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J Nanas

Publications and source records attributed to J Nanas.

23 records · Page 2Linked to original sources
PubMed1984

A cardiac output monitor and diagnostic unit for pneumatically driven artificial hearts.

The pneumatic artificial heart uses a flexible diaphragm to separate blood from air. The air space behind the diaphragm is connected to the atmosphere during diastole. Blood entering the heart during diastole displaces an equal volume of air into the atmosphere. A pneumotachograph is used to sense this flow of air. Integration of the airflow signal with respect to time yields the volume of air displaced during diastole, which is equal to the volume of blood entering the heart over the same period. This measured filling volume is equal to the cardiac output when averaged over a number of cardiac cycles. Allowance is made for regurgitant losses owing to the prosthetic heart valves. The output of the pneumotachograph is independent of absolute pressure, and so the device may also be used during the systolic (air compression) phase of the cardiac cycle. Analysis of the display of the airflow curves during diastole and systole has great diagnostic value. This device is accurate, easy to calibrate, stable, noninvasive, and does not require modification of any existing air-driven artificial hearts.

Air↗
PubMedDate not supplied

Experimental antifibrillatory effects of calcium channel blockade with diltiazem: comparison with beta-blockade and nitroglycerin.

Calcium channel blockade appears to be at least as effective as beta-blockade in the treatment of anginal syndromes, but whether a similar protective effect is afforded against sudden death is unknown. In order to compare experimental antifibrillatory effects of calcium channel blockade (diltiazem), beta-adrenoceptor blockade (timolol), and nitroglycerin, we measured ventricular fibrillation (VF) thresholds in anesthetized, open-chest dogs before and after 3 min of coronary ischemia before and after i.v. administration of each of these drugs or saline. In control studies, VF occurred after delivery of 11.8 +/- 5.3 mA (X +/- SD) in the nonischemic state and 9.4 +/- 4.6 mA during ischemia (n = 25). During saline administration, no significant change in VF threshold occurred during ischemia, and a minimal increase over time occurred in the nonischemic state. Diltiazem (0.04-0.08 mg/kg/min; n = 10) increased VF thresholds under both ischemic (by 7.7 mA, p less than .01) and nonischemic (by 5.5-5.8 mA, p less than .05) conditions. Timolol (0.03 mg/kg; n = 8) caused substantially greater increases in VFT during nonischemia and ischemia: 11.2 +/- 2.8 mA to 51.6 +/- 38.5 mA (nonischemia) and 8.4 +/- 3.8 mA to 28.7 +/- 16.4 mA (ischemia), both p less than 0.02. VF thresholds were not changed after nitroglycerin (n = 8). Differing experimental effects of these drugs emphasize the need for clinical studies to establish the relative potential of calcium channel blockade and nitroglycerin to reduce mortality in ischemic heart disease.

Adrenergic beta-Antagonists↗