Acute and Critical Care

Original Articles

Effects of Amrinone and Dobutamine on Regional Myocardial Function and Oxygen Balance in Normal and Stunned Myocardium in Dogs: Jun Suh Park, Jong Eun Park, Sung Tae Jeong, Seongwook Jeong, Sung Su Chung, Kyung Yeon Yoo; Korean J Crit Care Med. 2005;20(1):14-23.

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Abstract PDF: BACKGROUND
We examined the effects of amrinone and dobutamine on regional mechanical function, coronary blood flow (CBF), and myocardial oxygen consumption (MVO2) in normal and stunned myocardium in an open-chest canine model.
METHODS
Dogs were instrumented to measure aortic and left ventricular pressures, pulmonary and left anterior descending (LAD) coronary blood flows, and subendocardial segment length in the region supplied by LAD. Incremental doses of either amrinone (2~10microgram/ml of LAD flow, n=13) or dobutamine (0.05~0.375microgram/ml of LAD flow, n=14) were directly infused into a coronary artery before (normal) and after a 15 min of LAD occlusion and subsequent 30 min-reperfusion (stunned). Percent segment shortening (%SS) and percent post-systolic shortening (%PSS) were evaluated. Myocardial extraction of oxygen (EO2) and lactate (Elac) was calculated. RESULTS: Amrinone or dobutamine in the normal myocardium caused dose-dependent increases in %SS that were comparable (range, 20~40%) but had no effect on %PSS. MVO2 increased in parallel with %SS for both amrinone and dobutamine. With amrinone, CBF increased more than MVO2, resulting in a modest decrease in EO2, whereas with dobutamine, CBF increased in proportion to MVO2, resulting in no change in EO2. After the ischemia and reperfusion, %SS and Elac were reduced, but similar %SS and CBF responses to both agents were observed, except that both agents caused progressive reductions of %PSS. CONCLUSIONS: These results indicate that both amrinone and dobutamine exert positive inotropic effects in normal and stunned canine myocardium. It is also indicated that amrinone causes direct coronary vasodilation, which is not affected by ischemia and reperfusion, while dobutamine has no direct effect on coronary vascular tone in either normal or stunned myocardium.

Effects of Blood-Brain Barrier Disruption on Cerebral Oxygen Balance: Doo Ik Lee, Young Kyu Choi, Dong Ok Kim, Keon Sik Kim, Ok Young Shin, Moo Il Kwon; Korean J Crit Care Med. 1999;14(2):126-130.

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Abstract PDF: BACKGOUND: Disruption of the blood-brain barrier (BBB) can alter the internal milieu and may increase the release of excitatory amino acid neurotransmitters or catecholamines, which may affect metabolic rate or coupling. This study was performed to evaluate whether disruption of BBB by unilateral intracarotid injection of hyperosmolar mannitol would alter oxygen supply/consumption balance in the ipsilateral cortex.
METHODS
Rats were anesthetized with 1.4% isoflurane using mechanical ventilation via tracheostomy. 25% mannitol was administered at a rate of 0.25 mlxkg-1s-1 for 30 s through unilateral internal carotid artery. The BBB transfer coefficient (Ki) of 14C-alpha-aminoisobutyric acid was measured in one group (N=7) after administering mannitol. Regional cerebral blood flow (rCBF), regional arterial and venous O2 saturation and O2 consumption were measured in another group using a 14C-iodoantipyrine and microspectrophotometry (N=7).
RESULTS
Vital signs were similar before and after administering mannitol. Ki was significantly higher in the ipsilateral cortex (IC) than in the contralateral cortex (CC), (22.3+/-8.4 vs 4.4+/-1.1 microliterxg-1min-1). rCBF was similar between IC (105+/-21 mlxg-1min-1) and the CC (93+/-20). Venous O2 saturation was lower in the IC (43+/-7%) than in the CC (55+/-4). O2 consumption was higher in the IC (9.6+/-3.0 mlx100 g-1min-1) than in the CC (6.7+/-1.5).
CONCLUSIONS
Our data suggested that increasing permeability of the BBB increased cerebral O2 consumption and deteriorated cerebral oxygen balance.

The Effects of Nitric Oxide on Oxygen Balance in Cerebral Ischemia: Doo Ik Lee, Young Kyu Choi, Oak Za Chi; Korean J Crit Care Med. 1998;13(2):179-185.

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Abstract PDF: Bockground: Nitric oxide (NO) is an important regulator of blood flow and also works as a neuronal messenger via cyclic GMP. Recent studies regarding the therapeutic utility of nitric oxide synthase (NOS) inhibitors in reducing ischemia-induced neuronal damage are very controversial. The possible neuroprotective effect of NO or NOS inhibitors in ischemic neuronal damage could occur at the vascular and or neuronal level. This study investigated whether the NOS inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME) would alter oxygen balance in ischemic cerebrocortex of isoflurane-anesthetized rats.
METHODS
Fifteen minutes after middle cerebral artery occlusion, L-NAME (1.5 mgxmin-1kg-1) was infused intravenously to the L-NAME group (n=14), and normal saline was given to the control group (n=14) for 45 minutes. Regional cerebral blood flow was determined with [14C]iodoantipyrine, and arterial and venous oxygen saturations were determined by microspectrophotometry.
RESULTS
Regional cerebral blood flow of the ischemic cortex was significantly lower than that of the contralateral cortex in both groups. In the control group, ischemic cortex; 55+/-13, contralateral cortex; 110+/-29 mlxmin-1100 g-1, and in the L-NAME group, ischemic cortex; 35+/-13, contralateral cortex; 90+/-24 mlxmin-1100 g-1. Compared with the blood flow in the ischemic cortex of the control group, L-NAME significantly reduced ischemic blood flow by 36%. Venous oxygen saturation was significantly increased in the ischemic cortex (41+/-1% in control, 44+/-3% in L-NAME) but decreased in the contralateral cortex (65+/-3% in control, 61+/-3% in L-NAME) by L-NAME. Ischemic cortical oxygen consumption in the L-NAME group was 39% lower than that in the corresponding control group, whereas the difference was only 11% in the contralateral sides between groups. The ratio of oxygen supply to consumption was lower in the ischemic than in the nonischemic regions in both groups. In the ischemic cortex, this ratio was significantly lower in the control group (1.7+/-0.1) than in the L-NAME group (1.9+/-0.1). In contrast, the ratio tended to be decreased by L-NAME in nonischemic regions.
CONCLUSIONS
These observations suggest that despite a decrease in cerebral blood flow, inhibition of nitric oxide synthesis mildly improves the oxygen supply and consumption balance in the ischemic cortex.

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