Effect of converting enzyme inhibition on pulmonary edema after microembolization. 1982

C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik

We examined the effect of converting enzyme inhibition with captopril (SQ 14,225) on pulmonary hemodynamics and on accumulation of extravascular lung water after microembolization in dogs. Pulmonary microembolization, induced with glass beads (200 microns diam), increased the mean pulmonary arterial pressure to approximately 40 Torr in both control and captopril-treated animals. The increase in pulmonary vascular resistance (PVR) in control animals was sustained during the 75 min of study and was associated with an increase in the extravascular lung water content-to-bloodless dry lung weight ratio (W/D) from a normal value of 2.84 +/- 0.22 to 4.53 +/- 0.24 ml/g (P less than 0.01) after embolization. In the captopril-treated group, the PVR increased gradually, such that the value at 75 min postembolization was greater than in controls (P less than 0.05). The W/D in the captopril-treated group of 4.62 +/- 0.19 ml/g was greater than the value of 2.83 +/- 0.10 ml/g in nonembolized captopril-treated animals, but the degrees of edema in the control and captopril-treated animals were not different. A similar degree of embolization induced during infusion of 5 micrograms X kg-1 X h-1 of bradykinin also did not enhance the pulmonary edema, and there was also a greater increase in PVR than in control animals after embolization. These findings suggest that bradykinin does not contribute to the degree of pulmonary edema after microembolization.

UI MeSH Term Description Entries
D011652 Pulmonary Circulation The circulation of the BLOOD through the LUNGS. Pulmonary Blood Flow,Respiratory Circulation,Circulation, Pulmonary,Circulation, Respiratory,Blood Flow, Pulmonary,Flow, Pulmonary Blood,Pulmonary Blood Flows
D011654 Pulmonary Edema Excessive accumulation of extravascular fluid in the lung, an indication of a serious underlying disease or disorder. Pulmonary edema prevents efficient PULMONARY GAS EXCHANGE in the PULMONARY ALVEOLI, and can be life-threatening. Wet Lung,Edema, Pulmonary,Edemas, Pulmonary,Pulmonary Edemas,Lung, Wet,Lungs, Wet,Wet Lungs
D011655 Pulmonary Embolism Blocking of the PULMONARY ARTERY or one of its branches by an EMBOLUS. Pulmonary Thromboembolism,Thromboembolism, Pulmonary,Embolism, Pulmonary,Embolisms, Pulmonary,Pulmonary Embolisms,Pulmonary Thromboembolisms,Thromboembolisms, Pulmonary
D001794 Blood Pressure PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS. Systolic Pressure,Diastolic Pressure,Pulse Pressure,Pressure, Blood,Pressure, Diastolic,Pressure, Pulse,Pressure, Systolic,Pressures, Systolic
D001920 Bradykinin A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg,Bradykinin Acetate, (9-D-Arg)-Isomer,Bradykinin Diacetate,Bradykinin Hydrochloride,Bradykinin Triacetate,Bradykinin, (1-D-Arg)-Isomer,Bradykinin, (2-D-Pro)-Isomer,Bradykinin, (2-D-Pro-3-D-Pro-7-D-Pro)-Isomer,Bradykinin, (2-D-Pro-7-D-Pro)-Isomer,Bradykinin, (3-D-Pro)-Isomer,Bradykinin, (3-D-Pro-7-D-Pro)-Isomer,Bradykinin, (5-D-Phe)-Isomer,Bradykinin, (5-D-Phe-8-D-Phe)-Isomer,Bradykinin, (6-D-Ser)-Isomer,Bradykinin, (7-D-Pro)-Isomer,Bradykinin, (8-D-Phe)-Isomer,Bradykinin, (9-D-Arg)-Isomer,Arg Pro Pro Gly Phe Ser Pro Phe Arg
D002216 Captopril A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin. (S)-1-(3-Mercapto-2-methyl-1-oxopropyl)-L-proline,Capoten,Lopirin,SQ-14,225,SQ-14,534,SQ-14225,SQ-14534,SQ 14,225,SQ 14,534,SQ 14225,SQ 14534,SQ14,225,SQ14,534,SQ14225,SQ14534
D004285 Dogs The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065) Canis familiaris,Dog
D000806 Angiotensin-Converting Enzyme Inhibitors A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. ACE Inhibitor,ACE Inhibitors,Angiotensin Converting Enzyme Inhibitor,Angiotensin I-Converting Enzyme Inhibitor,Angiotensin-Converting Enzyme Inhibitor,Kininase II Inhibitor,Kininase II Inhibitors,Angiotensin I-Converting Enzyme Inhibitors,Angiotensin-Converting Enzyme Antagonists,Antagonists, Angiotensin-Converting Enzyme,Antagonists, Kininase II,Inhibitors, ACE,Inhibitors, Angiotensin-Converting Enzyme,Inhibitors, Kininase II,Kininase II Antagonists,Angiotensin Converting Enzyme Antagonists,Angiotensin Converting Enzyme Inhibitors,Angiotensin I Converting Enzyme Inhibitor,Angiotensin I Converting Enzyme Inhibitors,Antagonists, Angiotensin Converting Enzyme,Enzyme Antagonists, Angiotensin-Converting,Enzyme Inhibitor, Angiotensin-Converting,Enzyme Inhibitors, Angiotensin-Converting,II Inhibitor, Kininase,Inhibitor, ACE,Inhibitor, Angiotensin-Converting Enzyme,Inhibitor, Kininase II,Inhibitors, Angiotensin Converting Enzyme
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D014655 Vascular Resistance The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT. Peripheral Resistance,Total Peripheral Resistance,Pulmonary Vascular Resistance,Systemic Vascular Resistance,Peripheral Resistance, Total,Resistance, Peripheral,Resistance, Pulmonary Vascular,Resistance, Systemic Vascular,Resistance, Total Peripheral,Resistance, Vascular,Vascular Resistance, Pulmonary,Vascular Resistance, Systemic

Related Publications

C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
January 1979, Thrombosis research,
C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
January 1982, Journal of applied physiology: respiratory, environmental and exercise physiology,
C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
September 1979, Journal of applied physiology: respiratory, environmental and exercise physiology,
C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
August 2014, Zhonghua er ke za zhi = Chinese journal of pediatrics,
C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
January 2003, The American journal of cardiology,
C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
January 1980, Thrombosis research,
C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
June 1987, Critical care medicine,
C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
June 1974, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.),
C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
April 1996, Journal of clinical pharmacology,
C M Kivlen, and A Johnson, and T Pittman, and A J Guile, and A B Malik
January 1978, Circulation research,
Copied contents to your clipboard!