Biomedical subjects

J L Blackshear

Publications and source records attributed to J L Blackshear.

57 records · Page 4Linked to original sources

PubMedDate not supplied

Unruptured noncoronary sinus of Valsalva aneurysm: preoperative characterization by transesophageal echocardiography.

We describe a patient with a large unruptured sinus of Valsalva aneurysm that was discovered incidentally. Transesophageal echocardiography was used to characterize the aneurysm preoperatively, and was helpful intraoperatively in assessment of the degree of native aortic valvular regurgitation after repair. The use of transthoracic echocardiography, contrast echocardiography, Doppler echocardiography, and transesophageal echocardiography are discussed in this condition.

Adult↗

PubMedDate not supplied

Differential large and small vessel responses to serotonin in the dog hindlimb in vivo: role of the 5HT2 receptor.

Serotonin (5HT) constricts large arteries in vitro, an effect which seems contrary to 5HT-induced increases in blood flow observed in vivo. We used angiography to assess large artery responses, and blood flow (Q, electromagnetic flowmeter) to assess arteriolar responses to 5HT, norepinephrine (NE), and antagonists in the femoral circulation of the intact, anesthetized dog. 5HT constricted large arteries at a threshold dose of less than 10 micrograms/min, giving a 45 +/- 3% reduction of popliteal artery diameter at 100 micrograms/min (p less than 0.001). NE failed to constrict large arteries. With 100 micrograms/min 5HT, Q increased (delta Q = 108 +/- 26 ml/min; p = 0.001). NE decreased Q. Ketanserin, a 5HT and alpha 1-adrenergic antagonist, exerted a dose-dependent inhibition of 5HT-induced large artery constriction. Methysergide partially blocked the 5HT-induced large artery constriction. Ketanserin potentiated the Q response to 5HT whereas higher doses of methysergide reduced the Q response to 5HT. Neither indomethacin nor propranolol altered either response. Failure of NE to constrict large arteries in vivo and ketanserin antagonism of constriction produced by 5HT suggest the response to 5HT involves the 5HT2 receptor. No role for the 5HT2 receptor in blood flow responses is suggested. These observations may have implications for therapy of occlusive vascular disease.

Animals↗

PubMedDate not supplied

The renal response to diltiazem and nifedipine: comparison with nitroprusside.

We undertook a systematic comparison of the effects of diltiazem and nifedipine and a nonspecific vasodilator, sodium nitroprusside, on renal perfusion, function, and activation of potentially relevant neurohormonal systems in the anesthetized dog. These agents were employed to reduce blood pressure to two levels, a mean arterial pressure level of 100-110 mm Hg, and a subtherapeutic level of 75-85 mm Hg. Renal plasma flow (ERPF) and glomerular filtration rate (GFR) were estimated as the clearances of p-aminohippurate and inulin, respectively. All studies with vasodilators were compared with a group which received placebo over an identical time period. The agents differed both in their action on the renal blood supply and in their activation of the renin-angiotensin-aldosterone and sympathetic nervous systems. ERPF was better maintained at both blood pressure levels with nitroprusside than with either diltiazem (p less than 0.005) or nifedipine (p less than 0.005). GFR was better maintained with nitroprusside and diltiazem than with nifedipine. The rise in plasma catecholamines and plasma renin activity was greatest with nifedipine, least with nitroprusside, and intermediate with diltiazem. Diltiazem was also associated with substantially less stimulation of aldosterone release than was nifedipine. Diltiazem and nifedipine are known to have greater renal vasodilator action when infused into the renal artery than nitroprusside. The better-sustained renal plasma flow and glomerular filtration rate during systemic administration with the latter may well reflect the role of calcium in renal autoregulation and the angiotensin-renin feedback loop. Despite an apparent shared mechanism of action, the calcium-entry-blocking agents differ sufficiently that therapeutic implications are possible.

Animals↗