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D Brant

Publications and source records attributed to D Brant.

9 recordsLinked to original sources
PubMed1991

Changes in left ventricular diastolic filling during the development of left ventricular hypertrophy: observations using Doppler echocardiography in a unique canine model.

To examine changes in diastolic left ventricular filling during the development of left ventricular hypertrophy, serial pulsed Doppler echocardiographic studies were performed in a canine model of left ventricular hypertrophy induced by neurogenic pressor episodes. This model is unique since left ventricular hypertrophy develops without sustained hypertension. The neurogenic pressor episodes produced progressive increases in left ventricular mass of 17% by 3 weeks (p less than 0.03) and 23% by 9 weeks (p less than 0.001). During the course of hypertrophy development, there were no changes in resting heart rate, blood pressure, left ventricular volumes or ejection fraction, or end-systolic wall stress. However, peak early filling (peak E) velocity decreased from 65 +/- 5 cm/sec to 53 +/- 4 cm/sec by 3 weeks (p less than 0.05) and remained depressed at 9 weeks. In addition, peak E/A (the ratio of early to late peak filling) decreased by 3 weeks (p less than 0.01) and the contribution of atrial filling to total left ventricular diastolic filling increased by 9 weeks (p less than 0.005). There were significant correlations between the changes in left ventricular mass and the change in peak E velocity at 3 weeks (r = -0.92, p less than 0.001) but not at 9 weeks. These data indicate that left ventricular filling abnormalities occur early in the course of the development of left ventricular hypertrophy, are not a result of loading alterations related to sustained hypertension, and do not change significantly following increasing stages of hypertrophy.

Animals↗
PubMed1991

Quinapril, an angiotensin converting enzyme inhibitor, prevents cardiac hypertrophy during episodic hypertension.

Six control dogs, six dogs treated with 1.5 mg/kg b.i.d. quinapril, and six dogs treated with 8 mg/kg q.d. minoxidil underwent 6 hours daily of hindquarter compression for 9 weeks. Minoxidil significantly decreased baseline blood pressure (-17 mm Hg; p less than or equal to 0.01), whereas quinapril decreased baseline blood pressure 11 mm Hg but not significantly (p = 0.15). Hindquarter compression elicited blood pressure increases in all three groups (control +18, quinapril +13, minoxidil +19 mm Hg). After 9 weeks, left ventricular mass in control dogs increased 22% (p less than 0.004); a similar increase was seen in minoxidil-treated dogs (+22%, p less than 0.0001) but not in the quinapril-treated group (+4%, p less than 0.15). The increase in left ventricular mass in control dogs was concentric (increased epicardial volume only), whereas in the minoxidil group, the hypertrophy was eccentric (both epicardial and endocardial volumes increased). The minimal hypertrophy in the quinapril group was concentric (no change in epicardial, but a decrease in endocardial volume). Quinapril had little hypotensive effect, but prevented the development of left ventricular hypertrophy, whereas minoxidil did not prevent hypertrophy in spite of its hypotensive effect. The mechanism of this differential effect of direct vasodilation versus converting enzyme inhibition on left ventricular hypertrophy is not fully elucidated. The results with quinapril suggest that some antihypertensive agents may positively affect left ventricular hypertrophy in spite of the absence of a large effect on baseline blood pressure or on blood pressure reactivity.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Neurogenic pressor episodes fail to cause hypertension, but do induce cardiac hypertrophy.

Repeated neurogenic pressor episodes by hindquarter compression were elicited in nine experimental dogs. Conscious dogs underwent 6 hours of compression every day over a period of 9 weeks. The average mean blood pressure increase during the compression periods was 25 mm Hg, but after decompression the blood pressure promptly returned to baseline values. This blood pressure response was constant and did not change over the 9-week period. The blood pressure increase was associated with a significant increase of plasma norepinephrine values. After validity of the model was established, echocardiographic measurements were performed at baseline and after 3, 6, and 9 weeks of compression in six experimental and six time-control dogs. Concentric left ventricular hypertrophy was already detectable at 3 weeks, and at the ninth week, the left ventricular mass was 28% above the baseline value. The left ventricular mass in time-control dogs remained unchanged over the same period of time. The time-left ventricular mass curves in experimental dogs were significantly different (by profile analysis), had different means (p less than 0.005), were not parallel (p less than 0.0006), and the overall group difference was highly significant (p less than 0.00001). Since left ventricular hypertrophy, a poor prognostic sign in clinical situations, can evolve before established hypertension, present therapeutic recommendations based on permanently elevated blood pressure values may not be entirely justified.

Animals↗
PubMed1978

Nitroglycerin infusion during infrarenal aortic cross-clamping in dogs: an experimental study.

The effects of an intravenous infusion of nitroglycerin on cardiac index and peripheral vascular resistance during infrarenal aortic cross-clamping were determined in normal animals and in animals subjected to low cardiac output state. Both groups of untreated animals demonstrated progressive fall in cardiac index with a rise in total peripheral resistance during infrarenal aortic cross-clamping. The infusion of nitroglycerin during the period of aortic cross-clamping prevented the increase in total peripheral resistance and therefore prevented the progressive fall in cardiac index that occurred in untreated animals. In the animals with depressed myocardial function, the infusion of nitroglycerin produced a 44% increase in cardiac index during aortic cross-clamping. The results of this study showed that the infusion of nitroglycerin during abdominal aortic cross-clamping can prevent adverse cardiovascular sequelae from occurring and should be used in patients undergoing abdominal aortic resection, especially those with impairment of left ventricular function.

Animals↗
PubMedDate not supplied

Sustained blood pressure elevation to lower body compression in pigs and dogs.

Inflatable suits were constructed for lower body compression in pigs and dogs. The suit for pigs encompassed hindquarters and part of the abdomen, and the smaller suit for dogs compressed only the hindquarters, leaving free the abdominal cavity. In conscious, diazepam-pretreated pigs, the compression lasted 30 minutes; during that period the blood pressure increased 50/38 mm Hg over the baseline. In chloralose-anesthetized dogs, the compression was extended to 3 hours; the blood pressure increase was 44/53 mm Hg. Blood pressure fell to the baseline immediately after decompression in both animals. In both species the substantial blood pressure increase was due to an increase of vascular resistance; this did not induced the expected baroreceptor-mediated bradycardia. In dogs, the blood pressure increase was accompanied by a large increase of plasma norepinephrine (from 179 to 975 pg/ml). To test whether the increase of vascular resistance reflected the mechanical compression of the vessels under the suit, animals were pretreated with trimethaphan. In pigs the trimethaphan substantially decreased the vascular resistance and the blood pressure response. This indicated that a portion of the vasoconstriction occurred in areas outside the suit. Lower body compression is a new model to cause prolonged blood pressure elevation by noninvasive and nonpharmacologic means. The mechanism of the blood pressure elevation requires further investigation.

Abdomen↗