged compared with the solvent group. These biochemical derangements suggest that T4-treated rabbits were in a state of cardiac dysfunction. In contrast, a group which was assigned to concomitant treatment of T4 and CoQ10 (5 mg/kg) for 3 weeks showed no reductions in NE and ATP (0.9±0.2 µg/g wet weight and 44.6±1.9 nmol/mg protein, respectively) and protected an increase in the mitochondrial Ca2+ content (18.2±1.2 nmol/mg protein). A group treated with CoQ10 (5 mg/kg) for 3 weeks showed no changes in myocardial NE, ATP, and Ca2+ content in the mitochondria. These results suggest that exogenously administered CoQ10 may protect against biochemical derangements in the thyrotoxic heart.